Methods of identifying a subject for treatment with antibodies against oxidized low density lipoprotein using pericoronary fat attenuation index

Abstract

The disclosure provides methods of identifying a subject for treatment with an anti-ox-LDL antibody. The disclosure also provides methods of treating a subject with an anti-ox-LDL antibody, wherein the subject has been identified to as a candidate for anti-oxLDL antibody therapy. The methods described herein use computed tomography to identify subjects who are a candidate for anti-oxLDL antibody therapy, wherein a subject may be determined to be a candidate for anti-oxLDL antibody therapy by evaluating their fat attenuation index (FAI), perivascular adipose tissue (PVAT), pericoronary adipose tissue, FAI score, FAI percentile, or CaRi-Heart® Risk score.

Description

[0001]ATTORNEY DOCKET NO: 51473-028WO2 PATENT METHODS OF IDENTIFYING A SUBJECT FOR TREATMENT WITH ANTIBODIES AGAINST OXIDIZED LOW DENSITY LIPOPROTEIN USING PERICORONARY FAT ATTENUATION INDEX SEQUENCE LISTING The instant application contains a Sequence Listing which has been submitted electronically in XML format and is hereby incorporated by reference in its entirety. Said XML copy, created on January 6, 2025 is named “51473-028WO2_Sequence_Listing_1_3_25.xml” and is 11,397 bytes in size. BACKGROUND Oxidized low-density lipoprotein (oxLDL) is a proinflammatory mediator that is formed as a result of oxidative modification of LDL in tissue. OxLDL is most commonly associated with the development of atherosclerosis, which can have detrimental cardiovascular (CV) outcomes, including myocardial infarction, stroke, and death. Additionally, studies have linked oxLDL with disease progression in the context of inflammation in systemic lupus erythematosus (SLE), rheumatoid and associated arthritis, psoriasis, and cancer. OxLDL signals through various cellular scavenger receptors, including A-type scavenger receptors (SR-A), cluster of differentiation 36 (CD36), SRB1, dendritic cell-specific C-type lectin (DC-SIGN), CD68, mucin, Toll-like receptor (TLR) 4 and lectin-like oxLDL receptor-1 (LOX-1). Most of these receptors are expressed by endothelial cells, macrophages, smooth muscle cells, fibroblasts, and platelets. Additionally, LOX-1 is secreted in soluble form. Several studies have shown that oxLDL signaling through LOX-1 plays a major role in atherosclerosis development and progression along with a number of other diseases and conditions, while CD36 and TLR4 have also been associated with CV inflammation and metabolic dysfunction in diseases such as diabetes and fatty liver disease. Therefore, there remains a need to identify subjects and identify them earlier that would benefit from treatment with an ox-LDL antibody. SUMMARY OF THE INVENTION In an aspect, the disclosure provides a method of treating a subject in need thereof comprising: administering to the subject a therapeutically effective amount of an antibody or fragment thereof that binds to oxidized low density lipoprotein (oxLDL) if the subject is identified as being a candidate for anti- oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary fat attenuation index (FAI) of the blood vessel. In another aspect, the disclosure provides a method of identifying a subject as being a candidate for anti-oxLDL antibody therapy comprising using a computed tomography scan of a blood vessel in the subject to measure the pericoronary FAI of the blood vessel to identify the subject as being a candidate for anti-oxLDL antibody therapy. In another aspect, the disclosure provides a method preventing or reducing the risk of myocardial infarction in a subject comprising administering to the subject a therapeutically effect amount of an antibody or fragment thereof that binds to oxLDL, if the subject is identified as being a candidate for anti- oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary FAI of the blood vessel. ATTORNEY DOCKET NO: 51473-028WO2 PATENT In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a right coronary artery (RCA) FAI of ≥ -85 Hounsfield units (HU) (e.g., -86 HU, - 87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a left anterior descending artery (LAD) FAI of ≥ -85 HU (e.g., -86 HU, -87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a left circumflex artery (LCX) FAI of ≥ -81 HU (e.g., -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, -87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI Score of ≥ 2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI Score of ≥ 2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI Score of ≥ 3 (e.g., 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA Percentile of ≥ 28 (e.g., ≥29, ≥30, ≥35, ≥40, ≥45, ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD Percentile of ≥ 20 (e.g., ≥21, ≥ 22, ≥ 23, ≥25, ≥30, ≥35, ≥40, ≥45, ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX Percentile of ≥ 33 (e.g., ≥34, ≥35, ≥40, ≥45, ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi- Heart® Risk Score of >1.4 (e.g., ≥1.5, ≥ 1.6, ≥1.7, ≥1.8, ≥1.9, ≥2, ≥3, ≥4, ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, or ≥19). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a RCA FAI of ≥ -88 HU (e.g., -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, - 116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI of ≥ -80 HU (e.g., -81 HU, -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, -87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, - 106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a ATTORNEY DOCKET NO: 51473-028WO2 PATENT candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI of ≥ -72 HU (e.g., -72 HU, -73 HU, -74 HU, -75 HU, -76 HU, -77 HU, -78 HU, -79 HU, -80 HU, -81 HU, -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, -87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, - 110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI Score of ≥ 2.4 (e.g., 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI Score of ≥ 5 (e.g., 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI Score of ≥ 7 (e.g., 7, 8, 9, 10, 11, 12, 13, 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA Percentile of ≥ 14 (e.g., 14, 15, 1617, 18, 19, or 20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD Percentile of ≥ 48 (e.g., ≥48, ≥49, ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95); (ix) a LCX Percentile of ≥ 62 (e.g., ≥62, ≥63, ≥64, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi- Heart® Risk Score of >4.5 (e.g., ≥4.7, ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, or ≥19). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a RCA FAI of ≥ -70 HU (e.g., -70 HU, -71 HU, -72 HU, -73 HU, -74 HU, -75 HU, -76 HU, -77 HU, -78 HU, -79 HU, -80 HU, -81 HU, -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, 87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI of ≥ -73 HU (e.g., -73 HU, -74 HU, -75 HU, -76 HU, -77 HU, -78 HU, -79 HU, -80 HU, -81 HU, -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, 87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, - 94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, -104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, - 116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX) FAI of ≥ -67 HU (e.g., -67 HU, -68 HU, -69 HU -70 HU, -71 HU, -72 HU, -73 HU, -74 HU, -75 HU, -76 HU, -77 HU, -78 HU, -79 HU, - 80 HU, -81 HU, -82 HU, -83 HU, -84 HU, -85 HU, -86 HU, 87 HU, -88 HU, -89 HU, -90 HU, -91 HU, -92 HU, -93 HU, -94 HU, -95 HU, -96 HU, -97 HU, -98 HU, -99 HU, -100 HU, -101 HU, -102 HU, -103 HU, - 104 HU,-105 HU, -106 HU, -107 HU, -108 HU, -109 HU, -110 HU, -111 HU, -112 HU, -113 HU, -114 HU, -115 HU, -116 HU, -117 HU, -118 HU, -119 HU, or -120 HU). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI Score of ≥ 18 (e.g., ≥18, ≥19, or ≥20); (v) a LAD FAI Score of ≥ 10 (e.g., ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI Score of ≥ 9 (e.g., (e.g., ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ATTORNEY DOCKET NO: 51473-028WO2 PATENT ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has an RCA Percentile of ≥ 80 (e.g., 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, or 99). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD Percentile of ≥ 75 (e.g., 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, or 99). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX Percentile of ≥ 85 (e.g., 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, or 99). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi-Heart® Risk Score of >18 (e.g., ≥18, ≥19, or ≥20). In some embodiments, the subject is between the age of 30 and 39. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI score of ≥ 3 (e.g., ≥3, ≥4, ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI score of ≥ 3 (e.g., ≥3, ≥4, ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI Score ≥ 3 (e.g., ≥3, ≥4, ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi-Heart® Risk Score >4 (e.g., >4.5, >5, >6, ≥7, >8, >9, >10, >11, >12, >13, >14, >15, >16, >17, ≥18, or >19). In some embodiments, the subject is between the age of 40 and 59. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI score of ≥ 5 (e.g., ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI score of ≥ 5 (e.g., ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has a LCX FAI Score ≥ 5 (e.g., ≥5, ≥6, ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi-Heart® Risk Score ≥ 7 (e.g., ≥7, ≥8, ≥9, ≥10, ≥11, ≥12, ≥13, ≥14, ≥15, ≥16, ≥17, ≥18, ≥19, or ≥20). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a RCA percentile ≥ 50 (e.g., ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD percentile ≥ 50 (e.g., ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX percentile ≥ 50 (e.g., ≥50, ≥55, ≥60, ≥65, ≥70, ≥75, ≥80, ≥85, ≥90, or ≥95). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a RCA percentile ≥ 90 (e.g., 90, 91, 92, 93, 94, 95, 96, 97, 98, or 99). In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD percentile ≥ 90 (e.g., 90, 91, 92, 93, 94, 95, 96, 97, 98, or 99). In some embodiments, the ATTORNEY DOCKET NO: 51473-028WO2 PATENT subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi- Heart® Risk Score of >10. In some embodiments, the antibody or fragment thereof comprises at least one light chain complementarity determining region (LCDRs) that is at least 90% identical to an LCDR selected from the group consisting of SEQ ID NO: 7, SEQ ID NO: 8, and SEQ ID NO: 9. In some embodiments, the antibody or fragment thereof comprises at least one LCDR selected from the group consisting of SEQ ID NO: 7, SEQ ID NO: 8, and SEQ ID NO: 9. In some embodiments, the antibody or fragment thereof comprises at least one heavy chain complementarity determining region (HCDRs) that is at least 90% identical to a HCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO: 6. In some embodiments, the antibody or fragment thereof comprises at least one HCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO: 6. In some embodiments, the antibody or fragment thereof comprises a variable heavy region (VH) of SEQ ID NO: 10, a variable light region (VL) of SEQ ID NO: 11, or both. In some embodiments, the antibody or fragment thereof comprises a heavy chain of SEQ ID NO: 2, a light chain of SEQ ID NO: 3, or both. In some embodiments, the antibody is orticumab. In some embodiments, the subject has been diagnosed with a disease or condition. In some embodiments, the subject has been previously treated for a disease or condition. In some embodiments, the disease or condition comprises psoriasis, accelerated atherosclerosis, systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s Syndrome, Fabry disease, psoriatic arthritis, or a cardiovascular disease. In some embodiments, the cardiovascular disease comprises aortic valve stenosis or aortic valve sclerosis. In some embodiments, orticumab is administered subcutaneously or intravenously. In some embodiments, the risk of fatal myocardial infarction is reduced by at least 20% in comparison to a subject who is not administered orticumab. In an aspect, the disclosure provides an antibody or fragment thereof that binds to oxLDL for use in the treatment of a subject in need thereof, wherein the antibody or fragment thereof that binds to oxLDL is administered to the subject who is identified as being a candidate for anti-oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary fat attenuation index (FAI) of the blood vessel BRIEF DESCRIPTION OF THE FIGURES Exemplary embodiments are illustrated in referenced figures. It is intended that the embodiments and figures disclosed herein are to be considered illustrative rather than restrictive. FIG.1 is a schematic of the clinical study performed to assess the effect of orticumab on adults with moderate to severe psoriasis and cardiometabolic risk factors. FIGS.2A-2C are bar graphs showing the absolute change in FAI Scores (FIG.2A) and absolute change in CaRi-Heart Risk assessments (FIG.2B), and CaRi-Heart Risk measurements pre-treatment and post-treatment (FIG.2C) of the right coronary artery (RCA), left anterior descending artery (LAD), and left circumflex artery (LCX) in patients receiving orticumab treatment or placebo from the whole population. FIGS.3A-3C are bar graphs showing absolute change in FAI Scores (FIG.3A) and absolute change in CaRi-Heart Risk assessments (FIG.3B), and CaRi-Heart Risk measurements pre-treatment ATTORNEY DOCKET NO: 51473-028WO2 PATENT and post-treatment (FIG.3C) of three coronary arteries (RCA, LAD, and LCX) in patients receiving orticumab treatment or placebo of a high-risk population. All subjects were identified as to have elevated inflammatory risk, which was determined as patients who had a pretreatment FAI score of ≥ 50thpercentile in the RCA, LAD, or LCX arteries. FIGS.4A and FIG.4B are bar graphs showing absolute change in FAI Scores (FIG.4A) and CaRi-Heart Risk assessment before and after treatment (FIG.4B) of three coronary arteries (RCA, LAD, and LCX) in patients receiving orticumab treatment or placebo for a low-risk population. All subjects were identified as to have low inflammatory risk, which was determined as patients who had a pretreatment FAIscore of<50th percentile in the RCA, LAD, or LCX arteries.FIG.5 is representative images of changes in FAI score in the RCA and LAD in response to orticumab treatment and placebo. Definitions Terms used in the claims and specification are defined as set forth below unless otherwise specified. It must be noted that, as used in the specification and the appended claims, the singular forms “a,” “an,” and “the” include plural referents unless the context clearly dictates otherwise. As used herein, “about” will be understood by persons of ordinary skill and will vary to some extent depending on the context in which it is used. If there are uses of the term which are not clear to persons of ordinary skill given the context in which it is used, “about” will mean up to plus or minus 10% of the particular value. “Administering” and “administer,” as used herein, refer to any route for delivering a pharmaceutical composition to a subject. Routes of delivery may include non-invasive peroral (through the mouth), topical (skin), transmucosal (nasal, buccal / sublingual, vaginal, ocular and rectal) and inhalation routes, as well as parenteral routes, and other methods known in the art. Parenteral refers to a route of delivery that is generally associated with injection, including intraorbital, infusion, intraarterial, intracarotid, intracapsular, intracardiac, intradermal, intramuscular, intraperitoneal, intrapulmonary, intraspinal, intrasternal, intrathecal, intrauterine, intravenous, subarachnoid, subcapsular, subcutaneous, transmucosal, or transtracheal. Via the parenteral route, the compositions may be in the form of solutions or suspensions for infusion or for injection, or as lyophilized powders. As used herein, the terms “antibody” and “antibodies” are meant in a broad sense and includes immunoglobulin molecules including polyclonal antibodies, monoclonal antibodies including murine, human, human-adapted, humanized and chimeric monoclonal antibodies, antibody fragments, bispecific or multispecific antibodies, dimeric, tetrameric or multimeric antibodies, and single chain antibodies. Immunoglobulins can be assigned to five major classes, namely IgA, IgD, IgE, IgG and IgM, depending on the heavy chain constant domain amino acid sequence. IgA and IgG are further sub- classified as the isotypes IgA1, IgA2, IgG1, IgG2, IgG3 and IgG4. Antibody light chains of any vertebrate species can be assigned to one of two clearly distinct types, namely kappa (κ) and lambda (λ), based on the amino acid sequences of their constant domains. As used herein, the term “antibody fragment” refers to a portion of an immunoglobulin molecule that retains the heavy chain and / or the light chain antigen binding site, such as heavy chain ATTORNEY DOCKET NO: 51473-028WO2 PATENT complementarity determining regions (HCDR) 1, 2 and 3, light chain complementarity determining regions (LCDR) 1, 2 and 3, a heavy chain variable region (VH), or a light chain variable region (VL). Antibody fragments include a Fab fragment, a monovalent fragment consisting of the VL, VH, CL and CHI domains; a F(ab)2 fragment, a bivalent fragment comprising two Fab fragments linked by a disulfide bridge at the hinge region; a Fd fragment consisting of the VH and CHI domains; a Fv fragment consisting of the VL and VH domains of a single arm of an antibody; a domain antibody (dAb) fragment (Ward et al (1989) Nature 341:544-546), which consists of a VH domain. VH and VL domains can be engineered and linked together via a synthetic linker to form various types of single chain antibody designs where the VH / VL domains pair intramolecularly, or intermolecularly in those cases when the VH and VL domains are expressed by separate single chain antibody constructs, to form a monovalent antigen binding site, such as single chain Fv (scFv) or diabody; described for example in PCT Intl. Publ. NOs WO1998 / 44001, WO1988 / 01649, WO1994 / 13804, and WO1992 / 01047. These antibody fragments are obtained using well known techniques known to those of skill in the art, and the fragments are screened for utility in the same manner as are full length antibodies. “Beneficial results” may include, but are in no way limited to, lessening or alleviating the severity of the disease condition, preventing the disease condition from worsening, curing the disease condition, preventing the disease condition from developing, lowering the chances of a subject developing the disease condition and / or prolonging a subject’s life or life expectancy. In some embodiments, the disease condition is psoriasis, atherosclerosis, accelerated atherosclerosis, systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s Syndrome, Fabry disease, psoriatic arthritis, or a cardiovascular disease. “Bind” in reference to the interaction between antibody and epitope, “selectively binds” or “specifically binds” refers to the ability of an antibody or antibody fragment thereof described herein to bind to a target, such as a molecule present on the cell-surface, with a KD 10-5M (10000 nM) or less, e.g., 10-6M, 10-7M, 10-8M, 10-9M, 10-10M, 10-11M, 10-12M, or less. Specific binding can be influenced by, for example, the affinity and avidity of the polypeptide agent and the concentration of polypeptide agent. The person of ordinary skill in the art can determine appropriate conditions under which the polypeptide agents described herein selectively bind the targets using any suitable methods, such as titration of a polypeptide agent in a suitable cell binding assay. A “cardiovascular disease,” as used herein, refers to a disorder of the heart and blood vessels, and includes disorders of the arteries, veins, arterioles, venules, and capillaries. Non-limiting examples of cardiovascular diseases include congestive heart failure, arrhythmia, pericarditis, acute myocardial infarction, infarcted myocardium, coronary artery disease, coronary heart disease, ischemic heart disease, cardiomyopathy, stroke, hypertensive heart disease, heart failure, pulmonary heart disease, ischemic syndrome, coronary microvascular disease, cardiac dysrhythmias, rheumatic heart disease, aortic aneurysms, atrial fibrillation, congenital heart disease, endocarditis, inflammatory heart disease, endocarditis, inflammatory cardiomegaly, myocarditis, valvular heart disease, cerebrovascular disease, and peripheral artery disease, or any combination thereof. As used herein the term “a candidate for anti-oxLDL antibody therapy” refers to a subject who has been identified for administration of an anti-oxLDL antibody based on their fat attenuation index (FAI), FAI score, FAI percentile, or CaRi-Heart® Risk score as determined by using a computed tomography to scan of a blood vessel (e.g., RCA, LAD, or LCX) to measure perivascular adipose tissue present in the ATTORNEY DOCKET NO: 51473-028WO2 PATENT blood vessel. In some embodiments, a subject is considered to be a candidate for anti-oxLDL antibody therapy if the subject has a right coronary artery (RCA) FAI of ≥ -72 Hounsfield units (HU), a left anterior descending artery (LAD) FAI of ≥ -72 HU, a left circumflex artery (LCX) FAI of ≥ -72 HU, an RCA FAI Score of ≥ 10, a LAD FAI Score of ≥ 10; a LCX FAI Score of ≥ 6; an RCA Percentile of ≥ 70; a LAD Percentile of ≥ 70; a LCX Percentile of ≥ 95, or a CaRi-Heart® Risk Score of >9; or, if the subject is between the ages of 30 and 39 years old, an RCA FAI score of ≥ 3, a LAD FAI score of ≥ 3, a LCX FAI Score ≥ 3, or a CaRi-Heart® Risk Score >4; or, if the subject is between the ages of 50 and 59, an RCA FAI score of ≥ 5, a LAD FAI score of ≥ 5, a LCX FAI Score ≥ 5, or a CaRi-Heart® Risk Score ≥ 7. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a right coronary artery (RCA) FAI of ≥ --85 HU; a left anterior descending artery (LAD) FAI of ≥ -85 HU; a left circumflex artery (LCX) FAI of ≥ -81 HU; an RCA FAI Score of ≥ 2; a LAD FAI Score of ≥ 2; a LCX FAI Score of ≥ 3; an RCA Percentile of ≥ 28; a LAD Percentile of ≥ 20; a LCX Percentile of ≥ 33; or a CaRi-Heart® Risk Score of >1.4. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has RCA FAI of ≥ --88 HU; a LAD FAI of ≥ -80 HU; a LCX FAI of ≥ -72 HU; an RCA FAI Score of ≥ 2.4; a LAD FAI Score of ≥ 5; a LCX FAI Score of ≥ 7; an RCA Percentile of ≥ 14; a LAD Percentile of ≥ 48; a LCX Percentile of ≥ 62; or a CaRi-Heart® Risk Score of >4.5. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has RCA FAI of ≥ -70 HU; a LAD FAI of ≥ -73 HU; a LCX FAI of ≥ -67 HU; an RCA FAI Score of ≥ 18; a LAD FAI Score of ≥ 10; a LCX FAI Score of ≥ 9; an RCA Percentile of ≥ 80; a LAD Percentile of ≥ 75; a LCX Percentile of ≥ 85; or a CaRi-Heart® Risk Score of >18. An antibody variable region consists of a “framework” region interrupted by three “antigen binding sites.” The antigen binding sites are defined using various terms such as Complementarity Determining Regions (CDRs), three in the VH (HCDR1, HCDR2, HCDR3), and three in the VL (LCDR1, LCDR2, LCDR3), are based on sequence variability (Wu and Kabat J Exp Med 132:211-50, 1970; Kabat et al Sequences of Proteins of Immunological Interest, 5thEd. Public Health Service, National Institutes of Health, Bethesda, Md., 1991) or “Hypervariable regions”, “HVR”, or “HV”, three in the VH (H1, H2, H3) and three in the VL (L1, L2, L3), refer to the regions of an antibody variable domains which are hypervariable in structure as defined by Chothia and Lesk (Chothia and Lesk Mol Biol 196:901-17, 1987). Other terms include “IMGT-CDRs” (Lefranc et al., Dev Comparat Immunol 27:55-77, 2003) and “Specificity Determining Residue Usage” (SDRU) (Almagro, Mol Recognit 17:132-43, 2004). The International ImMunoGeneTics (IMGT) database provides a standardized numbering and definition of antigen-binding sites. The correspondence between CDRs, HVs and IMGT delineations is described in Lefranc et al., Dev Comparat Immunol 27:55-77, 2003. The term “effective amount” as used herein refers to the amount of a pharmaceutical composition to decrease at least one or more symptom of the disease or disorder and relates to a sufficient amount of pharmacological composition to provide the desired effect. The phrase “therapeutically effective amount” as used herein means a sufficient amount of the composition to treat a disorder, at a reasonable benefit / risk ratio applicable to any medical treatment. In various embodiments, the pharmaceutical compositions described herein further comprise a pharmaceutically acceptable carrier. In some embodiments, a therapeutic pharmaceutical composition is used, for example, to treat, inhibit, reduce the ATTORNEY DOCKET NO: 51473-028WO2 PATENT severity of and / or, reduce duration of psoriasis, or inflammation of one or more arteries, and / or related symptoms in a subject in need thereof. A therapeutically or prophylactically significant reduction in a symptom is, e.g., at least 5%, at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 100%, or more in a measured parameter as compared to a control or non- treated subject or the state of the subject prior to administering the compositions described herein. Measured or measurable parameters include clinically detectable markers of disease, for example, elevated or depressed levels of a biological marker, as well as parameters related to a clinically accepted scale of symptoms or markers for psoriasis and / or atherosclerosis. It will be understood, however, that the total daily usage of the compositions and formulations as disclosed herein will be decided by the attending physician within the scope of sound medical judgment. The exact amount required will vary depending on factors such as the type of disease being treated, gender, age, and weight of the subject. “Ineffective” treatment refers to when a subject is administered a treatment and there is less than 1%, 2%, 3%, 4% or 5%, improvement in symptoms. The term “epitope,” as used herein, means a portion of an antigen to which an antibody specifically binds. Epitopes usually consist of chemically active (such as polar, non-polar or hydrophobic) surface groupings of moieties such as amino acids or polysaccharide side chains and can have specific three-dimensional structural characteristics, as well as specific charge characteristics. An epitope can be composed of contiguous and / or discontiguous amino acids that form a conformational spatial unit. For a discontiguous epitope, amino acids from differing portions of the linear sequence of the antigen come in close proximity in 3-dimensional space through the folding of the protein molecule. As used herein, the term “Fc domain” refers to a dimer of two Fc domain monomers that is capable of binding an Fc receptor through the interaction between the two CH3 antibody constant domains. As used herein, the term “Fc domain monomer” refers to a polypeptide chain that includes that includes at least a hinge domain and second and third antibody constant domains (CH2 and CH3) or functional fragments thereof (e.g., fragments that that capable of (i) dimerizing with another Fc domain monomer to form an Fc domain, and (ii) binding to an Fc receptor. The Fc domain monomer can be any immunoglobulin antibody isotype, including IgG, IgE, IgM, IgA, or IgD (e.g., IgG). Additionally, the Fc domain monomer can be an IgG subtype (e.g., IgG1, IgG2a, IgG2b, IgG3, or IgG4) (e.g., IgG1). An Fc domain monomer does not include any portion of an immunoglobulin that is capable of acting as an antigen-recognition region, e.g., a variable domain or a complementarity determining region (CDR). Fc domain monomers in the conjugates as described herein can contain one or more changes from a wild- type Fc domain monomer sequence (e.g., 1-10, 1-8, 1-6, 1-4 amino acid substitutions, additions, or deletions) that alter the interaction between an Fc domain and an Fc receptor. Examples of suitable changes are known in the art. Unless otherwise specified herein, numbering of amino acid residues in the IgG or Fc domain monomer is according to the EU numbering system for antibodies, also called the Kabat EU index, as described, for example, in Kabat et al., Sequences of Proteins of Immunological Interest, 5thEd. Public Health Service, National Institutes of Health, Bethesda, MD, 1991. “Framework” or “framework sequences” are the remaining sequences of a variable region other than those defined to be antigen binding sites. Because the antigen binding sites can be defined by ATTORNEY DOCKET NO: 51473-028WO2 PATENT various terms as described above, the exact amino acid sequence of a framework depends on how the antigen-binding site was defined. “Human antibody” refers to an antibody having heavy and light chain variable regions in which both the framework and the antigen binding sites are derived from sequences of human origin. If the antibody contains a constant region, the constant region also is derived from sequences of human origin. “Humanized antibody” refers to an antibody in which the antigen binding sites are derived from non-human species and the variable region frameworks are derived from human immunoglobulin sequences. Humanized antibodies may include substitutions in the framework regions so that the framework may not be an exact copy of expressed human immunoglobulin or germline gene sequences. “Human-adapted” antibodies or “human framework adapted (HFA)” antibodies refer to humanized antibodies adapted according to methods described in U.S. Pat. Publ. No. US2009 / 0118127. Human- adapted antibodies are humanized by selecting the acceptor human frameworks based on the maximum CDR and FR similarities, length compatibilities and sequence similarities of CDR1 and CDR2 loops and a portion of light chain CDR3 loops. A human antibody comprises heavy or light chain variable regions that are “derived from” sequences of human origin wherein the variable regions of the antibody are obtained from a system that uses human germline immunoglobulin or rearranged immunoglobulin genes. Such systems include human immunoglobulin gene libraries displayed on phage, and transgenic non-human animals such as mice carrying human immunoglobulin loci as described herein. A “human antibody” may contain amino acid differences when compared to the human germline or rearranged immunoglobulin sequences due to for example naturally occurring somatic mutations or intentional introduction of substitutions in the framework or antigen binding sites. Typically, a human antibody is at least about 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99% or 100% identical in amino acid sequence to an amino acid sequence encoded by a human germline or rearranged immunoglobulin gene. In some cases, “human antibody” may contain consensus framework sequences derived from human framework sequence analyses, for example as described in Knappik et al., J Mol Biol 296:57-86, 2000), or synthetic HCDR3 incorporated into human immunoglobulin gene libraries displayed on phage, for example as described in Shi et al., J Mol Biol 397:385-96, 2010 and Intl. Pat. Publ. No. WO2009 / 085462. Antibodies in which antigen binding sites are derived from a non-human species are not included in the definition of human antibody. The term “in combination with” as used herein means that two or more therapeutics can be administered to a subject together in a mixture, concurrently as single agents or sequentially as single agents in any order. The term “monoclonal antibody” as used herein refers to a preparation of antibody molecules of single molecular composition. A monoclonal antibody composition displays a single binding specificity and affinity for a particular epitope, or in a case of a bispecific monoclonal antibody, a dual binding specificity to two distinct epitopes. As used herein, the term “psoriatic arthritis” refers to a form of inflammatory arthritis that affects some people who have psoriasis—a condition that features red patches of skin topped with silvery scales. For psoriatic arthritis, most people develop psoriasis first and are later diagnosed with psoriatic arthritis, but the joint problems can sometimes begin before skin lesions appear. ATTORNEY DOCKET NO: 51473-028WO2 PATENT The term “recombinant antibody” as used herein, includes all antibodies that are prepared, expressed, created or isolated by recombinant means, such as antibodies isolated from an animal (e.g., a mouse) that is transgenic or transchromosomal for human immunoglobulin genes or a hybridoma prepared therefrom (described further below), antibodies isolated from a host cell transformed to express the antibody, antibodies isolated from a recombinant, combinatorial antibody library, and antibodies prepared, expressed, created or isolated by any other means that involve splicing of human immunoglobulin gene sequences to other DNA sequences, or antibodies that are generated in vitro using Fab arm exchange such as bispecific antibodies. “Rheumatoid arthritis” is an autoimmune disease in which the body’s immune system – which normally protects its health by attacking foreign substances like bacteria and viruses – mistakenly attacks the joints. This creates inflammation that causes the tissue that lines the inside of joints (the synovium) to thicken, resulting in swelling and pain in and around the joints. The synovium makes a fluid that lubricates joints and helps them move smoothly. Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows, knees, and ankles. The joint effect is usually symmetrical. That means if one knee or hand if affected, usually the other one is, too. Because RA also can affect body systems, such as the cardiovascular or respiratory systems, it is called a systemic disease. Symptoms of rheumatoid arthritis include, but are not limited to, joint pain, tenderness, swelling or stiffness for six weeks or longer; morning stiffness for 30 minutes or longer; more than one joint is affected; small joints (wrists, certain joints of the hands and feet) are affected; and the same joints on both sides of the body are affected. “Variant” as used herein refers to a polypeptide or a polynucleotide that differs from a reference polypeptide or a reference polynucleotide by one or more modifications for example, substitutions, insertions or deletions. The term “statistically significant” or “significantly” refers to statistical evidence that there is a difference. It is defined as the probability of making a decision to reject the null hypothesis when the null hypothesis is actually true. The decision is often made using the p-value. By “substantially identical” is meant a nucleic acid or amino acid sequence that, when optimally aligned, for example using the methods described below, share at least 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% sequence identity with a second nucleic acid or amino acid sequence. “Substantial identity” may be used to refer to various types and lengths of sequence, such as full-length sequence, epitopes or immunogenic peptides, functional domains, coding and / or regulatory sequences, exons, introns, promoters, and genomic sequences. Percent identity between two polypeptides or nucleic acid sequences is determined in various ways that are within the skill in the art, for instance, using publicly available computer software such as Smith Waterman Alignment (Smith, T. F. and M. S. Waterman (1981) J Mol Biol 147:195-7); “BestFit” (Smith and Waterman, Advances in Applied Mathematics, 482-489 (1981)) as incorporated into GeneMatcher Plus™, Schwarz and Dayhof (1979) Atlas of Protein Sequence and Structure, Dayhof, M. O., Ed pp 353-358; BLAST program (Basic Local Alignment Search Tool; (Altschul, S. F., W. Gish, et al. (1990) J Mol Biol 215: 403-10), BLAST-2, BLAST- P, BLAST-N, BLAST-X, WU-BLAST-2, ALIGN, ALIGN-2, CLUSTAL, or Megalign (DNASTAR) software. In addition, those skilled in the art can determine appropriate parameters for measuring alignment, including any algorithms needed to achieve maximal alignment over the length of the sequences being compared. In general, for proteins, the length of comparison sequences will be at least 10 amino acids, ATTORNEY DOCKET NO: 51473-028WO2 PATENT preferably 20, 30, 40, 50, 60, 70, 80, 90, 100, 110, 120, 130, 140, 150, 200, 250, 300, 350, or 400 amino acids or more. For nucleic acids, the length of comparison sequences will generally be at least 25, 50, 100, 125, 150, 200, 250, 300, 350, 400, 450, 500, 550, 600, 650, 700, 800, 900, 1000, 1100, or 1200 or more. It is understood that for the purposes of determining sequence identity when comparing a DNA sequence to an RNA sequence, a thymine nucleotide is equivalent to an uracil nucleotide. Conservative substitutions typically include substitutions within the following groups: glycine, alanine; valine, isoleucine, leucine; aspartic acid, glutamic acid, asparagine, glutamine; serine, threonine; lysine, arginine; and phenylalanine, tyrosine. “Subject,” “individual,” “animal,” “patient,” and “mammal” are meant any subject, particularly a mammalian subject, for whom diagnosis, prognosis, or therapy is desired. Mammalian subjects include, but are not limited to, humans, domestic animals, farm animals, zoo animals, sport animals, pet animals such as guinea pigs, rabbits, rats, mice, cattle; primates such as apes, monkeys, orangutans, and chimpanzees; canids such as dogs and wolves; felids such as cats, lions, and tigers; equids such as horses, donkeys, and zebras; food animals such as cows, pigs, and sheep; and ungulates such as deer and giraffes. In certain embodiments, the mammal is a human subject. As used herein, the terms “treat,” “treatment,” “treating,” and “amelioration,” when used in reference to a disease, disorder or medical condition, refer to both therapeutic treatment and prophylactic or preventative measures, wherein the object is to prevent, reverse, alleviate, ameliorate, inhibit, lessen, slow down or stop the progression or severity of a symptom or condition. The term “treating” includes reducing or alleviating at least one adverse effect or symptom of a condition. Treatment is generally “effective” if one or more symptoms or clinical markers are reduced. Alternatively, treatment is “effective” if the progression of a disease-state is reduced or halted. That is, “treatment” includes not just the improvement of symptoms or markers, but also a cessation or at least slowing of progress or worsening of symptoms that would be expected in the absence of treatment. Also, “treatment” may mean to pursue or obtain beneficial results or lower the chances of the individual developing the condition even if the treatment is ultimately unsuccessful. Those in need of treatment include those already with the condition as well as those prone to have the condition or those in whom the condition is to be prevented. As used herein, the terms “pericoronary vascular adipose tissue,” “PVAT,” and “coronary PVAT attenuation” describe the average coronary computed tomography angiography (CCTA) attenuation in Hounsfield units (HU) of the adipose tissue inside the designated volume of interest, while adipose tissue may be defined as all voxels having attenuation between −190 and −30 HU. As used herein, the term “perivascular FAI” and “FAI” is defined as the weighted mean attenuation of all adipose tissue-containing voxels (−190 to −30 HU) lying within a radial distance from the outer vessel wall equal to the diameter of the relevant vessel around the coronary vessels. To avoid the effects of the aortic wall, the most proximal 10 mm segment may be excluded as well as the proximal 10– 50 mm of the coronary vessel in most of the studies. DETAILED DESCRIPTION The present disclosure features methods of treating a subject in need thereof by administering to the subject antibodies and antibody fragments capable of binding to oxidized-low density lipoproteins (ox- LDL). The present disclosure also provides methods of evaluating subjects for treatment with an antibody ATTORNEY DOCKET NO: 51473-028WO2 PATENT and antibody fragments capable of binding to ox-LDL. These subjects have been identified as being a candidate for anti-oxLDL antibody therapy. A subject may be identified as being a candidate for anti- oxLDL antibody therapy using computed tomography to assess one or more blood vessels in the subject. In some embodiments, a subject is determined to be a candidate for anti-oxLDL antibody therapy based on their associated fat attenuation (FAI), FAI score, FAI percentile, or CaRi-Heart® Risk score. It has presently been discovered that FAI, FAI score, FAI percentiles, and CaRi-Heart® Risk scores can be used to identify subjects that would be candidates for treatment with an anti-oxLDL antibody. The following sections provide a detailed description of the methods used to identify subjects for treatment with an anti-oxLDL antibody. Diagnostic Methods The disclosure provides methods of treating a subject with antibodies or antibody fragments capable of binding to ox-LDL, wherein the subject has been identified as being a candidate for anti-oxLDL antibody therapy. The disclosure also provides methods for evaluating a subject, wherein the method includes identifying the subject as a candidate for anti-oxLDL antibody therapy. A subject may be determined to be a candidate for anti-oxLDL antibody therapy using computed tomography (CT) to scan a blood vessel of the subject. For example, the computed tomography may be coronary computed tomography angiography (CCTA). The scan may be used to characterize the severity of the inflammation of the blood vessel. For example, the CT scan may be used measure the inflammation of the vessel wall by measuring the ratio of the thickness of the vascular wall to the thickness of the perivascular adipose tissue (PVAT) within the blood vessel. In some embodiments, a report is generated (e.g., a CaRi-Heart® report (Caristo Diagnostics)). Accordingly, a subject may be identified to be a candidate for anti-oxLDL antibody therapy by assessment of the subject’s fat attenuation index (FAI), FAI score, FAI percentile, and / or CaRi-Heart® Risk score. The CaRi-Hear® Risk score may be obtained from a CaRi-Heart® report. In some embodiments, additional factors such as the subject’s age may be considered in conjunction with the FAI, FAI percentile, and / or CaRi-Heart® Risk score to identify the subject as a candidate for anti-oxLDL antibody therapy. Fat Attenuation Index (FAI) The FAI is an unadjusted, visual representation of the extent of coronary inflammation in the blood vessels of a subject. To determine the FAI, the coronary inflammation is assessed in the three main epicardial coronary arteries including the right coronary artery (RCA), the left anterior descending artery (LAD), and the left circumflex artery (LCX). A subject may be identified as a candidate for anti-oxLDL antibody therapy based the FAI that is measured in one or more of the subject’s blood vessels. For example, in some embodiments, a subject may be identified as a candidate for anti-oxLDL antibody therapy, if the subject has a RCA FAI of ≥ -72 Hounsfield units (HU), a LAD FAI of ≥ -72 HU; or a LCX FAI of ≥ -72 HU. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a right coronary artery (RCA) FAI of ≥ -70, -71, -72, -73, -74, -75, -76, -77, -78, - 79, -80, -81, -82, -83, -84, -85, -86, -87, -88, -98, or -90 HU. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI of ≥ -70, -71, -72, 73, -74, -75, -76, -77, -78, -79, -80, -81, -82, -83, -84, -85, -86, -87, -88, -98, or -90 HU. In some ATTORNEY DOCKET NO: 51473-028WO2 PATENT embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI of ≥ -65, -71, -72, -73, -74, -75, -76, -77, -78, -79, -80, -81, -82, -83, -84, -85, -86, -87, -88, -98, or -90 HU. In some embodiments, the subject has an RCA FAI of ≥ -70.01 HU. In some embodiments, the subject has an LAD FAI of ≥ -73.12 HU. In some embodiments, the subject has an LCX LAI of ≥ -67.15 HU. In some embodiments, the subject has an RCA FAI of ≥ –87.09 HU. In some embodiments, the subject has an LAD FAI of ≥ -79.25 HU. In some embodiments, the subject has an LCX FAI of ≥-71.92 HU. In some embodiments, the subject has an RCA FAI of ≥-84.53 HU. In some embodiments, the subject has an LAD FAI of ≥ -85.70 HU. In some embodiments, the subject has an LCX FAI of ≥ -80.17 HU. The FAI measures changes in PVAT composition which are driven by inflammatory signals coming from the inflamed coronary artery via analyzing the 3D gradients of perivascular tissue attenuation, which then is adjusted for technical factors as well as anatomical and biological factors pertaining to the subject. The FAI is the weighted mean attenuation of all adipose tissue-containing voxels lying within a radial distance from the outer wall of the blood vessel equal to the diameter of the relevant vessel around the coronary vessels. Specifically, PVAT is defined as adipose tissue located within a radial distance equal to the diameter of the respective vessel extending from the outer vessel wall. This is based on a biological definition of PVAT derived from adipose tissue biopsies from the perivascular area which demonstrate a different adipose tissue phenotype: having smaller adipocytes as well as lower expression of adipogenic genes and less lipophilic / greater aqueous phase close to the vessel compared with adipose tissue 2 cm away from the vascular wall. Additionally, this method of measuring may be employed as the mean attenuation of PVAT has been shown to be independent of lumen attenuation, thus avoiding a partial volume effect. FAI values may be calculated to avoid the effects of the aortic wall, such as, the most proximal 10 mm segment as well as the proximal 10–50 mm of the coronary vessel, which are commonly excluded from calculations. As described in Sagris et al., European Heart Journal – Cardiovascular Imaging, 23(12), Dec.2022, 526–553, which is herein incorporated by reference in its entirety, the proximal 40 mm segment of the left anterior descending coronary artery (LAD), the left circumflex coronary artery (LCX), and the right coronary artery (RCA) may be manually traced. The analysis may be performed by segmenting the perivascular area into 20 concentric cylindrical layers of 1 mm thickness each. Voxel attenuation histograms are plotted, and the mean attenuation of all voxels characterized as adipose tissue within this volume are defined as FAIPVAT. Next, the respective FAI index is calculated for adipose tissue in each of the 20 concentric cylindrical layers and is plotted against the radial distance from the outer vessel wall. On the other hand, FAInon-PVAT is defined as the FAI value of adipose tissue in the most distal cylindrical layer (2 cm away from the vascular wall). In order to describe the change in adipose tissue attenuation between PVAT and non-PVAT, the volumetric perivascular characterization index ( VPCI ) is created and defined as the % change from FAIPVAT to FAInon-PVAT[ VPCI = 100x(FAIPVAT- FAInon- PVAT) / | FAIPVAT | ]. VPCI correlates with the presence of “soft atherosclerotic plaques,” as defined by using the standard plaque analysis methodology. Further methods of determining the FAI for a subject using computed tomography are also disclosed in U.S. Patent 10,695,023, U.S. Patent Publication No. US 2022 / 0139005, International Patent ATTORNEY DOCKET NO: 51473-028WO2 PATENT Application WO 2016 / 024128; Oikonomou et al. Lancet, 10151(392), Sept.2018, 929-939; Antonopoulos et al., Sci. Transl. Med., 9, 2017; which are herein incorporated by reference in their entirety. FAI Score The FAI score quantifies the changes in the perivascular adipose tissue triggered by inflammatory signals derived from the vascular wall and provides a quantitative metric of coronary inflammation with major prognostic value. It may be used monitor the effectiveness of anti-inflammatory agents on coronary inflammation. The FAI score is an individualized quantification of coronary inflammation in the three main epicardial coronary arteries, adjusted for age and gender and can be viewed as a measure of disease activity. A subject may be identified as a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI Score of ≥ 10, a LAD FAI Score of ≥ 10, or a LCX FAI Score of ≥ 6. If a subject is between the ages of 30 and 39, the subject may be identified as a candidate for anti-oxLDL antibody therapy if they have an RCA FAI score of ≥ 5, a LAD FAI score of ≥ 5, or a LCX FAI Score ≥ 5. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has an RCA FAI Score of ≥ 18, 17, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, or 4. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LAD FAI Score of ≥ 10, 9, 8, 7, 6, 5, 3, or 2. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX FAI Score of ≥ 9, 8, 7, 6, 5, 4, 3, or 2. In some embodiments, the subject has an RCA FAI Score of ≥ 18.14. In some embodiments, the subject has an LAD FAI Score of 10.33. In some embodiments, the subject has an LCX FAI Score of ≥ 9.61. In some embodiments, the subject has an RCA FAI Score of ≥ 2.47. In some embodiments, the subject has an LAD FAI Score of ≥ 5.61. In some embodiments, the subject has an LCX FAI Score of ≥ 7.33. In some embodiments, the subject has an RCA FAI Score of 2.03. In some embodiments, the subject has an LAD FAI Score of ≥ 2.14. In some embodiments, the subject has an LCX FAI Score of ≥ 3.17. The FAI Score standardizes the FAI for technical, anatomical, and biological factors before its introduction in the clinic as a potential risk stratification. The FAI Score utilizes the power of artificial intelligence to standardize FAI values, as described above, from coronary arteries for a clinical metric of coronary inflammation. The score was initially standardized using 3912 individuals, with 2040 from the United States and 1872 from Europe, having a mean age of 55.7, 41.1% of whom were women; all underwent clinically indicated coronary computed tomography angiography (CCTA) as described in Oikonomou et al. (Lancet, 10151(392), Sept.2018, 929-939), which is herein incorporated by reference in its entirety. FAI Score is measured at baseline in the proximal RCA, LAD, and LCX. As described by Oikonomou et al. (European Journal of Preventive Cardiology, 28(1), May 2021), which is herein incorporated by reference in its entirety, a dissimilarity index may be computed to classify individuals based on pre-randomization characteristics according to the Gower distance, which is a metric of dissimilarity between two subjects based on mixed numeric and non-numeric data. For continuous variables, Gower distance represents the absolute value of the difference between a pair of individuals divided by the range across all individuals. For categorical variables, the method assigns “1” if the values are identical and “0” if they are not. A Gower distance may ultimately be calculated as the mean of these terms. Alternatively, the dissimilarity index can be computed based on cosine similarity or other similarity ATTORNEY DOCKET NO: 51473-028WO2 PATENT measures. For each subject, a topological neighborhood may be identified as the 5% most phenotypically similar participants based on Gower’s distance. In sensitivity analyses, random neighborhood sizes between 2.5% and 10% may be iteratively evaluated, assessing the correlation of effect estimates in these iterations with those derived from the 5% neighborhood size. Within each subject-centered neighborhood, the association of undergoing anatomical vs. functional imaging is assessed with major adverse cardiac event in age- and sex-adjusted Cox regression models, which thus provides individualized risk estimates based on each subject’s unique neighborhood. The natural logarithmic transformations of the hazard ratio (HR) from the Cox models comparing anatomical and functional testing for each subject’s topological neighborhood represent their individualized effect estimate. Negative log-HRs favor anatomical testing, whereas positive values favor functional imaging. Furthermore, since an unbiased personalized effect estimate is contingent upon the similarity of individuals in their topological neighborhoods, a measure of neighborhood homogeneity may be created. This represents the square of 1 minus the average pairwise distance between the index subject and each one of their neighbors, with higher values reflecting a neighborhood of phenotypically more similar subjects. Methods of determining FAI scores are disclosed in US 2022 / 0336048 and Oikonomou et al., Cardiovascular Research 117(13), Nov.2021, 2677–2690, which are herein incorporated by reference in their entirety. FAI Score Percentiles The percentile curves associated with the FAI Score are estimates of how the score is distributed among a group of subjects who have undergone a clinically indicated CCTA. These curves provide a way to compare an individual’s FAI Score to the others in the same age and gender group. Subjects in the upper percentile curves have an increased risk of cardiovascular disease, regardless of the presence of traditional risk factors or established atherosclerotic changes. A subject may be identified as a candidate for anti-oxLDL antibody therapy if the subject has an RCA Percentile of ≥ 70, a LAD Percentile of ≥ 70, or a LCX Percentile of ≥ 95. In some embodiments, the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has an RCA Percentile of ≥ 80, 75, 70, 65, 60, 55, 50, 45, or 40, a LAD Percentile of ≥ 75, 70, 65, 60, 55, 50, 45, or 40. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a LCX Percentile of ≥ 85, 80, 75, 70, 65, 60, 55, 50, 45, or 40. In some embodiments, the subject has an RCA FAI Score Percentile of 81.45. In some embodiments, the subject has an LAD FAI Score Percentile of ≥ 76. In some embodiments, the subject has an LCX FAI Score Percentile of ≥ 86.90. In some embodiments, the subject has an RCA FAI Score Percentile of ≥ 14.00. In some embodiments, the subject has an LAD FAI Score Percentile of ≥ 48. In some embodiments, the subject has an LCX FAI Score Percentile of ≥ 62.00. In some embodiments, the subject has an RCA FAI Score Percentile of≥ 28.06. In some embodiments, the subject has an LAD FAI Score Percentile of ≥ 20. In some embodiments, the subject has an LCX FAI Score Percentile of ≥ 33.33. FAI Score percentiles emerged from FAI Score phenotyping of three main coronary areas as estimates of the distribution. Phenotyping of the FAI Score shows that there is a stepwise association between higher FAI Score percentiles and higher prospective risk of cardiac mortality in both univariate ATTORNEY DOCKET NO: 51473-028WO2 PATENT and multivariable Cox-regression. Nomograms and percentile curves are calculated for FAI Score around each one of the coronary vessels in a pooled analysis. The associated percentile curves represent estimates of the distribution of FAI Score in a representative sample of subjects undergoing clinically indicated CCTA. CaRi-Heart® Risk Score Artificial intelligence-enhanced cardiac risk prediction algorithm (CaRi-Heart® Risk Score) incorporates the FAI score with clinical risk factors and CCTA-derived plaque metrics to predict the 8-year risk of a fatal cardiac event. The CaRi-Heart® Risk score measures the absolute risk of a fatal cardiac event within the next 8 years, based on the personalized FAI-Score values, coronary atherosclerotic plaque burden and clinical risk factors. The CaRi-Hear® Risk score may be obtained from a CaRi-Heart® report. A subject may be identified as a candidate for anti-oxLDL antibody therapy if the subject has a CaRi-Heart® Risk Score of greater than 9. If a subject is between the ages of 30 and 39, the subject may be identified as a candidate for anti-oxLDL antibody therapy if they have a CaRi-Heart® Risk score of greater than 4. If a subject is between the ages of 40 and 59, the subject may be identified as a candidate for anti-oxLDL antibody therapy if they have a CaRi-Heart® Risk score of greater than or equal to 7. In some embodiments, the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has a CaRi-Heart® Risk Score of >18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, or 2. In some embodiments, the subject has a CaRi-Heart® Risk Score of greater than 18.09. In some embodiments, the subject has a CaRi-Heart® Risk Score of greater than 4.80. In some embodiments, the subject has a CaRi-Heart® Risk Score of greater than 1.41. CaRi-Heart® Risk Score is calculated by inputting a subject’s FAI Score and traditional risk factors, including concomitant conditions (e.g., hypertension, hypercholesterolemia, diabetes mellitus, smoking status, epicardial adipose tissue volume) and age into an algorithm to predict the likelihood of a fatal cardiac event using artificial intelligence. It was first trained in the US population and externally validated in Europe as described in Oikonomou et al. Cardiovasc. Res., 117:2677 (2021), which is herein incorporated by reference. The CaRi-Heart® then represents the individualized fatal cardiac event risk as a prognostic model for each coronary artery. CT scan data can be sent electronically to the system from a hospital’s picture archiving and communication systems (PACS) using a gateway appliance installed in the healthcare provider’s network. Reports are electronically sent back to the originating PACS or by email. Although the segmentation of epicardial adipose tissue and the perivascular space is done using a deep learning network, the device includes a quality control step by a trained analyst, who checks and edits the segmentations accordingly. The principal outputs of the CaRi-Heart® Risk Score are: (1) The FAI for the proximal segments of each of the major coronary arteries; (2) the FAI Score for each of the coronary arteries, representing the FAI weighted for technical scan parameters (e.g. tube voltage) and anatomical factors related with the fat distribution around the arteries and basic demographics (e.g., age and sex); FAI Score is also accompanied by vessel specific nomograms for each coronary territory to allow individualized interpretation of the degree of local coronary inflammation; and (3) the CaRi-Heart® Risk Score represents the individualized subject risk of a fatal cardiac event at 8 years. This metric incorporates the FAI Score values into a prognostic model that includes information about atherosclerotic plaque burden, ATTORNEY DOCKET NO: 51473-028WO2 PATENT as described through the modified Duke coronary artery disease index and clinical risk factors (e.g., diabetes, smoking, hyperlipidemia, and hypertension). Therapeutic Methods The disclosure also provides methods for treating a subject by administering to a subject a who has been diagnosed with or has been treated for one or more diseases or conditions. In some embodiments, the subject is diagnosed with a cancer or has been treated for a cancer. In some embodiments, the cancer is pancreatic cancer, breast cancer, colorectal cancer including rectal adenocarcinoma and colon adenocarcinoma, ovarian cancer, bladder urothelial carcinoma, kidney renal clear cell carcinoma, prostate cancer (prostate adenocarcinoma). In some embodiments, the cancer cells express and / or are identified as expressing LOX-1. In some embodiments, the subject is diagnosed with psoriasis or has been treated for psoriasis. In some embodiments, the subject shows symptoms of psoriasis or has been diagnosed with psoriasis. For example, subjects with psoriasis can be characterized by an elevated amount of tumor necrosis factor-alpha (TNFa), interleukin 17 (IL-17), C-reactive protein (CRP), or a combination thereof, compared to a control subject free of psoriasis. In some embodiments, the subjects that are refractory to typical therapies for psoriasis (e.g., UVA or UVB therapy; topical steroids). In some embodiments, the subject is diagnosed with or has been treated for plaque psoriasis, where the subject does not have non-plaque forms of psoriasis such as erythrodermic, guttate or pustular at least at the time of the administration. Various embodiments provide the psoriasis in the disclosed methods herein is plaque psoriasis and does not include a non-plaque form of psoriasis, such as erythrodermic, guttate or pustular psoriasis. Other embodiments of the methods of treating or reducing the severity of psoriasis include selecting a subject exhibiting symptoms of or having been diagnosed with plaque psoriasis and administering to the subject an antibody or antibody fragment described herein. In some embodiments, the subject is diagnosed with a cardiovascular disease (e.g., aortic valve stenosis or aortic valve sclerosis) or has been treated for a cardiovascular disease. In some embodiments, the subject has an elevated level of Lp(a) and / or is exhibiting symptoms of aortic valve sclerosis and / or aortic stenosis. In some embodiments, the level of Lp(a) and / or symptoms of aortic valve sclerosis or aortic stenosis are quantified after the administration, and if the level of Lp(a) or the symptoms persist or appear, the antibody or antibody fragment is continued to be administered. In some embodiments, a reduced amount or level of Lp(a) after the administration of the antibody or antibody fragment is relative to the amount of the same subject before the administration, or relative to the amount from subjects not having aortic valve sclerosis or aortic stenosis or having been successfully treated from aortic valve sclerosis or aortic stenosis. In some embodiments, an elevated amount or level of Lp(a) is relative to the amount or level of subject not having aortic valve sclerosis or aortic stenosis or having been successfully treated from aortic valve sclerosis or aortic stenosis. In some embodiments, the subject is diagnosed with systemic lupus erythematosus (SLE) or treated for SLE. In some embodiments, the subject with SLE is diagnosed with or is suspected of having cardiovascular disease. In some embodiments, the subject is diagnosed with rheumatoid arthritis or treated for rheumatoid arthritis. In some embodiments, the subject is diagnosed with accelerated atherosclerosis or ATTORNEY DOCKET NO: 51473-028WO2 PATENT treated for accelerated atherosclerosis. In some embodiments, a subject is showing symptoms of rheumatoid arthritis, accelerated atherosclerosis, or both or has been diagnosed with rheumatoid arthritis, accelerated atherosclerosis, or both. For example, subjects with rheumatoid arthritis, accelerated atherosclerosis, or both can be characterized by an elevated amount of TNFa, IL-6, CRP, MCP-l, or a combination thereof, compared to a control subject free of rheumatoid arthritis, accelerated atherosclerosis, or both. Subjects with rheumatoid arthritis can be further characterized by having joint pain, tenderness, swelling or stiffness for six weeks or longer; or morning stiffness for 30 minutes or longer. In some embodiments, the subject is diagnosed with psoriatic arthritis or treated for psoriatic arthritis. The subject in some embodiments is diagnosed with, shows symptoms of, or has psoriatic arthritis. Psoriatic arthritis is a chronic disease that worsens over time. However, there may be periods when the symptoms of psoriatic arthritis improve or go away temporarily in the subject. Psoriatic arthritis can affect joints on one or both sides of the body, and the signs and symptoms of psoriatic arthritis often resemble those of rheumatoid arthritis and may include in addition to joint pain, swelling of the fingers and toes, foot pain, lower back pain, changes to the nails, and / or eye inflammation. In some embodiments, the subject is diagnosed with Sjogren’s syndrome or treated for Sjorgren’s syndrome. The subject in some embodiments is diagnosed with, shows symptoms of, or has Sjogren’s syndrome. Subjects suffering from Sjogren’s syndrome often have symptoms of dry eyes and a dry mouth. Other symptoms that are associated with Sjogren’s syndrome include cavities and infections of the mouth such as oral thrush and vision problems including corneal ulcers, dryness in the nose, throat, or skin, swollen glands, specifically behind the jaw and in front of the ears, joint pain, prolonged dry skin, skin rashes, chronic dry cough, vaginal dryness, problems urinating, numbness or tingling in your fingers and toes, and prolonged fatigue. In some embodiments, the subject is diagnosed with Fabry disease or treated for Fabry disease. The subject in some embodiments is diagnosed with, shows symptoms of, or has Fabry disease. Symptoms of Fabry disease may include episodes of pain, especially in the hands and feet, clusters of small, dark red spots on the skin called angiokeratomas, a decreased ability to sweat (e.g., hypohidrosis), cloudiness of the front part of the eye (e.g., corneal opacity), and hearing loss. Internal organs, such as the kidney, heart or brain, may also be affected, leading to progressive kidney damage, heart attacks, and strokes. Milder forms of Fabry disease may appear later in life and affect only the heart or kidneys. In some embodiments, any one of the antibodies described herein may be used to treat classic type Fabry disease, which appears during childhood or the teenage years, in a subject in need thereof. In some embodiments, any one of the antibodies described herein may be used to treat late-onset / atypical type Fabry disease, which appears in subjects in their late thirties. Anti-Ox-LDL Antibodies The disclosure provides methods of identifying subjects for treatment with antibodies or antibody fragments capable of binding to ox-LDL. Particularly, the anti-oxLDL antibodies are administered to a subject who has been identified as a candidate for anti-oxLDL antibody therapy. In some embodiments, the antibodies or antibody fragments are capable of binding to the ox-LDL ApoB100. In some embodiments, ApoB100 has an amino acid sequence of IEIGLEGKGFEPTLEALFGK (SEQ ID NO: 1). ATTORNEY DOCKET NO: 51473-028WO2 PATENT As discussed herein, the disclosure provides anti- ox-LDL antibodies conjugated to one or more detectable labels. In some embodiments, the anti- oxLDL antibody is an anti- ApoB100 antibody. FIG.2 of WO 2009 / 08205 describes the amino acid sequence of the 2D03 heavy chain and the 2D03 light chain, underlining the complementarity determining regions (CDRs). WO 2007 / 025781, which is hereby incorporated by reference in its entirety, discloses an antibody that selectively binds to the oxidized-LDL epitope that is selectively bound by antibody 2D03 and further includes an antibody comprising at least one, two, three, four, five, or all six-complementarity determining region(s) (CDRs) that has the amino acid sequence of the corresponding CDR of antibody 2D03. Furthermore, an antibody with three or four CDRs having sequences corresponding to the 2D03 antibody CDRs preferably has all three heavy chain or all three light chain CDRs that have the sequence of the corresponding CDRs of antibody 2D03; that thus this aspect of the disclosure includes an antibody comprising three light chain CDRs that have the sequence of the corresponding three light chain CDRs of antibody 2D03, or three heavy chain CDRs that have the sequence of the corresponding three heavy chain CDRs of antibody 2D03; that yet more preferably, the antibody comprises three light chain CDRs and three heavy chain CDRs that have the sequence of the corresponding CDRs of antibody 2D03; that if the antibody does not comprise all six CDRs that have the sequence of the corresponding CDRs of antibody 2D03, it is preferred if some or all of the 1, 2, 3, 4 or 5 “non-identical” CDRs comprise a variant of the sequence of the corresponding CDRs of antibody 2D03, (by “a variant” WO 2007 / 025781 includes the meaning that the variant has at least 50% sequence identity with the sequence of the corresponding CDR, more preferably at least 70%, yet more preferably at least 80% or at least 90% or at least 95%; most preferably, the variant has 96% or 97% or 98% or 99% sequence identity with the sequence of the corresponding CDR of antibody 2D03; typically the “variant” CDR sequence has 5 or 4 or 3 or 2 or only 1 amino acid residue difference from the sequence of the corresponding CDR of antibody 2D03); and that this aspect of the disclosure includes antibody 2D03. The heavy chain complementarity determining region (HCDR) 1 (HCDR1), 2 (HCDR2) and 3 (HCDR3) are set forth in SEQ ID NOs: 4, 5 and 6, respectively; and light chain complementarity determining regions (LCDR) 1 (LCDR1), 2 (LCDR2) and 3 (LCDR3) are set forth in SEQ ID NOs: 7, 8 and 9, respectively. HCDR1: FSNAWMSWVRQAPG (SEQ ID NO: 4). HCDR2: SSISVGGHRTYYADSVKGR (SEQ ID NO: 5). HCDR3: ARIRVGPSGGAFDY (SEQ ID NO: 6). LCDR1: CSGSNTNIGKNYVS (SEQ ID NO: 7). LCDR2: ANSNRPS (SEQ ID NO: 8). LCDR3: CASWDASLNGWV (SEQ ID NO: 9). In one embodiment, the antibody contains a variable heavy region (VH) amino acid sequence of SEQ ID NO: 10, and a variable light region (VL) amino acid sequence of SEQ ID NO: 11. The antibody may contain between one and five (e.g., one, two, three, four, or five) amino acid substitutions in the heavy chain amino acid sequence of SEQ ID NO: 2, which includes a VH, a hinge region, and three constant ATTORNEY DOCKET NO: 51473-028WO2 PATENT heavy chain regions. In some embodiments, the antibody includes a light chain amino acid sequence of SEQ ID NO: 3, including a VL and constant light chain region. EVQLLESGGGLVQPGGSLRLSCAASGFTFSNAWMSWVRQAPGKGLEWVSSISVGGHRTYYADSVKGR STISRDNSKNTLYLQMNSLRAEDTAVYYCARIRVGPSGGAFDYWGQGTLVTVSSASTKGPSVFPLAPSS KSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNV NHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPE VKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKG QPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLT VDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK (SEQ ID NO: 2) QSVLTQPPSASGTPGQRVTISCSGSNTNIGKNYVSWYQQLPGTAPKLLIYANSNRPSGVPDRFSGSKSG TSASLAISGLRSEDEADYYCASWDASLNGWVFGGGTKLTVLGQPKAAPSVTLFPPSSEELQANKATLVC LISDFYPGAVTVAWKADSSPVKAGVETTTPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVE KTVAPTECS (SEQ ID NO: 3) EVQLLESGGGLVQPGGSLRLSCAASGFTFSNAWMSWVRQAPGKGLEWVSS ISVGGHRTYY ADSVKGRSTISRDNSKNTLYLQMNSLRAEDTAVYYCARIRVGPSGGAFDYWGQGTLVTVS (SEQ ID NO: 10), QSVLTQPPSASGTPGQRVTISCSGSNTNIGKNYVSWYQQLPGTAPKLLIYANSNRPSGVPDRFSGSKSG TSASLAISGLRSEDEADYYCASWDASLNGWVFGGGTKLTVL (SEQ ID NO: 11). In some embodiments, the disclosure provides an antibody or antibody fragment that binds to oxLDL and one or more of HCDR1, HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4-9, respectively. In some embodiments, the disclosure provides an antibody comprising at least one CDR that has the amino acid sequence of the corresponding CDR of orticumab. More preferably, the antibody has two or three or four or five CDRs that have the sequence of the corresponding CDRs of orticumab. If the antibody has three or four CDRs that have the sequence of the corresponding CDRs of orticumab, it is preferred if the antibody has all three heavy chain or all three light chain CDRs that have the sequence of the corresponding CDRs of orticumab. Thus, this aspect of the methods includes an antibody comprising three light chain CDRs that have the sequence of the corresponding three light chain CDRs of orticumab, or three heavy chain CDRs that have the sequence of the corresponding three heavy chain CDRs of orticumab. Yet more preferably, the antibody includes three light chain CDRs and three heavy chain CDRs that have the sequence of the corresponding CDRs of orticumab. If the antibody does not include all six CDRs that have the sequence of the corresponding CDRs of orticumab, it is preferred if some or all of the 1, 2, 3, 4 or 5 “non-identical” CDRs comprise a variant of the sequence of the corresponding CDRs of orticumab. By “a variant,” we include the meaning that the variant has at least 50% sequence identity with the sequence of the corresponding CDR, more preferably at least 70%, yet more preferably at least 80% or at least 90% or at least 95%. Most preferably, the ATTORNEY DOCKET NO: 51473-028WO2 PATENT variant has 96% or 97% or 98% or 99% sequence identity with the sequence of the corresponding CDR of orticumab. Typically, the “variant” CDR sequence has 5 or 4 or 3 or 2 or only 1 amino acid residue difference from the sequence of the corresponding CDR of orticumab. In particular, the disclosure provides an antibody containing “one or more of HCDR1, HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3” encompasses embodiments that the antibody contains one, any two, any three, any four, any five or all six of the CDRs (i.e., HCDR1, HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3). For example, one aspect of the embodiment provides that the antibody contains HCDR1 as set forth in SEQ ID NO: 4. Another aspect provides that the antibody contains HCDR2 as set forth in SEQ ID NO: 5. Another aspect provides that the antibody contains HCDR3 as set forth in SEQ ID NO: 6. Yet another aspect provides that the antibody contains LCDR1 as set forth in SEQ ID NO: 7. Another aspect provides that the antibody contains LCDR2 as set forth in SEQ ID NO: 8. Another aspect provides that the antibody contains LCDR3 as set forth in SEQ ID NO:9. Yet another aspect provides that the antibody contains HCDR1 as set forth in SEQ ID NO:4 and HCDR2 as set forth in SEQ ID NO: 5. Another aspect provides that the antibody contains HCDR1 as set forth in SEQ ID NO:4 and HCDR3 as set forth in SEQ ID NO: 6. Another aspect provides that the antibody contains HCDR1 as set forth in SEQ ID NO:4 and LCDR1 as set forth in SEQ ID NO: 7. Another aspect provides that the antibody contains HCDR1 as set forth in SEQ ID NO:4 and LCDR2 as set forth in SEQ ID NO: 8. Another aspect provides that the antibody contains HCDR1 as set forth in SEQ ID NO:4 and LCDR3 as set forth in SEQ ID NO: 9. Another aspect provides that the antibody contains HCDR2 as set forth in SEQ ID NO:5 and HCDR3 as set forth in SEQ ID NO: 6. Another aspect provides that the antibody contains HCDR2 as set forth in SEQ ID NO:5 and LCDR1 as set forth in SEQ ID NO: 7 Another aspect provides that the antibody contains HCDR2 as set forth in SEQ ID NO:5 and LCDR2 as set forth in SEQ ID NO: 8. Another aspect provides that the antibody contains HCDR2 as set forth in SEQ ID NO:5 and LCDR3 as set forth in SEQ ID NO: 9. Another aspect provides that the antibody contains HCDR3 as set forth in SEQ ID NO:6 and LCDR1 as set forth in SEQ ID NO: 7. Another aspect provides that the antibody contains HCDR3 as set forth in SEQ ID NO:6 and LCDR2 as set forth in SEQ ID NO: 8. Another aspect provides that the antibody contains HCDR3 as set forth in SEQ ID NO:6 and LCDR3 as set forth in SEQ ID NO: 9. Another aspect provides that the antibody contains LCDR1 as set forth in SEQ ID NO:7 and LCDR2 as set forth in SEQ ID NO: 8. Another aspect provides that the antibody contains LCDR1 as set forth in SEQ ID NO:7 and LCDR3 as set forth in SEQ ID NO: 9. Another aspect provides that the antibody contains LCDR2 as set forth in SEQ ID NO:8 and LCDR3 as set forth in SEQ ID NO: 9. Another aspect provides that the antibody contains HCDR1, HCDR2 and HCDR3 as set forth in SEQ ID NOs: 4-6, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2 and LCDR1 as set forth in SEQ ID NOs: 4, 5 and 7, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2 and LCDR2 as set forth in SEQ ID NOs: 4, 5 and 8, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 5 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3 and LCDR1 as set forth in SEQ ID NOs: 4, 6 and 7, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3 and LCDR2 as set forth in SEQ ID NOs: 4, 6 and 8, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3 and LCDR3 as set forth in SEQ ID NOs: 4, 6 and 9, respectively. Another aspect provides that the antibody contains HCDR1, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 4, 8 and 9, respectively. Another aspect ATTORNEY DOCKET NO: 51473-028WO2 PATENT provides that the antibody contains HCDR1, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 4, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3 and LCDR1 as set forth in SEQ ID NOs: 5, 6 and 7, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3 and LCDR2 as set forth in SEQ ID NOs: 5, 6 and 8, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3 and LCDR3 as set forth in SEQ ID NOs: 5, 6 and 9, respectively. Another aspect provides that the antibody contains HCDR2, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 5, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR2, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 5, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR2, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 5, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR3, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 6, 7 and 8, respectively. Another aspect provides that the antibody contains HCDR3, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 6, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR3, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 6, 8 and 9, respectively. Another aspect provides that the antibody contains LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 7-9, respectively. Yet another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3 and LCDR1 as set forth in SEQ ID NOs: 4-7, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3 and LCDR2 as set forth in SEQ ID NOs: 4-6 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3 and LCDR3 as set forth in SEQ ID NOs: 4-6 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 4, 5, 7 and 8, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 4, 5, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 5, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 4, 6, 7 and 8, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 4, 6, 7 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 6, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR1, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 7, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 5-8, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 5-7 and 9, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 5, 6, 8 and 19, respectively. Another aspect provides that the antibody contains HCDR2, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 5, 7, 8 and 9, respectively. Another aspect provides that the antibody contains HCDR3, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 6-9, respectively. Yet another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3, LCDR1 and LCDR2 as set forth in SEQ ID NOs: 4-8 respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3, LCDR1 and LCDR3 as set forth in SEQ ID NOs: 4-7 and 9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4-6, 8 and 9, respectively. Another aspect provides that the antibody ATTORNEY DOCKET NO: 51473-028WO2 PATENT contains HCDR1, HCDR2, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 5, 7-9, respectively. Another aspect provides that the antibody contains HCDR1, HCDR3, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4, 6-9, respectively. Another aspect provides that the antibody contains HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 5-9, respectively. Yet another aspect provides that the antibody contains HCDR1, HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3 as set forth in SEQ ID NOs: 4-9, respectively. When making and using variants of any of the polypeptide sequences (e.g., CDRs) provided herein, it is understood that a given amino acid can be replaced by a residue having similar physiochemical characteristics, e.g., substituting one aliphatic residue for another (such as Ile, Val, Leu, or Ala for one another), or substitution of one polar residue for another (such as between Lys and Arg; Glu and Asp; or Gln and Asn). Other such conservative substitutions, e.g., substitutions of entire regions having similar hydrophobicity characteristics or substitutions of residues with similar side chain volume are well known. Isolated antibodies comprising conservative amino acid substitutions can be tested in any one of the assays described herein to confirm that a desired activity, as determined by the assays described elsewhere herein. Amino acids can be grouped according to similarities in the properties of their side chains (in A. L. Lehninger, in Biochemistry, second ed., pp.73-75, Worth Publishers, New York (1975)): (1) non-polar: Ala (A), Val (V), Leu (L), Ile (I), Pro (P), Phe (F), Trp (W), Met (M); (2) uncharged polar: Gly (G), Ser (S), Thr (T), Cys (C), Tyr (Y), Asn (N), Gln (Q); (3) acidic: Asp (D), Glu (E); (4) basic: Lys (K), Arg (R), His (H). Alternatively, naturally occurring residues can be divided into groups based on common side-chain properties: (1) hydrophobic: Norleucine, Met, Ala, Val, Leu, Ile, Phe, Trp; (2) neutral hydrophilic: Cys, Ser, Thr, Asn, Gln, Ala, Tyr, His, Pro, Gly; (3) acidic: Asp, Glu; (4) basic: His, Lys, Arg; (5) residues that influence chain orientation: Gly, Pro; (6) aromatic: Trp, Tyr, Phe, Pro, His, or hydroxyproline. Non- conservative substitutions will entail exchanging a member of one of these classes for another class. Particularly preferred conservative substitutions for use in the variants described herein are as follows: Ala into Gly or into Ser; Arg into Lys; Asn into Gln or into His; Asp into Glu or into Asn; Cys into Ser; Gln into Asn; Glu into Asp; Gly into Ala or into Pro; His into Asn or into Gln; Ile into Leu or into Val; Leu into Ile or into Val; Lys into Arg, into Gln or into Glu; Met into Leu, into Tyr or into Ile; Phe into Met, into Leu or into Tyr; Ser into Thr; Thr into Ser; Trp into Tyr or into Phe; Tyr into Phe or into Trp; and / or Phe into Val, into Tyr, into Ile or into Leu. In general, conservative substitutions encompass residue exchanges with those of similar physicochemical properties (i.e., substitution of a hydrophobic residue for another hydrophobic amino acid). Any cysteine residue not involved in maintaining the proper conformation of the isolated peptide as described herein can also be substituted, generally with serine, to improve the oxidative stability of the molecule and prevent aberrant crosslinking. Conversely, cysteine bond(s) can be added to the isolated peptide as described herein to improve its stability or facilitate multimerization. In some embodiments, an antibody as described herein can comprise naturally occurring amino acids commonly found in polypeptides and / or proteins produced by living organisms, e.g., Ala (A), Val (V), Leu (L), Ile (I), Pro (P), Phe (F), Trp (W), Met (M), Gly (G), Ser (S), Thr (T), Cys (C), Tyr (Y), Asn (N), Gln (Q), Asp (D), Glu (E), Lys (K), Arg (R), and His (H). In some embodiments, the antibody can comprise alternative amino acids. Non-limiting examples of alternative amino acids include, D-amino acids; beta- ATTORNEY DOCKET NO: 51473-028WO2 PATENT amino acids; homocysteine, phosphoserine, phosphothreonine, phosphotyrosine, hydroxyproline, gamma-carboxyglutamate; hippuric acid, octahydroindole-2-carboxylic acid, statine, 1,2,3,4,- tetrahydroisoquinoline-3-carboxylic acid, penicillamine (3-mercapto-D-valine), ornithine, citruline, alpha- methyl-alanine, para-benzoylphenylalanine, para-amino phenylalanine, p-fluorophenylalanine, phenylglycine, propargylglycine, sarcosine, and tert-butylglycine), diaminobutyric acid, 7-hydroxy- tetrahydroisoquinoline carboxylic acid, naphthylalanine, biphenylalanine, cyclohexylalanine, amino- isobutyric acid, norvaline, norleucine, tert-leucine, tetrahydroisoquinoline carboxylic acid, pipecolic acid, phenylglycine, homophenylalanine, cyclohexylglycine, dehydroleucine, 2,2-diethylglycine, 1-amino-1- cyclopentanecarboxylic acid, 1-amino-1-cyclohexanecarboxylic acid, amino-benzoic acid, amino- naphthoic acid, gamma-aminobutyric acid, difluorophenylalanine, nipecotic acid, alpha-amino butyric acid, thienyl-alanine, t-butylglycine, trifluorovaline; hexafluoroleucine; fluorinated analogs; azide-modified amino acids; alkyne-modified amino acids; cyano-modified amino acids; and derivatives thereof. In some embodiments, an antibody can be modified, e.g., a moiety can be added to one or more of the amino acids. In some embodiments, the antibody can comprise one or more moiety molecules, e.g., one or more moiety molecules per peptide, two or more moiety molecules per peptide, five or more moiety molecules per peptide, 10 or more moiety molecules per antibody or more moiety molecules per antibody. In some embodiments, an antibody as described herein can comprise one or more types of modifications and / or moieties, e.g., one type of modification, two types of modifications, three types of modifications or more types of modifications. Non-limiting examples of modifications and / or moieties include PEGylation; glycosylation; HESylation; ELPylation; lipidation; acetylation; amidation; end-capping modifications; cyano groups; phosphorylation; and cyclization. In some embodiments, an end-capping modification can comprise acetylation at the N-terminus, N-terminal acylation, and N-terminal formylation. In some embodiments, an end-capping modification can comprise amidation at the C-terminus, introduction of C-terminal alcohol, aldehyde, ester, and thioester moieties. Pharmaceutical Compositions In various embodiments, the present disclosure provides a pharmaceutical composition for use in the methods. The pharmaceutical composition includes the anti-oxLDL antibody or fragment thereof conjugated to a detectable label and a pharmaceutically acceptable carrier. “Pharmaceutically acceptable carrier” as used herein refers to a pharmaceutically acceptable material, composition, or vehicle that is involved in carrying or transporting a compound of interest from one tissue, organ, or portion of the body to another tissue, organ, or portion of the body. For example, the carrier may be a liquid or solid filler, diluent, excipient, solvent, or encapsulating material, or a combination thereof. Examples of excipients include but are not limited to starches, sugars, microcrystalline cellulose, diluents, granulating agents, lubricants, binders, disintegrating agents, wetting agents, emulsifiers, coloring agents, release agents, coating agents, sweetening agents, flavoring agents, perfuming agents, preservatives, antioxidants, plasticizers, gelling agents, thickeners, hardeners, setting agents, suspending agents, surfactants, humectants, carriers, stabilizers, and combinations thereof. Generally, each component of the carrier must be “pharmaceutically acceptable” in that it must be compatible with the other ingredients of the formulation. It must also be suitable for use in contact with any tissues or organs with which it may come ATTORNEY DOCKET NO: 51473-028WO2 PATENT in contact, meaning that it must not carry a risk of toxicity, irritation, allergic response, immunogenicity, or any other complication that excessively outweighs its therapeutic benefits. The pharmaceutical compositions may be delivered in a therapeutically or diagnostically effective amount. The precise diagnostically or therapeutically effective amount is that amount of the composition that will yield the most effective results in terms of efficacy of detection of atherosclerosis in a given subject. This amount will vary depending upon a variety of factors, including but not limited to the characteristics of the compound (including activity, pharmacokinetics, pharmacodynamics, and bioavailability), the physiological condition of the subject (including age, sex, disease type and stage, general physical condition, responsiveness to a given dosage, and type of medication), the nature of the pharmaceutically acceptable carrier or carriers in the formulation, and the route of administration. One skilled in the clinical and pharmacological arts will be able to determine a therapeutically effective amount through routine experimentation, for instance, by monitoring a subject's response to administration of a compound and adjusting the dosage accordingly. For additional guidance, see Remington: The Science and Practice of Pharmacy (Gennaro ed.20th edition, Williams & Wilkins PA, USA) (2000). In various embodiments, the anti-ox-LDL antibody to be administered in the disclosed methods is formulated for delivery via any route of administration. For example, the methods include administration via an aerosol, nasal, oral, transmucosal, transdermal, parenteral or enteral route. “Parenteral” refers to a route of administration that is generally associated with injection, including intraorbital, infusion, intraarterial, intracapsular, intracardiac, intradermal, intramuscular, intraperitoneal, intrapulmonary, intraspinal, intrasternal, intrathecal, intrauterine, intravenous, subarachnoid, subcapsular, subcutaneous, transmucosal, or transtracheal. Via the parenteral route, the compositions may be in the form of solutions or suspensions for infusion or for injection, or as lyophilized powders. Via the parenteral route, the compositions may be in the form of solutions or suspensions for infusion or for injection. Via the enteral route, the pharmaceutical compositions can be in the form of tablets, gel capsules, sugar-coated tablets, syrups, suspensions, solutions, powders, granules, emulsions, microspheres or nanospheres or lipid vesicles or polymer vesicles allowing controlled release. Typically, the compositions are administered by injection. Antibody Preparation In some embodiments, the aforementioned methods involve antibodies that bind to a specific antigen epitope, where the antibodies contain one or more defined sequences. For example, modern recombinant library technology is used to prepare therapeutic antibodies against native ApoB or oxidized ApoB. While murine hybridomas cells produce large amounts of identical antibodies, these non-human antibodies are recognized by human body as foreign, and as a consequence, their efficacy and plasma half-lives are decreased in addition to eliciting allergic reactions. To solve this problem, one approach is to make chimeric antibodies where the murine variable domains of the antibody are transferred to human constant regions resulting in an antibody that is mainly human. A further refinement of this approach is to develop humanized antibodies where the regions of the murine antibody that contacted the antigen, the Complementarity Determining Regions (CDRs) are transferred to a human antibody framework, resulting in a humanized antibody. Another approach is to produce completely human antibodies using recombinant technologies, which do not rely on immunization of animals to generate the specific ATTORNEY DOCKET NO: 51473-028WO2 PATENT antibody. Instead, recombinant libraries comprise a huge number of pre-made antibody variants and it is likely that a library will have at least one antibody specific for any antigen. A phage display system may be used where antibody fragments are expressed, displayed, as fusions with phage coat proteins on the surface of filamentous phage particles, while the phage display system simultaneously carries the genetic information encoding the displayed molecule. Phage displaying antibody fragments specific for a particular antigen may be selected through binding to the antigen in question. Isolated phage may then be amplified and the gene encoding the selected antibody variable domains may optionally be transferred to other antibody formats as e.g., full length immunoglobulin and expressed in high amounts using appropriate vectors and host cells well known in the art. The format of displayed antibody specificities on phage particles may differ. The most commonly used formats are Fab and single chain (scFv) both containing the variable antigen binding domains of antibodies. The single chain format is composed of a variable heavy domain (VH) linked to a variable light domain (VL) via a flexible linker. Before use as analytical reagents, or therapeutic agents, the displayed antibody specificity is transferred to a soluble format, e.g., Fab or scFv, and analyzed as such. In later steps the antibody fragment identified to have desirable characteristics may be transferred into yet other formats such as full-length antibodies. Antibody Production from Hybridomas The cell fusions are accomplished by standard procedures well known to those skilled in the field of immunology. Fusion partner cell lines and methods for fusing and selecting hybridomas and screening for mAbs are well known in the art. See, e.g., Ausubel, Harlow, and Colligan, the contents of which references are incorporated entirely herein by reference. An anti-MDA-ApoB100 antibody, or an anti-apo(a) antibody, can be produced in large quantities by injecting hybridoma or transfectoma cells secreting the antibody into the peritoneal cavity of mice and, after appropriate time, harvesting the ascites fluid which contains a high titer of the mAb, and isolating the mAb therefrom. For such in vivo production of the mAb with a non-murine hybridoma (e.g., rat or human), hybridoma cells are preferably grown in irradiated or athymic nude mice. Alternatively, the antibodies can be produced by culturing hybridoma or transfectoma cells in vitro and isolating secreted mAb from the cell culture medium or recombinantly, in eukaryotic or prokaryotic cells. Recombinant Expression of Antibodies Recombinant murine or chimeric murine-human or human-human antibodies that inhibit oxidized LDL can be provided according to the present disclosure using known techniques based on the teaching provided herein. See, e.g., Ausubel et al., eds. Current Protocols in Molecular Biology, Wiley Interscience, N.Y. (1987, 1992, 1993); and Sambrook et al. Molecular Cloning: A Laboratory Manual, Cold Spring Harbor Laboratory Press (1989). The DNA encoding an anti- oxLDL antibody can be genomic DNA or cDNA which encodes at least one of the heavy chain constant region (Hc), the heavy chain variable region (Hc), the light chain variable region (Lv) and the light chain constant regions (Lc). A convenient alternative to the use of chromosomal gene fragments as the source of DNA encoding the murine V region antigen-binding segment is the use of cDNA for the construction of chimeric immunoglobulin genes, e.g., as reported by Liu et al. (Proc. Natl. Acad. Sci., USA 84:3439 (1987) and J. Immunology 139:3521 (1987). The use of ATTORNEY DOCKET NO: 51473-028WO2 PATENT cDNA requires that gene expression elements appropriate for the host cell be combined with the gene in order to achieve synthesis of the desired protein. The use of cDNA sequences is advantageous over genomic sequences (which contain introns), in that cDNA sequences can be expressed in bacteria or other hosts which lack appropriate RNA splicing systems. EXAMPLES The following examples are provided to better illustrate the claimed invention and are not to be interpreted as limiting the scope of the invention. To the extent that specific materials are mentioned, it is merely for purposes of illustration and is not intended to limit the invention. One skilled in the art may develop equivalent means or reactants without the exercise of inventive capacity and without departing from the scope of the invention. Example 1. A Phase 2, Randomized, Double-blind, Placebo-controlled to Assess the Effect of Orticumab 1245 mg in Adults with Moderate to Severe Psoriasis and Cardiometabolic Risk Factors. Here, we report results of a randomized, double-blind, placebo-controlled phase 2a trial in subjects with psoriasis, a disease known to be associated with increased cardiovascular risk, carried out in 13 centers in the US assessing the effects of orticumab on both skin and coronary disease inflammation as measured by FAI Score (CaRi-Heart®, Caristo Diagnostics Ltd, Oxford, UK) derived from CCTA. A Phase 2a, randomized, double-blind, placebo-controlled study was performed and enrolled adults > 30 years of age with moderate to severe plaque psoriasis along with cardiometabolic risk factors. Subjects with psoriasis (n=77) were randomized in a 2:1 ratio to receive either 1245 mg orticumab or placebo weekly for 4 weeks then monthly for 8 weeks, for a total of 12 weeks of treatment. The primary efficacy endpoints were the mean percent change from baseline in Psoriasis Area and Severity Index (PASI) at Week 15 and the percentage of patients with treatment success using the static Investigator’s Global Assessment (sIGA) at Week 15. Secondary endpoints included the mean percent change from baseline in PASI at Weeks 1, 3, 7, and 11. Coronary CT angiograms (CCTA) were performed during screening and at 15 weeks. Coronary inflammation was assessed from CCTA using pericoronary Fat Attenuation Index (FAI) Score, and the 8-year risk for cardiac mortality (CaRi-Risk) was determined using the CaRi-Heart® device. The CaRi-Heart Risk score is determined using artificial intelligence-enhanced cardiac risk prediction algorithm that incorporates the FAI score with clinical risk factors and CCTA- derived plaque metrics to predict the 8-year risk of a fatal cardiac event. Exploratory endpoints utilized CaRi-Heart® technology with CCTA to examine change in coronary artery perivascular Fat Attenuation Index (FAI), FAI scores (calculated relative risk %) and CaRi- Heart Risk (% absolute risk of 8-year fatal cardiac event). The Per Protocol Population and the high-risk subgroup (by CaRi-Heart Risk and / or FAI-Score) was examined. Safety was also assessed. Study Design Described herein is a Phase-2, randomized, double-blind, placebo-controlled study to evaluate the safety and efficacy of orticumab 1245 mg or placebo in subjects with moderate to severe psoriasis, as described in FIG.1. A total of 75 subjects with psoriasis were randomized in a double-blind fashion to ATTORNEY DOCKET NO: 51473-028WO2 PATENT receive either a single IV infusion of orticumab or placebo for a total of six IV infusions for up to 78 days. Participants were randomized to receive orticumab or placebo in a 2:1 ratio. The randomization scheme was generated by a qualified statistician designated by Sponsor or its designee. The study comprised three periods: screening, randomized control trial, and end of study assessments. Before any study-related procedures were conducted, the subjects signed a written informed consent. Subjects were screened (Day -28 to -1) for the study, which included clinical laboratory evaluations and CCTA. Prior to dosing on study Day 1, Baseline assessments were performed. During treatment periods, dosing was performed under supervision at the research center. Subjects visited the research center on the morning of Days 1, 8, 15, 22, 50, and 78 for a pre-dose blood sample for PK purposes, Day 106 for End of Study assessments, and Day 120 for Follow-up assessments. Following the Screening Period, participants were enrolled into one of the two groups: 1245 mg (50 mL infusion) orticumab or placebo. Subjects were randomized in a 2:1 ratio, orticumab to placebo and receive up to 12 weeks of treatment. Planned treatments were weekly for 4 weeks, then monthly IV infusions of 1245 mg of orticumab or placebo. The results of the prior in vivo safety studies supported the proposed clinical program and provided adequate safety factors to support x 4 weekly, followed by x 2 monthly administration of 1245 mg orticumab in this planned Phase 2 study in psoriasis. The dosing regimen was designed to administer the maximal allowable concentration of orticumab to the subjects in the first 4 weeks of treatment. Given that the mean elimination half-life of orticumab at this dose was approximately 2-3 weeks, a weekly dosing regimen was consistent with the therapeutic goal of ensuring pharmacologically relevant blood concentrations of orticumab over the initial 4-week period. Since the link between PK and PD had not been established, blood samples were taken just prior to dosing (minimum concentration [Cmin]) on days 8, 15, 22, 29, 58 and 87 to confirm trough levels of orticumab to ascertain intersubject differences concentrations associated with potential differences in PD measures. Preparation of a dose required that a 10 mL syringe and needle withdrew 8.45 mL from the contents of six (6) vials in the kit and injected into a 50 mL 0.9% Sodium Chloride IV bag. This was prepared using aseptic technique by an unblinded pharmacist or other trained medical personnel designated by the Investigator. Allowing for an estimated 0.15 mL retained in the needle after injection into the IV bag, this delivered 1245 mg of orticumab (consult the pharmacy manual for dose preparation instructions). Orticumab was diluted (in 50 mL of sterile normal saline) and administered for over 30 minutes without premedication. The Internal Safety Review Committee (ISRC) reviewed the blinded safety data after the first subject completed the first dose (Day 1), the first five subjects completed the first dose (Day 1), and the first ten subjects completed the first dose (Day 1). The IRSC reviewed all adverse reactions to all administered doses at these times. At the Investigator’s discretion, subjects were eligible for psoriasis rescue medications, such as topical hydrocortisone 2.5% (cream or ointment) that could be applied twice daily if needed to the face and sensitive intertriginous regions (axilla, groin, breast). Over the counter (non-prescription) applications of coal tar and emollients could be used as necessary. Participants made every effort to maintain the regular dosing intervals. However, deviations of ± 1 day were acceptable if they cannot be avoided. No dosage modification was permitted in this trial. If a ATTORNEY DOCKET NO: 51473-028WO2 PATENT subject had a reaction while study drug was being infused and the injection was stopped, the volume infused prior to stopping study drug administration was recorded and the Medical Monitor was contacted. Efficacy Measurements The Psoriasis Area and Severity Index (PASI) combined assessments of 4 body areas: the head and neck (H), the upper limbs (UL), the trunk (T) and the lower limbs (LL). The percentage of skin affected by psoriasis in each area was given a numerical score representing the Percentage involved: 1(0–9%), 2 (10–29%), 3 (30–49%), 4 (50–69%), 5 (70–89%) or 6 (90–100%). Within each area (H, UL, T, LL) the severity of three plaque signs–erythema (E), thickness / induration (I) and desquamation / scaling (D) –was assessed on a 5-point scale: 0 (none), 1 (mild), 2 (moderate), 3 (severe) or 4 (very severe). The assessment of lesion severity and area affected were combined into a single score. The final PASI was = sum of severity parameters for each region*area score*weight of region (where head: 0.1, arms: 0.2, body: 0.3, legs: 0.4); total possible score range: 0=no disease to 72=maximal disease. The maximum PASI score that could be measured was <72 since the PASI assessment excluded scalp, palms, fingernails, soles, and toenails. Reduction in PASI score from Baseline indicated improvement. The percentage change was calculated by subtracting weeks 1, 3, 7, 11 and 15 values from the Baseline values. The percentage change was calculated for each entire treatment group (not for each participant). A positive percentage change from Baseline indicated improvement. Scored as the percentage body area affected by psoriasis; 0–100%. A commonly used method to estimate the body surface area (BSA) of psoriatic lesions is the “rule of nines”, which was originally developed for estimating the surface area of burns. It was defined as 9% coverage for the head and neck, 9% for each arm, 9% for the anterior and posterior legs, and 9% for each of 4 trunk quadrants, leaving 1% for the genitalia. The BSA could also be estimated by the number of a subject’s hand areas affected, on the assumption that one “handprint” reflected approximately 1% of BSA. The Investigator Global Assessment (IGA) was a 5-category scale including “0 = clear”, “1 = almost clear”, “2 = mild”, “3 = moderate” or “4 = severe” indicating the physician’s overall assessment of the psoriasis severity focusing on induration, erythema and scaling. Treatment success of “clear” or “almost clear” consisted of no signs of psoriasis or normal to pink coloration of lesions, no thickening of the plaque, and none to minimal focal scaling. The IGA captured and categorized the global assessment of all clinical signs and symptoms of disease. This scale was scored as a static assessment, i.e., without regard to a previous assessment. To have IGA success, one must have had a designation of ‘clear’ or ‘almost clear’ and exhibit a two-point improvement from Baseline. Hence, if a subject had ‘mild’ disease at Baseline, he / she must reach ‘clear’. If a subject had ‘moderate’ disease at Baseline, he / she must reach ‘almost clear’. And, if a subject was classified as ‘severe’ at Baseline, he / she must still reach ‘almost clear’, even though that required a three-point improvement. The Itch Numeric Rating Scale (NRS) was a self-administered subject reported outcome questionnaire that was completed during protocol specified clinic visits. Participants indicated itch severity by circling the integer that best described the worst level of itching due to psoriasis in the past 24 h on an 11-point scale anchored at 0, representing ‘no itching’ and 10, representing ‘worst itch imaginable’. ATTORNEY DOCKET NO: 51473-028WO2 PATENT Dermatology Life Quality Index (DLQI) was the dermatology-specific quality of life measure used for psoriatic population. The 10-item questionnaire assesses participant health-related quality of life (daily activities, personal relationships, symptoms and feelings, leisure, work and school, and treatment). The DLQI questions were rated by the participant as 0 (not at all / not relevant) to 3 (very much) with a total score range of 0 (best) to 30 (worst); higher scores indicated poor quality of life. Patient's Global Assessment (PtGA)-The PtGA asked the participant to evaluate the overall cutaneous disease at that point in time on a single item, 5-point scale (0=clear; 1=almost clear;2=mild; 3=moderate; 4=severe). Mean change from Baseline in cardiometabolic and inflammatory biomarkers at Weeks 3 and 15 was in blood serum parameters, ApoB, Apo A1, VLDL-c, oxLDL, oxHDL, Lp(a), oxLp(a), NMR-LP-4. Mean change was also observed in cardiometabolic and inflammatory biomarkers at Weeks 3 and 15 in blood serum inflammation biomarkers, Interleukin-6 (IL-6), IL-1b, IL-17, tumor necrosis factor-alpha (TNF- α), osteoprotegerin, high-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA), and monocyte chemoattractant protein-1 (MCP-1). Further, there was a mean change in blood serum HDL efflux efficiency, ABCA-1. Change in coronary artery perivascular fat attenuation index (FAI) was measured by coronary computed tomography angiography (CCTA) at Week 15 for participants. Change in Noncalcified and low attenuation coronary artery plaque volume was assessed by CCTA at week 15 as compared to Baseline, in active and placebo patients. Change in total plaque volume, assessed by CCTA at week 15 as compared to Baseline, in active and placebo patients. Efficacy Variables The primary efficacy endpoints were two-fold: (i) mean percent change from Baseline in PASI at Week 15, compared to placebo and (ii) percentage of participants achieving treatment success (clear =0 or almost clear =1) and greater than or equal to (>=) 2 Point Improvement at Week 15 on the 5-point static Investigator’s Global Assessment modified 2011 version (sIGA). There were secondary efficacy endpoints. Mean percent change from Baseline in PASI at Weeks 1, 3, 7, and 11 was measured. Percentage of Participants achieving PASI75 and PASI50 from Baseline at Weeks 1, 3, 7, and 11 was compared to placebo. Percentage of participants achieving treatment success (clear =0 or almost clear =1) and greater than or equal to (>=) 2 was assessed. Point Improvement at Weeks 1, 3, 7, and 11 on the 5-point static Investigator’s Global Assessment modified 2011 version (sIGA) was calculated. Mean percent change from Baseline in BSA at Weeks 1, 3, 7, 11, and 15 was compared to placebo. Mean change from Baseline in Dermatology Life Quality Index (DLQI) at Weeks 3, 7, 11, and 15 was compared to placebo. Mean change from Baseline in Itch Numerical Rating Scale Score at Weeks 3 and 15 was compared to placebo. There were several exploratory efficacy endpoints. One was mean change from Baseline in cardiometabolic and inflammatory biomarkers at Weeks 3 and 15 in blood serum lipid parameters (ApoB, Apo A1, VLDL-c, oxLDL, oxHDL, Lp(a), oxLp(a), NMR-LP4), blood serum inflammation biomarkers (Interleukin-6 (IL-6), IL-1b, IL-17, tumor necrosis factor-alpha (TNF-α), osteoprotegerin, high-sensitivity C- reactive protein (hs-CRP), serum amyloid A (SAA), and monocyte chemoattractant protein-1 (MCP-1)), ATTORNEY DOCKET NO: 51473-028WO2 PATENT and blood serum HDL efflux efficiency (ABCA-1). A second is the change in coronary artery perivascular fat attenuation index (FAI) measured by coronary computed tomographic angiography (CCTA) at Week 15 as compared to Baseline in active and placebo treated subjects. Also, the change in noncalcified and low attenuation coronary artery plaque volume was assessed by CCTA at week 15 as compared to Baseline, in active and placebo subjects. CCTA was performed in 32 patients in the group receiving orticumab and 19 patients in the placebo group. Finally, the change in total plaque volume was assessed by CCTA at week 15 as compared to Baseline, in active and placebo subjects. Population Each subject had to meet the following criteria to be eligible for the study: (i) stable / chronic plaque psoriasis with PASI score of ≥ 12 AND involving ≥ 10% of the subject’s BSA; (ii) Males and Females ≥ 30 years of age at time of consent; (iii) Females of childbearing age were to use 2 forms of birth control; (iv) BMI ≥ 30 kg / m2; (v) LDL ≥ 100 mg / dL at Screening; and (vi) all females were to have a negative serum pregnancy test result at Screening and a negative urine pregnancy test at Day 1 (Visit 1) prior to dosing. The study subjects were overweight (Table 2), with moderate to severe skin disease (PASI Score 17.02 ± 6.7) (Table 3). Subjects who met any of the following criteria were to have been excluded from the study: (i) past use of orticumab; (ii) any of the non-plaque forms of psoriasis: erythrodermic, guttate, or pustular; (iii) scalp, palmar or plantar psoriasis only, at Screening or Baseline; (iv) had evidence of skin conditions (e.g., eczema) at the time of Screening or Baseline visit that would have interfered with the evaluation of psoriasis; (v) newly discovered Type 2 diabetes mellitus (T2DM) within 90 days of Screening (prior to study entry) or medical treatment for T2DM started < 90 days prior to Screening; (vi) moderate or high- intensity statin use or new use of a low-intensity statin therapy within 90 days of Screening. Low-intensity statin therapy was permitted provided it is limited to lovastatin, fluvastatin, pravastatin ≤ 40 mg daily, simvastatin ≤ 20 mg daily, or pitavastatin ≤ 2 mg daily AND the dose had remained stable and unchanged for ≥ 90 days prior to the Screening visit and NO DOSE change was anticipated for the approximate 20- week duration of the trial. No other non-statin lipid-modifying therapy was permitted; (vii) No use of anti- coagulating agents or anti-thrombotic agents within 90 days prior to the Screening visit. Low dose aspirin limited to ≤ 81 mg daily provided the dose had remained stable and unchanged for ≥ 90 days prior to the Screening visit. Nonsteroidal anti-inflammatory drugs were not permitted for the duration of the trial from the Screening Visit; (viii) Poorly controlled hypertension defined as: (a) systolic blood pressure (BP) > 160 mm Hg or (b) diastolic BP > 90 mm Hg; (ix) antihypertensive medication was permitted provided it was limited to two or less medications and all had been stable and unchanged for ≥ 90 days prior to the Screening visit and NO DOSE change was anticipated for the approximate 20-week duration of the trial; (x) use of topical therapies, phototherapy (UVA or UVB) or tanning salons for the treatment of psoriasis in the past 4 weeks; (xi) use of an IL-23 blocker in the past 180 days, an IL-17 blocker in the past 16 weeks, or a TNF blocker in the past 12 weeks; (xii) use of methotrexate, cyclosporine, or apremilast in the past 4 weeks; (xiii) history of hypersensitivity or allergies to any contents in the orticumab formulation; (xiv) participation in any clinical study with an investigational drug / device within 4 weeks prior to the first day of dosing; (xv) was pregnant or breastfeeding; (xvi) had an underlying condition that predisposed to infections (e.g., immunodeficiency, HIV, or splenectomy); (xvii) chronic or acute hepatitis B and C, or ATTORNEY DOCKET NO: 51473-028WO2 PATENT carrier status; (xviii) history of tuberculosis, tuberculosis, or a positive tuberculin skin test (TST) for tuberculosis. Participants who previously received BCG vaccination could participate in the study after showing negative responses in Interferon-Gamma Release Assays (IGRA); (xix) history of malignancy in the past 5 years or suspicion of active malignant disease except treated cutaneous squamous cell or basal cell carcinoma and treated carcinoma in situ of the cervix uteri; (xx) diagnosis of major depressive disorder, schizophrenia, bipolar disorder, personality disorder or other DSM-V disorders which the Investigator believed could have interfered significantly with study compliance; (xxi) a history of any clinically important abnormalities in cardiac rhythm or conduction; (xxii) a history of prolonged QT intervals or a family history of long QT-syndrome at Screening; (xxiii) a history of first, second or third- degree atrioventricular (AV) block, or AV dissociation; (xxiv) a history of complete bundle branch block; (xxv) unstable angina pectoris, myocardial infarction, transient ischemic attack, or stroke within 3 months prior to Screening, or participants who underwent percutaneous coronary intervention or a coronary artery bypass graft within 6 months prior to Screening or who were due to undergo these procedures at the time of Screening; (xxvi) severe congestive heart failure (NYHA III or IV); (xxvii) prior history of contrast- induced nephropathy; (xxviii) known or suspected allergy to iodinated x-ray contrast; (xxix) estimated GFR < 60 mL / min / 1.73 m2{MDRD formula}; (xxx) contraindications to intravenous metoprolol (beta adrenergic blocker) during CCTA imaging procedure; (xxxi) contraindications to sublingual nitroglycerine during CCTA imaging procedure; or (xxxii) subject was a user of recreational or illicit drugs or has had a recent history (within 1 year of Screening) of drug or alcohol abuse or dependence. (Note: Alcohol abuse included heavy alcohol intake as defined by >3 drinks per day or >14 drinks per week, or binge drinking) at Screening. Occasional intermittent use of cannabinoid products was allowed provided that no cannabinoid products were used during the 1 week prior to each visit. A summary of subject disposition comparing orticumab and placebo for the safety population is presented in Table 1. Table 1. Summary of Subject Disposition (Safety Population) ATTORNEY DOCKET NO: 51473-028WO2 PATENT Demographic and Baseline characteristics for all subjects in the safety population are presented in Table 2. Majority of the subjects were males (57.14%) and 92.21% of the population was white. The mean age of treated subjects was 51.23 years. At Screening, the mean BMI was recorded to be 36.77 kg / m2. All subjects in the safety population had their psoriasis condition diagnosed nearly 13 years prior to Screening. Table 2. Summary of Demographics and Baseline Characteristics (Safety Population) ATTORNEY DOCKET NO: 51473-028WO2 PATENT Max = maximum; Min = minimum The baseline characteristics of the subjects that participated in the CCTA study are summarized below in Table 3. Table 3. Baseline characteristics of the CCTA population ATTORNEY DOCKET NO: 51473-028WO2 PATENT The cardiovascular characteristics of the baseline population for study using CCTA are summarized in Table 4 below. ATTORNEY DOCKET NO: 51473-028WO2 PATENT Table 4. Baseline cardiovascular characteristics of CCTA population Treatment Subjects were randomly allocated in a 2:1 ratio to receive either orticumab (1245 mg) or placebo by a single IV infusion based on the Schedule of Visits (Table 5). Subjects received a total of six (6) IV infusions of either orticumab or placebo during the study. Preparation of a dose required that a 10 mL syringe and needle withdrew 8.45 mL from the contents of six (6) vials in the kit and injected into a 50 mL 0.9% Sodium Chloride IV bag. This was prepared using aseptic technique by an unblinded pharmacist or other trained medical personnel designated by the Investigator. Allowing for an estimated 0.15 mL retained in the needle after injection into the IV bag, this delivered 1245 mg of orticumab (consult the pharmacy manual for dose preparation instructions). Orticumab was diluted (in 50 mL of sterile normal saline) and administered for over 30 minutes without premedication. No dosage modification was permitted in this trial. If a subject had a reaction while study drug was being infused and the injection was stopped, the volume infused prior to stopping study drug administration was recorded and the Medical Monitor was contacted. ATTORNEY DOCKET NO: 51473-028WO2 PATENT Table 5. Schedule of Events Results In the primary efficacy assessment, Psoriasis Area and Severity Index (PASI) (Mean Percent Change from Baseline in PASI at Week 15), there were no differences in mean PASI percent change from Baseline at Week 15 among placebo and orticumab regimens. For the static Investigator Global Assessment (sIGA) (Percentage of Participants Achieving Treatment Success at Week 15), the sIGA treatment success response rates for both treatment groups were similar and non-significant. In the secondary efficacy assessments, Psoriasis Area and Severity Index (PASI) (Mean Percent Change from Baseline in PASI at Weeks 1, 3, 7, and 11), subjects in the orticumab group demonstrated a significant reduction in the PASI total score at Week 7, while no differences were observed at Weeks 1, 3, and 11. During Visit 5 (Week 7), subjects receiving orticumab showed a decrease of 13.39 (p-value = 0.0121) in the mean PASI percent change from Baseline at Week 7, compared to placebo. The ATTORNEY DOCKET NO: 51473-028WO2 PATENT reductions in PASI percentage change from Baseline were consistently greater for the orticumab group and progressively increased from Week 1 (Visit 2) to Week 3 (Visit 4), reaching statistical significance (p = 0.01) at Week 7 (Visit 5). Subjects were dosed once weekly at Visits 2 and 4 and received their first monthly administration of orticumab at Visit 5. Thereafter, for the monthly administered injections at Weeks 11 and 15 (Visits 6 and 7), the orticumab difference over placebo declined and was not statistically significant. With Psoriasis Area and Severity Index (PASI) (Percent of Participants Achieving PASI75 and PASI50 from Baseline at Weeks 1, 3, 7, 11, and 15), there were no differences in subjects achieving 50% and 75% improvement in the PASI total score between the two treatment groups. With static Investigator Global Assessment (sIGA) (Percent of Participants Achieving Treatment Success at Weeks 1, 3, 7, and 11), the sIGA treatment success response rates at Weeks 7 and 11 were non- significant, while there were no successful responders at Weeks 1 and 3. With Psoriasis Body Surface Area (BSA) Involvement (Mean Percent Change from Baseline at Weeks 1, 3, 7, 11, and 15), subjects in the orticumab group demonstrated a significant reduction in the PASI total score at Week 7, while no differences were observed at Weeks 1, 3, 11, and 15. During Visit 5 (Week 7), subjects receiving orticumab showed a decrease of 12.36 (p-value = 0.0357) in the mean percent change from Baseline in BSA at Week 7, compared to placebo. This shows a similar pattern of reduction to the mean percentage change in PASI, which demonstrated a steady decline during weekly dosing up to the first monthly administration of orticumab [Week 7 (Visit 5)] and was not sustained at subsequent visits involving monthly injections. With Dermatology Life Quality Index (DLQI) (Mean Percent Change from Baseline at Weeks 3, 7, 11, and 15), subjects in either treatment group did not report an improvement in the DLQI at Weeks 3, 7, 11, and 15. With Itch Numeric Rating Scale (I-NRS) (Observed Means at Weeks 3 and 15), the observed itch numerical rating scale means were similar among the two treatment groups at Weeks 3 and 15. Overall, based on the primary and secondary efficacy results, IV infusions of orticumab (1245 mg) for up to 78 days (11 weeks) were similar to placebo and did not prove to be efficacious in treating subjects with moderate to severe psoriasis and cardiometabolic risk factors. In the overall study population, there was a downward trend in FAI Score as well as CaRi-Risk after treatment in the orticumab group (P=0.11 vs baseline and P=0.08 vs placebo) (FIGS.2B and 2C). Regarding the characterization of the subjects’ cardiovascular characteristics specifically, in the whole population of subjects on active treatment, there was a reduction in LCX FAI from baseline. The change from baseline in LCX FAI Score in subjects on orticumab was significant when compared to subjects on placebo (FIG.2A). However, in those patients identified by CaRi-Heart® to have elevated coronary inflammatory risk prior to treatment (n=28), the FAI Score was significantly reduced in the right and left circumflex coronary arteries in the orticumab group vs placebo. The CaRi-Risk (8-year risk for a fatal cardiac event) was significantly reduced by ~50% in this population (P=0.02 vs baseline and P=0.01vs placebo) (FIGS.3B and 3C). There was no significant effect of orticumab on the CaRi-Heart risk score in the low inflammation subgroup (FIG.4B). Representative images of changes in FAI score in response to orticumab treatment and placebo are shown in FIG.5. Treatment with orticumab had no significant effect on LDL, HDL, or triglyceride levels (data not shown). Subjects were divided into low (FAI score <50thpercentile) and high (FAI score ≥50thpercentile) coronary inflammation groups, allowing analysis of the importance of baseline coronary inflammation. ATTORNEY DOCKET NO: 51473-028WO2 PATENT Using the FAI score, which adjusts for technical scan parameters, anatomical factors, age and sex, we found a trend towards reduced coronary inflammation in response to orticumab in all three arteries of the whole population. For subjects who were determined to be in the 50thpercentile of FAI score for the right coronary artery (RCA), left anterior descending artery (LAD), or left circumflex artery (LCX) and on active treatment, there was a significant reduction in absolute Cari-heart risk % from baseline. There was also a significant reduction in absolute RCA FAI (HU) from baseline (P=0.01 vs baseline and P=0.02 vs placebo) and a significant reduction in absolute LCX FAI (HU) from baseline (P=0.01 vs baseline and P=0.05 vs placebo) (FIG.3A). Subjects in this group also had a significant reduction in absolute RCA FAI Score from baseline and a significant reduction in absolute LCX FAI Score from baseline (FIG.3A). In the LAD there was a trend towards reduction in FAI score (P=0.06 vs baseline) in the orticumab group. There were no significant changes in FAI score in any of the arteries of the low inflammation groups (FIG.4A). Subjects in this group also had a significant reduction in absolute RCA FAI Score Percentile from baseline, a significant reduction in absolute LAD FAI Score Percentile from baseline, and a significant reduction in absolute LCX FAI Score Percentile from baseline (FIG.3D). Lastly, these subjects, who were determined to be in the high-risk group of being in the 50thpercentile FAI score for RCA, LAD, or LCX at baseline also saw a significant reduction in their CaRi-Heart Risk % over the 15 weeks (FIGS.3B and 3C). Orticumab demonstrated a direct anti-inflammatory effect on the coronary arteries of patients with psoriasis during a 15-week period and reduced the FAI score in patients with psoriasis who have high coronary inflammation while no effect was observed in those with a low level of coronary inflammation. According to the predicted CaRi-Heart risk, this could translate into a 50% reduction of the predicted risk of fatal cardiac events in the group with elevated coronary inflammation. The blockade of oxidized LDL with orticumab demonstrated a strong trend towards reduced inflammation in all 3 epicardial coronary arteries, as measured by the CaRi heart device using CCTA, with a statistically significant reduction of inflammation in the LCX artery. In the high-risk population, there was a consistent reduction in vascular inflammation in the coronary arteries by CaRi technology, with a 50% decrease in the predicted absolute risk of a fatal cardiac event over the next 8 years. This study also showed that orticumab improved psoriasis skin disease severity using PASI and BSA after 7 weeks of treatment in obese subjects with active, chronic moderate to severe psoriasis. No serious adverse events due to the study drug were reported, and there was no increase in treatment-emergent adverse events (TEAEs) in the orticumab group compared to placebo (38.5% versus 36% of subjects experienced a TEAE in each group, respectively). The most common adverse events were infections (17.3% of subjects experienced an infection in the orticumab group versus 16 % in the placebo group). There were no drug-related treatment discontinuations. In conclusion, the present study provides the first clinical evidence suggesting that pharmacological inhibition of oxLDL with an anti-oxLDL antibody reduces coronary inflammation. Residual inflammation remains an important risk factor for recurrent events in cardiovascular patients receiving guideline preventive therapy. ATTORNEY DOCKET NO: 51473-028WO2 PATENT OTHER EMBODIMENTS Various modifications and variations of the described disclosure will be apparent to those skilled in the art without departing from the scope and spirit of the disclosure. Although the disclosure has been described in connection with specific embodiments, it should be understood that the disclosure as claimed should not be unduly limited to such specific embodiments. Indeed, various modifications of the described modes for carrying out the disclosure that are obvious to those skilled in the art are intended to be within the scope of the disclosure. Other embodiments are in the claims.

Claims

ATTORNEY DOCKET NO: 51473-028WO2 PATENT CLAIMS 1. A method of treating a subject in need thereof, the method comprising: administering to the subject a therapeutically effective amount of an antibody or fragment thereof that binds to oxidized low density lipoprotein (oxLDL) if the subject is identified as being a candidate for anti-oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary fat attenuation index (FAI) of the blood vessel.

2. A method of identifying a subject as being a candidate for anti-oxLDL antibody therapy, the method comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary FAI of the blood vessel to identify the subject as being a candidate for anti-oxLDL antibody therapy.

3. A method preventing or reducing the risk of myocardial infarction in a subject the method comprising administering to the subject a therapeutically effect amount of an antibody or fragment thereof that binds to oxLDL, if the subject is identified as being a candidate for anti-oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary FAI of the blood vessel.

4. The method of any one of claims 1-3, wherein the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has: (i) a right coronary artery (RCA) FAI of ≥ -85 Hounsfield units (HU); (ii) a left anterior descending artery (LAD) FAI of ≥ -85 HU; (iii) a left circumflex artery (LCX) FAI of ≥ -81 HU; (iv) an RCA FAI Score of ≥ 2; (v) a LAD FAI Score of ≥ 2; (vi) a LCX FAI Score of ≥ 3; (vii) an RCA Percentile of ≥ 28; (viii) a LAD Percentile of ≥ 20; (ix) a LCX Percentile of ≥ 33; or (x) a CaRi-Heart® Risk Score of >1.

4.

5. The method of any one of claims 1-3, wherein the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has: (i) a RCA FAI of ≥ --88 HU; (ii) a LAD FAI of ≥ -80 HU; (iii) a LCX FAI of ≥ -72 HU; (iv) an RCA FAI Score of ≥ 2.4; (v) a LAD FAI Score of ≥ 5; (vi) a LCX FAI Score of ≥ 7;ATTORNEY DOCKET NO: 51473-028WO2 PATENT (vii) an RCA Percentile of ≥ 14; (viii) a LAD Percentile of ≥ 48; (ix) a LCX Percentile of ≥ 62; or (x) a CaRi-Heart® Risk Score of >4.

5.

6. The method of any one of claims 1-3, wherein the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has: (i) a RCA FAI of ≥ -70 HU; (ii) a LAD FAI of ≥ -73 HU; (iii) a LCX FAI of ≥ -67 HU; (iv) an RCA FAI Score of ≥ 18; (v) a LAD FAI Score of ≥ 10; (vi) a LCX FAI Score of ≥ 9; (vii) an RCA Percentile of ≥ 80; (viii) a LAD Percentile of ≥ 75; (ix) a LCX Percentile of ≥ 85; or (x) a CaRi-Heart® Risk Score of >18.

7. The method of any one of claims 1-6, wherein the subject is between the age of 30 and 39.

8. The method of claim 7, wherein the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has: (i) an RCA FAI score of ≥ 3; (ii) a LAD FAI score of ≥ 3; (iii) a LCX FAI Score ≥ 3; or (iv) a CaRi-Heart® Risk Score >4.

9. The method of any one of claims 1-6, wherein the subject is between the age of 40 and 59.

10. The method of claim 9, wherein the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has: (i) an RCA FAI score of ≥ 5; (ii) a LAD FAI score of ≥ 5; (iii) a LCX FAI Score ≥ 5; or (iv) a CaRi-Heart® Risk Score ≥ 7.

11. The method of any one of claims 1-3, wherein the subject is identified as being a candidate for anti- oxLDL antibody therapy if the subject has: i) a RCA percentile ≥ 50; ii) a LAD percentile ≥ 50; or iii) a LCX percentile ≥ 50.ATTORNEY DOCKET NO: 51473-028WO2 PATENT 12. The method of claim 11, wherein the subject is identified as being a candidate for anti-oxLDL antibody therapy if the subject has: i) a RCA percentile ≥ 90; ii) a LAD percentile ≥ 90; or iii) a CaRi-Heart® Score of >10.

13. The method of any one of claims 1-12, wherein the antibody or fragment thereof comprises at least one light chain complementarity determining region (LCDRs) that is at least 90% identical to an LCDR selected from the group consisting of SEQ ID NO: 7, SEQ ID NO: 8, and SEQ ID NO:

9.

14. The method of claim 13, wherein the antibody or fragment thereof comprises at least one LCDR selected from the group consisting of SEQ ID NO: 7, SEQ ID NO: 8, and SEQ ID NO:

9.

15. The method of any one of claims 1-14, wherein the antibody or fragment thereof comprises at least one heavy chain complementarity determining region (HCDRs) that is at least 90% identical to a HCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO:

6.

16. The method of claim 15, wherein the antibody or fragment thereof comprises at least one HCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO:

6.

17. The method of any one of claims 1-16, wherein the antibody or fragment thereof comprises a variable heavy region (VH) of SEQ ID NO: 10, a variable light region (VL) of SEQ ID NO: 11, or both.

18. The method of any one of claims 1-13, wherein the antibody or fragment thereof comprises a heavy chain of SEQ ID NO: 2, a light chain of SEQ ID NO: 3, or both.

19. The method of any one of claims 1-18, wherein the antibody is orticumab.

20. The method of any one of claims 1-19, wherein the subject has been diagnosed with a disease or condition.

21. The method of any one of claims 1-20, wherein the subject has been previously treated for a disease or condition.

22. The method of claim 20 or 21, wherein the disease or condition comprises psoriasis, accelerated atherosclerosis, systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s Syndrome, Fabry disease, psoriatic arthritis, or a cardiovascular disease.

23. The method of claim 22, wherein the cardiovascular disease comprises aortic valve stenosis or aortic valve sclerosis.ATTORNEY DOCKET NO: 51473-028WO2 PATENT 24. The method of claims 1 or 3, wherein orticumab is administered subcutaneously or intravenously.

25. The method of claims 1 or 3, wherein the risk of fatal myocardial infarction is reduced by at least 20% in comparison to a subject who is not administered orticumab.

26. An antibody or fragment thereof that binds to oxLDL for use in the treatment of a subject in need thereof, wherein the antibody or fragment thereof that binds to oxLDL is administered to the subject who is identified as being a candidate for anti-oxLDL antibody therapy, wherein said identifying comprises using a computed tomography scan of a blood vessel in the subject to measure the pericoronary FAI of the blood vessel.

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