Compositions and methods for reducing risk of major adverse cardiovascular event

Abstract

The disclosure provides methods of reducing the risk of a major adverse cardiovascular event (MACE) in a subject having previously experienced acute coronary syndrome (ACS) and for reducing risk of a MACE in a patient who is diagnosed with coronary artery disease and has blood high-sensitivity C- reactive (hs-CRP) of >2.0 mg / L. The methods include administering to the subject an anti-oxLDL antibody. The anti-oxLDL antibody may be administered to the subject alone or in combination with one or more additional therapeutic agents, such as one or more lipid lowering agents.

Description

[0001]ATTORNEY DOCKET NO.: 51473-029WO4 PATENT COMPOSITIONS AND METHODS FOR REDUCING RISK OF MAJOR ADVERSE CARDIOVASCULAR EVENT 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 “51473-029WO4_Sequence_Listing_1_6_25.xml” and is 11,333 bytes in size. BACKGROUND OF THE INVENTION Cardiovascular diseases (CVDs) are a leading cause of death, affecting an estimated more than 70 million people in the United States alone. CVD events include major adverse cardiac events (MACEs), which include stroke, need for revascularization (e.g., a need to restore blood flow to parts of the heart when that flow is limited or blocked), cardiac arrhythmia, and acute coronary syndrome (ACS), including unstable angina and myocardial infarction. Patients with prior ACS face higher risk of experiencing a MACE and poorer clinical outcomes.1 in 4 patients who are discharged from a hospital after surviving ACS will experience a MACE within the following 5 years. Therefore, it is desirable to identify methods to reduce the risk of a MACE in a patient, e.g., one who has experienced a prior ACS of subsequently experience a MACE which may result in severe morbidity or death to the patient. SUMMARY OF THE INVENTION In an aspect, the disclosure provides a method for reducing risk of a major adverse cardiovascular event (MACE) in a patient who has had a prior acute coronary syndrome (ACS). The method comprises administering to the patient an antibody or antibody fragment capable of binding to an oxidized fragment of apolipoprotein B100 (ApoB100), wherein the antibody or antibody fragment is administered to the patient in a pharmaceutically effective amount to reduce the risk in the patient. In some embodiments, the antibody or antibody fragment is administered to the patient within 24 hours of the prior ACS. In some embodiments, the antibody or antibody fragment is administered to the patient prior to the patient being discharged from the hospital for treatment of the ACS. In some embodiments, the antibody or antibody fragment is administered to the patient within 5 years of a prior ACS (e.g., within 5 years, within 4 years, within 3 years, within 2 years, within 1 year, within 6 months, within 3 months, within 1 month, or within 1 week). In some embodiments, the antibody or antibody fragment is administered to the patient from one week to five years (e.g., the patient may have had the ACS from 1 week to 5 years, 2 weeks to 5 years, 1 month to 5 years, 2 months to 5 years, 4 months to 5 years, 6 months to 5 years, 9 months to 5 years, 1 year to 5 years, 18 months to 5 years, 2 years to 5 years, 30 months to 5 years, 1 week to 30 months, 1 week to 2 years, 1 week to 18 months, 1 week to 1 year, 1 week to 9 months, 1 week to 6 months, 1 week to 4 months, 1 week to 2 months, 1 week to 4 weeks, 1 week to 2 weeks, 1 month to 1 year, 1 week to 3 years, 2 years to 4 years, 1 year to 3 years, or 2 years to 4 years) following the prior ACS. In some embodiments, the antibody or antibody fragment is administered to the patient from one week to two years (e.g., 1 week to 2 years, 1 week to 18 months, 1 week to 12 months, 1 week to 10 months, 1 week to 8 months, 1 week to 6 months, 1 week to 4 months, 1 week to 3 months, 1 week to 2 months, 1 week to 1 month, 1 week to 3 weeks, 1 week to 2 weeks, 2 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT weeks to 2 years, 3 weeks to 2 years, 1 month to 2 years, 2 months to 2 years, 3 months to 2 years, 4 months to 2 years, 6 months to 2 years, 8 months to 2 years, 10 months to 2 years, 1 year to 2 years, 14 months to 2 years, 18 months to 2 years, 20 months to 2 years, or 5 months to 18 months) following the prior ACS. In some embodiments, the antibody or antibody fragment is administered to the patient from two weeks to one year (e.g., 2 weeks to 1 year, 2 weeks to 10 months, 2 weeks to 8 months, 2 weeks to 6 months, 2 weeks to 4 months, 2 weeks to 3 months, 2 weeks to 2 months, 2 weeks to 1 month, 2 weeks to 3 weeks, 3 weeks to 1 year, 1 month to 1 year, 2 months to 1 year, 3 months to 1 year, 4 months to 1 year, 6 months to 1 year, 8 months to 1 year, 10 months to 1 year, 5 months to 10 months or 3 months to 6 months) following the prior ACS. In some embodiments, the prior ACS comprises a myocardial infarction (MI). In another aspect, the disclosure provides a method for reducing risk of a MACE in a patient who is diagnosed with coronary artery disease and has blood high-sensitivity C-reactive (hs-CRP) of >2.0 mg / L. The method comprises administering to the patient an antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100, wherein the antibody or antibody fragment is administered to the patient in a pharmaceutically effective amount to reduce the risk in the patient. In some embodiments of either of the above aspects, the fragment of ApoB100 comprises an amino acid sequence of SEQ ID NO: 1 and is an aldehyde derivative. 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 or the antibody fragment comprises heavy chain complementarity determining regions (HCDRs) HCDR1, HCDR2, and HCDR3 sequences of SEQ ID Nos: 2, 3, and 4, respectively, and light chain complementarity determining regions (LCDRs) LCDR1, LCDR2, and LCDR3 sequences of SEQ ID NOs: 5, 6, and 7, respectively. In some embodiments, the antibody is orticumab. In some embodiments of either of the above aspects, the method further comprises administering a lipid-lowering agent to the patient. In some embodiments, the patient was previously on a lipid-lowering agent. In some embodiments, the lipid-lowering agent comprises an antibody, an siRNA, an antisense oligonucleotide, a small molecule, an omega-3 fatty acid, a bile acid sequestrant, or a peptide. In some embodiments, the small molecule is a statin. In some embodiments, the statin is lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, or pitavastatin. In some embodiments, the small molecule is ezetimibe. In some embodiments, the small molecule is a fibrate. In some embodiments, the fibrate is fenofibrate, bezafibrate, gemfibrozil, or pemafibrate. In some embodiments, the lipid-lowering agent is a bile acid sequestrant. In some embodiments, the bile acid sequestrant is cholestyramine, ATTORNEY DOCKET NO.: 51473-029WO4 PATENT colesevelam or colestipol. In some embodiments, the small molecule is bempedoic acid or lomitapide. In some embodiments, the lipid-lowering agent is an omega-3 fatty acid. In some embodiments, the omega- 3 fatty acid is docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), or docosapentaenoic acid (DPA). In some embodiments, the lipid-lowering agent is an antibody. In some embodiments, the antibody is a PCSK9 antibody. In some embodiments, the PCSK9 antibody is evolocumab or alirocumab. In some embodiments, the antibody is evinacumab. In some embodiments, the lipid-lowering agent is an siRNA. In some embodiments, the siRNA is a PCSK9 siRNA. In some embodiments, the PCSK9 siRNA is inclisiran. In some embodiments, the siRNA is olpasiran. In some embodiments, the lipid-lowering agent is an antisense oligonucleotide. In some embodiments, the antisense oligonucleotide is mipomersen, volanesorsen, pelacarsen, or olezarsen. In some embodiments, the peptide is NNC0385- 0434A. In some embodiments, the method further comprises administering colchicine to the patient. In some embodiments, the method further comprises administering ziltivekimab to the patient. In some embodiments of either of the above aspects, the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 is administered in one, two or more doses of at least 5 mg / kg each or at least 8 mg / kg each. In some embodiments, further comprising administering a plurality of subsequent doses of the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 in an amount of at least 2 mg / kg / week, at least 2.5 mg / kg / two weeks, or at least 6 mg / kg / month. In some embodiments, the two or more doses are administered over at least 8 weeks, 10 weeks, or 12 weeks. In some embodiments, the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 is administered at 1-10 µg / kg, 10-100 µg / kg, 100-500 µg / kg, 200-500 µg / kg, 300- 500 µg / kg, 400-500 µg / kg, 1-5 mg / kg, 5-10 mg / kg, 10-15 mg / kg, 15-20 mg / kg, 20-25 mg / kg, 25-50 mg / kg, 50-75 mg / kg. In some embodiments of either of the above aspects, the MACE comprises a stroke, need for revascularization, cardiac arrhythmia, ACS, unstable angina, or myocardial infarction. In some embodiments, the MACE is ACS. In some embodiments, the ACS comprises unstable angina (UA) or an acute myocardial infarction (MI). In some embodiments, the MI is ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation myocardial infarction (NSTEMI). 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 (shaded background) or placebo (white background) from the whole population. FIGS.3A, 3B, and 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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-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 FAI score of < 50thpercentile in the RCA, LAD, or LCX arteries. FIG.5 shows 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. 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” means plus or minus 10% of the particular value. The term “acute coronary syndrome,” as used herein, encompasses any group of clinical symptoms compatible with acute myocardial ischemia. Acute myocardial ischemia causes chest pain due to insufficient blood supply to the heart muscle that results from coronary artery disease, which is also known as coronary heart disease. Acute myocardial ischemia includes unstable angina (UA) and (acute) myocardial infarction (AMI or MI), in which the heart muscle is damaged. UA, which may also be referred to as crescendo angina, refers to angina pectoris that changes or worsens. AMI refers to both non-ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI). These two types of MI may be determined using an electrocardiogram (EKG). “Administering” and “administer,” as used herein, refer to any route for delivering a pharmaceutical composition to a patient. 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, IgG3and IgG4. Antibody light chains of any vertebrate ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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. 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. “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. 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 terms “effective amount” and “pharmaceutically effective amount” refer to at least the minimum amount of the pharmaceutical composition required to achieve the desired therapeutic or prophylactic result, such as a measurable improvement, prevention, or reduction of risk of a particular disorder (e.g., MACE, e.g., UA and MI). An effective amount herein may vary according to factors such ATTORNEY DOCKET NO.: 51473-029WO4 PATENT as the disease state, age, sex, and weight of the animal, and the ability of the antibody to elicit a desired response in the animal. An effective amount is also one in which any toxic or detrimental effects of the treatment are outweighed by the therapeutically beneficial effects. For prophylactic use, beneficial or desired results include results such as eliminating or reducing the risk, lessening the severity, or delaying the onset of the disease, including biochemical, histological and / or behavioral symptoms of the disease, its complications, and intermediate pathological phenotypes presenting during development of the disease. For therapeutic use, beneficial or desired results include clinical results such as decreasing one or more symptoms resulting from the disease, increasing the quality of life of those suffering from the disease, decreasing the dose of other medications required to treat the disease, enhancing effect of another medication such as via targeting, delaying the progression of the disease, and / or prolonging survival. An effective amount can be administered in one or more administrations. For purposes of this invention, an effective amount of drug, compound, or pharmaceutical composition is an amount sufficient to accomplish prophylactic or therapeutic treatment either directly or indirectly. As is understood in the clinical context, an effective amount of a drug, compound, or pharmaceutical composition may or may not be achieved in conjunction with another drug, compound, or pharmaceutical composition. Thus, an “effective amount” may be considered in the context of administering one or more therapeutic agents, and a single agent may be considered to be given in an effective amount if, in conjunction with one or more other agents, a desirable result may be or is achieved. In some embodiments, a therapeutic pharmaceutical composition is used, for example, to treat, inhibit, reduce the risk of a MACE, and / or related symptoms in a patient in need thereof. As used herein, the term “reduce the risk of a major cardiovascular event” refers to reducing the likelihood that a patient undergoes a major adverse cardiovascular event (MACE). A reduced risk of MACE is assessed for a given patient population (e.g., patients who have experienced a prior ACS). The reduction in risk for MACE is understood by comparing rates for a MACE in patients having prior ACS being treated by the methods described herein with the rates of MACE in patients having prior who are not treated by the methods described herein. A therapeutically or prophylactically significant reduction in a occurrence of a MACE 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 patient or the state of the patient prior to administering the compositions described herein. 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. “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 various terms as described above, the exact amino acid sequence of a framework depends on how the antigen-binding site was defined. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT “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. 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 patient together in a mixture, concurrently as single agents or sequentially as single agents in any order. As used herein, the term “major cardiovascular event” or “MACE” encompasses stroke, need for revascularization (e.g., a need to restore blood flow to parts of the heart when that flow is limited or blocked), cardiac arrhythmia, and ACS, including UA and MI. Potential outcomes of MACEs include fatal MI, fatal stroke, nonfatal MI, nonfatal stroke, nonfatal UA, and heart failure requiring hospitalization. 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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. 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. “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, 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” refer to any subject, particularly a mammalian subject, for whom diagnosis, prognosis, or therapy is desired. Mammalian subjects include, ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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. DETAILED DESCRIPTION The present disclosure features compositions and methods of reducing the risk of a major adverse cardiovascular event (MACE) in a patient who has had a prior acute coronary syndrome (ACS). The method includes administering to the patient antibodies and antibody fragments capable of binding to oxidized-low density lipoproteins (ox-LDL). Also provided herein are methods of preparing recombinant murine or chimeric murine-human or human-human anti-ox-LDL antibodies for administration to a patient. Anti-ox-LDL antibodies may be incorporated into a pharmaceutical composition, which can be administered to a patient alone or in combination with another therapeutical agent, such as a lipid- lowering agent to reduce a patient’s risk of experiencing a MACE. During an ACS, patients are exposed to significant oxidative stress and coronary inflammation. This inflammation leads to a significant risk of a vulnerable plaque rupture and, consequently, for a MACE to occur in the patient. In patients having been identified as having high coronary inflammation by way of suffering from an ACS or through clinical assessment, inflammation must be lowered in order reduce the risk of a MACE occurring the patient. Accordingly, there is a need to reduce coronary inflammation in order to reduce the risk for a MACE occurring in the patient. Patients who are being treated by methods of the disclosure have had a prior ACS, such as unstable angina (UA) or acute myocardial infarction (MI). The patient may be administered the anti-ox-LDL antibody within 24 hours of the ACS. For example, the patient may have the ACS within 1 hour, 2 hours, 4 hours, 8 hours, 10 hours, 12 hours, 14 hours, 16 hours, 18 hours, 20 hours, 22 hours, or 24 hours prior to administration of the anti-ox-LDL antibody. The patient may be administered the anti-ox-LDL antibody 1 day to 3 days after the ACS (e.g., 24 hours to 36 hours, 24 hours to 48 hours, 24 hours to 60 hours, 24 hours to 70 hours, 70 hours to 72 hours, 60 hours to 72 hours, 48 hours to 72 hours, 36 hours to 72 hours, or 30 hours to 72 hours). In some embodiments, the patient is administered the anti-ox-LDL antibody within 5 years of an ACS (e.g., within 1 year, within 2 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT years, within 3 years, within 4 years, within 5 years, within 1 week, within 1 month, within 6 months, within 3 months. For example, the patient is administered the anti-ox-LDL antibody between 24 hours and 5 years after suffering from the ACS. The patient may have had the ACS 1 week to 5 years prior to administration of the anti-ox-LDL antibody (e.g., the patient may have had the ACS from 1 week to 5 years, 2 weeks to 5 years, 1 month to 5 years, 2 months to 5 years, 4 months to 5 years, 6 months to 5 years, 9 months to 5 years, 1 year to 5 years, 18 months to 5 years, 2 years to 5 years, 30 months to 5 years, 1 week to 30 months, 1 week to 2 years, 1 week to 18 months, 1 week to 1 year, 1 week to 9 months, 1 week to 6 months, 1 week to 4 months, 1 week to 2 months, 1 week to 4 weeks, 1 week to 2 weeks, 1 month to 1 year, 1 year and 3 years, 2 years and 4 years, 1 week and 4 years, 1 month and 4 years, or 1 year and 2 years prior to administration of the anti-ox-LDL antibody or may have had the ACS). The ACS may have occurred in the patient 1 week to 2 years (e.g., 1 week to 2 years, 1 week to 18 months, 1 week to 12 months, 1 week to 10 months, 1 week to 8 months, 1 week to 6 months, 1 week to 4 months, 1 week to 3 months, 1 week to 2 months, 1 week to 1 month, 1 week to 3 weeks, 1 week to 2 weeks, 2 weeks to 2 years, 3 weeks to 2 years, 1 month to 2 years, 2 months to 2 years, 3 months to 2 years, 4 months to 2 years, 6 months to 2 years, 8 months to 2 years, 10 months to 2 years, 1 year to 2 years, 14 months to 2 years, 18 months to 2 years, 20 months to 2 years, or 5 months to 18 months) prior to treatment by methods of the disclosure. For example, the ACS may have occurred in the patient 2 weeks to 1 year (e.g., 2 weeks to 1 year, 2 weeks to 10 months, 2 weeks to 8 months, 2 weeks to 6 months, 2 weeks to 4 months, 2 weeks to 3 months, 2 weeks to 2 months, 2 weeks to 1 month, 2 weeks to 3 weeks, 3 weeks to 1 year, 1 month to 1 year, 2 months to 1 year, 3 months to 1 year, 4 months to 1 year, 6 months to 1 year, 8 months to 1 year, 10 months to 1 year, 5 months to 10 months or 3 months to 6 months) prior to treatment by methods of the disclosure. The risk of developing a MACE is higher in patients who have had a prior ACS. MACE encompasses stroke, need for revascularization (e.g., a need to restore blood flow to parts of the heart when that flow is limited or blocked), cardiac arrhythmia, and ACS, including UA and MI. Potential outcomes of a patient experiencing a MACE include cardiovascular death as a result of fatal MI and fatal stroke, nonfatal MI, nonfatal stroke, nonfatal UA, or heart failure requiring hospitalization. The methods described herein reduce the risk of a MACE in a patient who has had a prior ACS, where the risk of a MACE refers to the potential likelihood that a patient experiences a MACE. A reduced risk of MACE is assessed for a given patient population (e.g., patients who have experienced a prior ACS) of a particular severity comparing rates for a MACE in patients being treated by a method of the invention alone or in combination with a lipid-lowering agent to patients relying solely on a lipid-lowering agent. As a result of treatment by the methods described herein, the patient may have a reduced risk of having a MACE. The risk may be reduced by 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 in comparison to a patient who has not been administered an anti-ox-LDL antibody after an ACS. For example, the patient who is administered an any one of the anti-ox-LDL antibodies described herein may reduce their risk of a MACE by 5% to 100% (e.g., 5% to 95%, 5% to 90%, 5% to 85%, 5% to 80%, 5% to 75%, 5% to 70%, 5% to 65%, 5% to 60%, 5% to 55%, 5% to 50%, 5% to 45%, 5% to 40%, 5% to 35%, 5% to 30%, 5% to 25%, 5% to 20%, 5% to 15%, 5% to 10%, 10% to 15%, 10% to 20%, 10% to 25%, 10% to 30%, 10% to 35%, 10% to 40%, 10% to 45%, 10% to 50%, 10% to 55%, 10% to 60%, 10% to 65%, 10% to 70%, 10% to 75%, 10% to 80%, 10% to 85%, 10% to 90%, 10% to 95%, 10% to 100%, 20% to 50%, 50% to 80%). In ATTORNEY DOCKET NO.: 51473-029WO4 PATENT some embodiments, the patient’s risk of a MACE is reduced by 20% to 90%. Embodiments of the present methods can also be used to assess the patient’s risk of experiencing an adverse cardiac event within the ensuing 30 days, 60 days, 90 days, five years, four years, three years, two years, or one year. In another embodiment, the present methods are used to determine if a patient presenting with chest pain is at risk of experiencing a heart attack or other MACE, such as a near term MI, reinfarction, stroke, the need for revascularization (e.g., a need to restore blood flow to parts of the heart when that flow is limited or blocked), or death. As used in this context, the term “near term” means within one year. Thus, patients who are at near term risk may be at risk of experiencing a MACE within the following day, 3 months, or 6 months after presenting with chest pain. Anti-Ox-LDL Antibodies The disclosure provides methods of reducing the risk of a MACE in a patient having previously had an ACS by administering to the patient an antibody or antibody fragment capable of binding to ox- LDL. 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). 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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- 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 method of reducing the risk of a patient having a MACE described herein. 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 patient. 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 patient (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 patient'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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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. Methods of Administration The antibodies that bind ox-LDL may be administered to a patient in need thereof. The antibodies may be administered to the patient in a pharmaceutically effect amount to reduce the patient’s risk of a MACE after an ACS. The antibody may be administered to the patient in order to reduce the patient’s risk of MACE either alone or in combination with one or more therapeutic agents. For example, the antibody may be administered to the patient with one or more lipid lowering agents. In some embodiments the patient is assessed using Coronary Computed Tomography Angiography (CCTA). For example, the CCTA may be used to assess the pericoronary vascular adipose tissue or perivascular Fat Attenuation Index in the patient. Combination Therapies The antibodies and antibody fragments capable of binding oxidized ApoB100 described herein may be administered to the patient in combination with one or more additional therapeutic agents. For example, the antibody or antibody fragment capable of binding oxidized ApoB100 may be administered in combination with a lipid-lowering agent. In some embodiments, the patient may have been administered a lipid-lowering agent prior to experiencing ACS. The lipid-lowering agent may be an antibody, an siRNA, an antisense oligonucleotide, a small molecule, an omega-3 fatty acid, a bile acid sequestrant, or a ATTORNEY DOCKET NO.: 51473-029WO4 PATENT peptide. The lipid-lowering agent may be a small molecule. In some embodiments, the lipid-lowering agent is a statin. For example, the statin may be lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, or pitavastatin, or a combination thereof. Statins inhibit 2-hydroxyl-methyl- glutaryl coenzyme A (HMG-CoA) reductase, which is the rate-limiting step in cholesterol synthesis. As a result, there may be a reduced intracellular cholesterol concentration and subsequent upregulation of LDL receptors which encourages the removal of low-density lipoprotein cholesterol (LDL-C) from the circulation. The resulting reduction in LDL-C as a result of administering a statin to the patient may be dose dependent. The statin may also reduce the level of triglycerides in a patient upon administration. While statins are generally safe and generally tolerated by most patients, higher doses that achieve greater LDL-C reduction may cause more side effects such as gastrointestinal disturbances and myopathy. Increase in liver enzymes particularly alanine and aspartate transaminases may occur in some patients who are administered a statin therapy and may normalize on reducing the dose or stopping the statin. A baseline measurement of liver function test may be performed prior to beginning the statin therapy. Statin therapy may be discontinued if transaminases are found to be well over a reference limit. In some embodiments, the small molecule is ezetimibe. Ezetimibe acts by inhibiting cholesterol absorption through inhibition of the duodenal Niemann-Pick C1-like protein. Ezetimibe may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, ezetimibe may be administered to a patient in combination with a statin. In some embodiments, the small molecule is a fibrate. For example, the fibrate may be fenofibrate, bezafibrate, gemfibrozil, or pemafibrate. Fibrates reduce concentrations of triglycerides. Treatment with fibrates may cause side effects including gastrointestinal pain, skin rashes, myopathy, and liver enzyme elevation. The fibrate may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the fibrate may be administered to a patient in combination with a statin. In some embodiments, the lipid-lowering agent is a bile acid sequestrant. For example, the bile acid sequestrant may be cholestyramine, colesevelam or colestipol. Bile acid sequestrants bind to intestinal cholesterol and thereby inhibit the absorption cholesterol in the small intestine. As a result, intestinal cholesterol may be effectively removed from the enterohepatic cholesterol circulation. Treatment with bile sequestrants is associated with a significant reduction in LDL-Cs. The bile acid sequestrant may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the bile acid sequestrant may be administered to a patient in combination with a statin. In some embodiments, the lipid-lowering agent is an omega-3 fatty acid. For example, the omega-3 fatty acid may be docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), or docosapentaenoic acid (DPA). The omega-3 fatty acid may be administered to the patient alone or in combination with one or more additional lipid-lowering agents. For example, the patient may be administered a statin and an omega-3 fatty acid. The omega-3 fatty acid may reduce triglycerides in the patient in a dose-dependent manner. In some embodiments, the lipid-lowering agent may be an antibody. For example, the antibody may be evinacumab. Evinacumab inhibits angiopoietin-like 3 (ANGPTL3), which results in decreased blood lipid levels. In some embodiments, the antibody may be a PCSK9 antibody, such as evolocumab or alirocumab. PCSK9 antibodies inhibit PCSK9, thereby reducing the concentration of PCSK9 plasma ATTORNEY DOCKET NO.: 51473-029WO4 PATENT levels. As a result, LDL-C receptor expression is increased, and LDL-C levels are reduced. PCSK9 inhibitors also lower triglycerides and lipoprotein(a). The antibody may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the antibody may be administered to a patient in combination with a statin. In some embodiments, the lipid-lowering agent may be an siRNA. For example, the siRNA may be olpasiran. Olpasiran acts by reducing Lp(a) levels. In some embodiments, the siRNA may be a PCSK9 siRNA, such as inclisiran. The PCSK9 siRNA may act by inhibiting PCSK9 biosynthesis. The underlying method of action is similar to evolocumab and alirocumab. The siRNA permits infrequent subcutaneous administration with fewer injection site reactions. The siRNA may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the siRNA may be administered to a patient in combination with a statin. In some embodiments, the lipid-lowering agent may be an antisense oligonucleotide. For example, the antisense oligonucleotide may be mipomersen, volanesorsen, pelacarsen, or olezarsen. The antisense oligonucleotide may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the antisense oligonucleotide may be administered to a patient in combination with a statin. In some embodiments, the lipid-lowering agent may be a peptide. For example, the peptide may be NNC0385-0434A. NNC0385-0434A is a PCSK9 inhibitor. The peptide may be administered to the patient alone or in combination with one or more lipid-lowering agents. For example, the peptide may be administered to a patient in combination with a statin. Dosing Typically, an effective amount of the anti-oxLDL or an anti-LDL antibody, or the antibody that binds SEQ ID NO: 1, in the method disclosed herein, results in a plasma concentration of at least 4 pg / mL, preferably at least 12 pg / mL in the patient. Embodiments provide the method of treating or reducing the risk of a MACE in a patient who has had a prior ACS, includes administering to the patient an antibody or antibody fragment disclosed above subcutaneously at about 330 mg / month for about 3, 4, 5, 6, 7, 8, 9, 10, 11 or 12 months or longer, and the patient is an adult human. Other embodiments provide administering the antibody or antibody fragment to treat reduce the risk of a MACE in a patient who has had a prior ACS or provide passive immunity with at least 8 mg orticumab / kg of a patient (e.g., 664 mg for an averaged human patient of 83 kg). Some embodiments provide administering the antibody or antibody fragment at between 5 mg orticumab / kg of a patient (e.g., 415 mg for an average human patient of 83 kg) and 8 mg / kg. Some embodiment provides administering orticumab at a monthly dosing regimen at the above-mentioned dosage. Other embodiments provide administering the antibody or antibody fragment to reduce the risk of a MACE in a patient who has had a prior ACS weekly at no less than 2 mg / kg / week (166 mg for an averaged human patient of 83 kg); preferably, 4 mg / kg / week (332 mg for an averaged human patient of 83 kg). In another aspect, the composition of an anti-oxLDL antibody is administered biweekly at >2.5 mg / kg / two weeks (e.g., 208 mg for an averaged human patient of 83 kg). In yet another aspect, the composition of an anti-oxLDL antibody is administered monthly at about 6 mg / kg / month (e.g., about 498 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT mg for an average human patient of 83 kg). For example, the monthly dosing may be carried out for 12 months or 3 months. Yet other embodiments provide administering an antibody or antibody fragment to reduce the risk of a MACE in a patient who has had a prior ACS with at least an initial dose of 800-900 mg, 900-1000 mg, 1000-1100 mg, 1100-1200 mg, 1200-1300 mg, 1300-1400 mg, 1400-1500 mg, or 1500-1600 mg. In some aspects, the effective amount in the method described herein includes an initial dose of orticumab of approximately 1000-1500 mg, followed by subsequent doses of the antibody at 700-900 mg administered weekly for 2, 3, 4 or 5 weeks and / or even administered monthly for 1, 2 or 3 months. Other embodiments provide administering step-wise escalating doses of an antibody against native or oxidized LDL (e.g., binding SEQ ID NO: 1). In this embodiment, an exemplary (starting) dose of a single-dose administration of an antibody (e.g., orticumab) against native or oxidized LDL is between 0.005 and 0.01 mg / kg (e.g., intravenously); and other exemplary dosage levels to be administered in the single-dose administration are between 0.01 and 0.15, between 0.15 and 0.75, between 0.75 and 2.5, between 2.5 and 7.5, and between 7.5 and 30 mg / kg (e.g., intravenously). For example, a starting dose of orticumab in a single-dose intravenous administration is 0.007 mg / kg; and other exemplary dosages can be 0.05, 0.25, 1.25, 5.0 or 15.0 mg / kg in subsequent single-dose intravenous administration. In another embodiment, a single-dose subcutaneous administration of an antibody against native or oxidized LDL is between 0.5 and 5 mg / kg, and a multiple-dose subcutaneous administration is also between 0.5 and 5 mg / kg. For example, an antibody against native or oxidized LDL at 1.25 mg / kg is administered subcutaneously. In various embodiments, the dosage is administered within a specified hour range of the day in each administration, and each dose in a multiple-dose treatment (e.g., 4 doses, 3 doses, 5 doses, or 6 doses) is administered at weekly intervals with a time window of ± 1 day. In another example, an antibody (such as orticumab) against native or oxidized LDL is administered at between 300 mg and 450 mg (e.g., 360 mg) to a human patient, optionally followed by another dose between 300 mg and 450 mg (e.g., 360 mg) to the human patient where the second dose is at least 70 days (up to 91 days) apart from the first dose. The antibody (such as orticumab) may be formulated at a concentration of 100-170 mg / mL (e.g., 150 mg / mL) and for use in subcutaneous administration without further dilution, or diluted to a large volume for intravenous infusion. Further embodiments include administering to a patient an effective amount of an antibody or antibody fragment that binds SEQ ID NO: 1 and having a sequence of one or more of SEQ ID NOs: 2-11, which is in the range of about 10-50 pg / period, 50-100 pg / period, 100-150 pg / period, 150-200 pg / period, 100-200 pg / period, 200-300 pg / period, 300-400 pg / period, 400-500 pg / period, 500-600 pg / period, 600- 700 pg / period, 700-800 pg / period, 800-900 pg / period, 900-1000 pg / period, 1000-1100 pg / period, 1100- 1200 pg / period, 1200- 1300 pg / period, 1300-1400 pg / period, 1400-1500 pg / period, 1500-1600 pg / period, 1600-1700 pg / period, 1700-1800 pg / period, 1800-1900 pg / period, 1900-2000 pg / period, 2000-2100 pg / period, 2100-2200 pg / period, 2200-2300 pg / period, 2300-2400 pg / period, 2400-2500 pg / period, 2500- 2600 pg / period, 2600-2700 pg / period, 2700-2800 pg / period, 2800-2900 pg / period or 2900-3000 pg / period. A period is a day, a week, a month, or another length of time. One aspect is the antibody (e.g., orticumab) is administered at a weekly, biweekly or monthly frequency of any of above-mentioned dosage per period. In some embodiments, the methods include administering an inhibitor of oxidized LDL (e.g., orticumab) to the patient for 1-5 days, 1-5 weeks, 1-5 months, or 1-5 years. For example, the antibody is ATTORNEY DOCKET NO.: 51473-029WO4 PATENT administered to the patient in 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 or 20 doses, each dose separated by at least 3 days, 5 days, one week, two weeks, one month, two months, or a combination thereof. In other embodiments, the second dose is administered about 2-3 weeks, or about 3 weeks after the first dose and the third dose is administered about 5-6 weeks or about 6 weeks after the first dose, etc. In another embodiment, the second dose is administered about 2-3 months, about 2 months, about 3 months or about 4 months after the first dose and the third dose is administered about 4- 6 months, about 5-6 months, about 5 months or about 6 months after the first dose. Other embodiments provide administering step-wise escalating doses of an antibody against native or oxidized LDL to reduce the risk of a MACE in a patient who has had a prior ACS. In this embodiment, an exemplary (starting) dose of a single-dose administration of an antibody (e.g., orticumab) against native or oxidized LDL is between 0.005 and 0.01 mg / kg (e.g., intravenously); and other exemplary dosage levels to be administered in the single-dose administration are between 0.01 and 0.15, between 0.15 and 0.75, between 0.75 and 2.5, between 2.5 and 7.5, and between 7.5 and 30 mg / kg (e.g., intravenously). For example, a starting dose of orticumab in a single-dose intravenous administration is 0.007 mg / kg; and other exemplary dosages can be 0.05, 0.25, 1.25, 5.0 or 15.0 mg / kg in subsequent single-dose intravenous administration. In another embodiment, a single-dose subcutaneous administration of an antibody against native or oxidized LDL is between 0.5 and 5 mg / kg, and a multiple- dose subcutaneous administration is also between 0.5 and 5 mg / kg. For example, an antibody against native or oxidized LDL at 1.25 mg / kg is administered subcutaneously. In various embodiments, the dosage is administered within a specified hour range of the day in each administration, and each dose in a multiple-dose treatment (e.g., 4 doses, 3 doses, 5 doses, or 6 doses) is administered at weekly intervals with a time window of ± 1 day. In another example, an antibody (such as orticumab) against native or oxidized LDL is administered at between 300 mg and 450 mg (e.g., 360 mg) to a human patient, optionally followed by another dose between 300 mg and 450 mg (e.g., 360 mg) to the human patient where the second dose is at least 70 days (up to 91 days) apart from the first dose. The antibody (such as orticumab) may be formulated at a concentration of 100-170 mg / mL (e.g., 150 mg / mL) and for use in subcutaneous administration without further dilution, or diluted to a large volume for intravenous infusion. In some embodiments, the therapeutically effective amount of an anti-LDL antibody or an anti-oxLDL antibody, or analogs, pharmaceutical equivalents or a peptidomimetics thereof, for use with the methods described herein is per dose: 1-10 pg / kg, 10-100 pg / kg, 100-500 pg / kg, 200-500 pg / kg, 300-500 pg / kg, 400-500 pg / kg, 1-5 mg / kg, 5-10 mg / kg, 10-15 mg / kg, 15-20 mg / kg, 20-25 mg / kg, 25-50 mg / kg, 50-75 mg / kg of the patient; where each dose is administered daily, weekly, monthly, or at other intervals. 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. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Example 1. Administration of an anti-ox-LDL antibody to reduce the risk of MACE in a patient who had a prior ACS Patients who had a prior ACS may be administered a therapeutically effective amount of an anti- ox-LDL antibody to reduce the risk of a MACE in the patient. Patients may have had an ACS within the past 24 hours. Patients may have had an ACS one week to three years prior. Patients may have had an ACS from one week to two years prior to the administration of the anti-ox-LDL antibody. Patients may have had an ACS from two weeks to one year prior. An anti-ox-LDL antibody or antibody fragment capable of binding to an oxidized fragment of apolipoprotein B100 may be administered to the patient having been identified as having had an ACS. The antibody or antibody fragment may comprise 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. The antibody or antibody fragment may comprise 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. The antibody or antibody fragment may comprise at least one LCDR selected from the group consisting of SEQ ID NO: 7, SEQ ID NO: 8, and SEQ ID NO: 9. The antibody or antibody fragment may comprise at least one heavy chain complementarity determining region (HCDRs) that is at least 90% identical to an LCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO: 6. The antibody or antibody fragment may comprise at least one LCDR selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, and SEQ ID NO: 6. The antibody or fragment thereof may comprise a variable heavy region (VH) of SEQ ID NO: 10, a variable light region (VL) of SEQ ID NO: 11, or both. The antibody or antibody fragment may comprise a heavy chain of SEQ ID NO: 2, a light chain of SEQ ID NO: 3, or both. The antibody or the antibody fragment may comprise heavy chain complementarity determining regions (HCDRs) HCDR1, HCDR2, and HCDR3 sequences of SEQ ID NOs: 2, 3, and 4, respectively, and light chain complementarity determining regions (LCDRs) LCDR1, LCDR2, and LCDR3 sequences of SEQ ID NOs: 5, 6, and 7, respectively. The antibody may be orticumab. The anti-ox-LDL antibody may be administered to the patient in doses of at least 5 mg / kg or at least 8 mg / kg. The anti-ox-LDL antibody may be administered at 1-10 ug / kg, 10-100 ug / kg, 100-500 ug / kg, 200-500 ug / kg, 300-500 ug / kg, 400-500 ug / kg, 1-5 mg / kg, 5-10 mg / kg, 10-15 mg / kg, 15-20 mg / kg, 20-25 mg / kg, 25-50 mg / kg, 50-75 mg / kg. The anti-ox-LDL antibody may be administered in a plurality of subsequent doses of the antibody or antibody fragment in an amount of at least 2 mg / kg / week, at least 2.5 mg / kg / two weeks, or at least 6 mg / kg / month. The subsequent doses of anti-ox-LDL antibody may be administered in two or more doses over at least 8 weeks, 10 weeks, or 12 weeks. The anti-ox-LDL antibody may be administered to the patient intravenously, subcutaneously, intramuscularly, intraperitoneally, intracerebroventricularly, or by intrathecal injection. The risk of a MACE may be measured within the ensuing 30 days, 60 days, 90 days, five years, four years, three years, two years, or one year. A reduced risk of a MACE may be determined if the patient does not experience a MACE in the ensuing five years, four years, three years, two years, or one year. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Example 2. Administration of an anti-ox-LDL antibody and lipid-lowering therapy to reduce the risk of MACE in a patient who had a prior ACS Patients who had a prior ACS may be administered a therapeutically effective amount of an anti- ox-LDL antibody to reduce the risk of a MACE in the patient. Patients may have had an ACS within the past 24 hours. Patients may have had an ACS one week to three years prior. Patients may have had an ACS from one week to two years prior to the administration of the anti-ox-LDL antibody. Patients may have had an ACS from two weeks to one year prior The patient is also administered a lipid-lowering therapy. The lipid-lowering therapy may include administration of a lipid-lowering agent to the patient. The lipid-lowering agent may be a statin, wherein the statin may be lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, or pitavastatin, or a combination thereof. The lipid-lowering agent may be ezetimibe or NNC0385-0434A. The lipid-lowering agent may be an antibody, wherein the antibody may be evinacumab or a PCSK9 antibody, such as evolocumab or alirocumab. The lipid-lowering agent may be an siRNA, wherein the siRNA may be olpasiran or a PCSK9 siRNA, such as inclisiran. The lipid-lowering agent may be an antisense oligonucleotide, wherein the antisense oligonucleotide may be mipomersen, volanesorsen, pelacarsen, or olezarsen. The lipid-lowering agent may be a small molecule. The small molecule may be a fibrate, wherein the fibrate may be fenofibrate, bezafibrate, gemfibrozil, or pemafibrate. The small molecule may be an omega-3 fatty acid, wherein the omega-3 fatty acid may be docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), or docosapentaenoic acid (DPA). The small molecule may be a bile acid sequestrant, wherein the bile acid sequestrant may be cholestyramine, colesevelam, or colestipol. The small molecule may be bempedoic acid or lomitapide. The anti-ox-LDL antibody may be administered to the subject while they receive treatment by a lipid-lowering therapy. The anti-ox-LDL antibody may be administered to the subject who has previously been treated by a lipid-lowering therapy. The anti-ox-LDL antibody may be administered in doses of at least 5 mg / kg or at least 8 mg / kg. The anti-ox-LDL antibody may be administered at 1-10 ug / kg, 10-100 ug / kg, 100-500 ug / kg, 200-500 ug / kg, 300-500 ug / kg, 400-500 ug / kg, 1-5 mg / kg, 5-10 mg / kg, 10-15 mg / kg, 15-20 mg / kg, 20-25 mg / kg, 25-50 mg / kg, 50-75 mg / kg. The anti-ox-LDL antibody may be administered in a plurality of subsequent doses of the antibody or antibody fragment in an amount of at least 2 mg / kg / week, at least 2.5 mg / kg / two weeks, or at least 6 mg / kg / month. The subsequent doses of anti-ox-LDL antibody may be administered in two or more doses over at least 8 weeks, 10 weeks, or 12 weeks. The anti-ox-LDL antibody may, e.g., be administered to the patient intravenously, subcutaneously, intramuscularly, or intraperitoneally. There may be a reduced risk of a MACE when comparing rates for a MACE in patients treated with the anti-ox-LDL antibody in combination with a lipid-lowering therapy to patients relying solely on a lipid-lowering agent. There may further be a reduction risk of MACE when comparing severity of MACEs (e.g., number of MACEs) during or after the treatment. The patient’s risk of experiencing an adverse cardiac event may be measured within the ensuing 30 days, 60 days, 90 days, five years, four years, three years, two years, or one year. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Example 3. 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. In this Example, patients having psoriasis and determined to have a high amount of inflammation in the coronary artery experienced a reduction in coronary inflammation when administered orticumab. 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 FAI score quantified 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 to monitor the effectiveness of anti-inflammatory agents on coronary inflammation. Artificial intelligence-enhanced cardiac risk prediction algorithm (CaRi-Heart® Risk Score) incorporated the FAI score with clinical risk factors and CCTA-derived plaque metrics to predict the 8-year risk of a 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 77 subjects with psoriasis were randomized in a double-blind fashion to 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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 four body areas: the head and neck (H), the upper limbs (UL), the trunk (T) and the lower limbs (LL). The percentage of skin ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 3 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’. 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. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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)), 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. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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 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- ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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) ^ 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. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Table 2. Summary of Demographics and Baseline Characteristics (Safety Population) Max = maximum; Min = minimum The baseline characteristics of the subjects that participated in the CCTA study are summarized below in Table 3. ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Table 3. Baseline characteristics of the CCTA population ATTORNEY DOCKET NO.: 51473-029WO4 PATENT The cardiovascular characteristics of the baseline population for study using CCTA are summarized in Table 4 below. Table 4. Baseline cardiovascular characteristics of CCTA population ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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. Table 5. Schedule of Events ATTORNEY DOCKET NO.: 51473-029WO4 PATENT Study Period SCR BSL 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 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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=0.01 vs 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. 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 thewhole population. For subjects who were determined to be in the 50th percentile of FAI score for the rightcoronary 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). 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). 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 ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 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.

Claims

ATTORNEY DOCKET NO.: 51473-029WO4 PATENT CLAIMS 1. A method for reducing risk of a major adverse cardiovascular event (MACE) in a patient who has had a prior acute coronary syndrome (ACS), the method comprising administering to the patient an antibody or antibody fragment capable of binding to an oxidized fragment of apolipoprotein B100 (ApoB100), wherein the antibody or antibody fragment is administered to the patient in a pharmaceutically effective amount to reduce the risk in the patient.

2. The method of claim 1, wherein the antibody or antibody fragment is administered to the patient within 24 hours of the prior ACS.

3. The method of claim 1, wherein the antibody or antibody fragment is administered to the patient prior to the patient being discharged from the hospital for treatment of the ACS.

4. The method of claim 1, wherein the antibody or antibody fragment is administered to the patient from one week to five years following the prior ACS.

5. The method of claim 4, wherein the antibody or antibody fragment is administered to the patient from two weeks to one year following the prior ACS.

6. The method of any one of claims 1-5, wherein the prior ACS comprises a myocardial infarction (MI).

7. A method for reducing risk of a MACE in a patient who is diagnosed with coronary artery disease and has blood high-sensitivity C-reactive (hs-CRP) of >2.0 mg / L, the method comprising administering to the patient an antibody or antibody fragment capable of binding to an oxidized fragment of apolipoprotein B100 (ApoB100), wherein the antibody or antibody fragment is administered to the patient in a pharmaceutically effective amount to reduce the risk in the patient.

8. The method of any one of claims 1-7, wherein the fragment of ApoB100 comprises an amino acid sequence of SEQ ID NO: 1 and is an aldehyde derivative.

9. The method of any one of claims 1-8, 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.

10. The method of claim 9, 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.

11. The method of any one of claims 1-10, 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.ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 12. The method of claim 11, 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.

13. The method of any one of claims 1-9, 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.

14. The method of claim 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.

15. The method of any one of claims 1-14, wherein the antibody or the antibody fragment comprises HCDR1, HCDR2, and HCDR3 sequences of SEQ ID Nos: 2, 3, and 4, respectively, and light chain complementarity determining regions (LCDRs) LCDR1, LCDR2, and LCDR3 sequences of SEQ ID NOs: 5, 6, and 7, respectively.

16. The method of any one of claims 1-15, wherein the antibody is orticumab.

17. The method of any one of claims 1-16, wherein the method further comprises administering a lipid- lowering agent to the patient.

18. The method of any one of claims 1-17, wherein the patient was previously on a lipid-lowering agent.

19. The method of claim 17 or 18, wherein the lipid-lowering agent comprises an antibody, an siRNA, an antisense oligonucleotide, a small molecule, an omega-3 fatty acid, a bile acid sequestrant, or a peptide.

20. The method of claim 19, wherein the small molecule is a statin.

21. The method of claim 20, wherein the statin is lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, or pitavastatin.

22. The method of claim 19, wherein the small molecule is ezetimibe.

21. The method of claim 19, wherein the small molecule is a fibrate.

22. The method of claim 21, wherein the fibrate is fenofibrate, bezafibrate, gemfibrozil, or pemafibrate.

23. The method of claim 19, wherein the lipid-lowering agent is a bile acid sequestrant.

24. The method of claim 23, wherein the bile acid sequestrant is cholestyramine, colesevelam or colestipol.

25. The method of claim 19, wherein the small molecule is bempedoic acid or lomitapide.ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 26. The method of claim 19, wherein the lipid-lowering agent is an omega-3 fatty acid.

27. The method of claim 26, wherein the omega-3 fatty acid is docosahexaenoic acid, eicosapentaenoic acid, or docosapentaenoic acid.

28. The method of claim 19, wherein the lipid-lowering agent is an antibody.

29. The method of claim 28, wherein the antibody is a PCSK9 antibody.

30. The method of claim 29, wherein the PCSK9 antibody is evolocumab or alirocumab.

31. The method of claim 28, wherein the antibody is evinacumab.

32. The method of claim 19, wherein the lipid-lowering agent is an siRNA.

33. The method of claim 32, wherein the siRNA is a PCSK9 siRNA.

34. The method of claim 33, wherein the PCSK9 siRNA is inclisiran.

35. The method of claim 32, wherein the siRNA is olpasiran.

36. The method of claim 19, wherein the lipid-lowering agent is an antisense oligonucleotide.

37. The method of claim 36, wherein the antisense oligonucleotide is mipomersen, volanesorsen, pelacarsen, or olezarsen.

38. The method of claim 19, wherein the peptide is NNC0385-0434A.

39. The method of any one of claims 1-38, wherein the method further comprises administering colchicine to the patient.

40. The method of any one of claims 1-39, wherein the method further comprises administering ziltivekimab to the patient.

41. The method of any one of claims 1-40, wherein the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 is administered in one, two or more doses of at least 5 mg / kg each or at least 8 mg / kg each.

42. The method of claim 41, further comprising administering a plurality of subsequent doses of the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 in an amount of at least 2 mg / kg / week, at least 2.5 mg / kg / two weeks, or at least 6 mg / kg / month.ATTORNEY DOCKET NO.: 51473-029WO4 PATENT 43. The method of claim 41 or 42, wherein two or more doses are administered over at least 8 weeks, 10 weeks, or 12 weeks.

44. The method of any one of claims 1-43, wherein the antibody or antibody fragment capable of binding to an oxidized fragment of ApoB100 is administered at 1-10 ug / kg, 10-100 ug / kg, 100-500 ug / kg, 200-500 ug / kg, 300-500 ug / kg, 400-500 ug / kg, 1-5 mg / kg, 5-10 mg / kg, 10-15 mg / kg, 15-20 mg / kg, 20-25 mg / kg, 25-50 mg / kg, 50-75 mg / kg.

45. The method of any one of claims 1-44, wherein the MACE comprises a stroke, need for revascularization, cardiac arrhythmia, ACS, unstable angina, or myocardial infarction.

46. The method of claim 45, wherein the MACE is ACS.

47. The method of claim 46, wherein the ACS comprises unstable angina or an acute MI.

48. The method of claim 47, wherein the MI is ST-segment elevation myocardial infarction or non-ST- segment elevation myocardial infarction.

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