34 results about "Arteriogenesis" patented technology

Method and system for using segmentation and three-dimensional image-processing techniques of a method to create an automatic method to detect coronary artery calcification deposits and identify their location with respect to a major coronary artery. Finally, different scoring algorithms can be applied to generate calcium scores such as Agatston Janovitz, Mass, and Volume. A total score and a more detailed score can be generated based on the major arteries such as right coronary artery, left anterior descending artery, or left circumflex artery to be incorporated into the patient report.

A method for determining an arteriovascular condition of a subject having an arterial blood flow is shown. The method involves determining a temporal progression of an instantaneous blood flow condition of the arterial blood flow as well as deriving a slew rate of the temporal progression during an increase of the temporal progression. In addition, an arteriovascular condition indicator device is shown, which comprises: an input for receiving an input signal representing an instantaneous arterial blood flow condition of a subject and a slew rate monitor connected to the input. A corresponding control device for providing an activation signal is also shown. The control device comprises a maximum detector connected to the slew rate monitor. A method for stimulation of arteriogenesis is also shown, wherein a temporal progression of an instantaneous blood flow condition is monitored, a slew rate of the temporal progression is derived, and the maximum of the slew rate is determined. An external pressure is applied repeatedly to the arteriovascular section in synchronization with the occurrence of the determined maximum.

The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF− / −) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monoclonal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.

VEGF-B is shown to be needed for cardiac muscle revascularization after heart infarction, and methods of promoting or stimulating vascular development, e.g. angiogenesis and / or arteriogenesis, particularly in ischemic mammals, are disclosed.

A method for modulating vasculogenesis or arteriogenesis or angiogenesis, especially for treating heart and limb ischemia, using the core domain protein of PDGF-C, a new member of the PDGF / VEGF family of growth factors, or a homodimer or a heterodimer comprising the core domain. Also disclosed are pharmaceutical compositions comprising the core protein, nucleotide sequences encoding the protein, and uses thereof in medical and diagnostic applications.

A method for promoting muscle or tendon regeneration, and / or arteriogenesis in a subject includes administering to the subject a pharmaceutical composition that contains a synthetic peptide, which has an amino acid sequence that has 20-39 amino acid residues and has at least 20 consecutive residues that has at least 90% amino acid sequence identity to residues 11-30 of SEQ ID NO: 1. The synthetic peptide may have the amino acid sequence of SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 5, SEQ ID NO: 6, SEQ ID NO: 8, or SEQ ID NO: 9.

The present invention provides methods of promoting arteriogenesis in a subject. Embodiments include methods comprising: administering an effective dose of tocotrienol to the subject; causing an increase in Tissue Inhibitor of Metalloproteinase Metallopeptidase Inhibitor 1 (TIMP1) in vessels of cerebrovascular collateral circulation in the subject; attenuating the activity of Matrix Metalloproteinase-2 (MMP2); thereby promoting arteriogenesis.

The present invention relates, e.g., to a method for inducing arteriogenesis, lymphangiogenesis, vasculogenesis, or cardiomyogenesis, and / or for inducing mitosis or proliferation of a smooth muscle cell, a skeletal muscle cell, or a cardiomyocyte, comprising administering to a cell or tissue in need thereof a dose of a polynucleotide that encodes a vascular endothelial growth factor (VEGF), or that encodes a polypeptide comprising an active site of the VEGF. The coding sequence is operably linked to an expression control sequence; and the dose is sufficient to induce arteriogenesis, lymphangiogenesis, vasculogenesis, or cardiomyogenesis, and / or to induce mitosis or proliferation of a smooth muscle cell, a skeletal muscle cell, or a cardiomyocyte. In preferred embodiments of the invention, the method is a method of tissue regeneration, particularly of cardiomyogenesis; and the polynucleotide (or a polypeptide encoded by such a polynucleotide) is administered into the myocardium.

A method of delivering an arteriogenic factor. The factor is delivered in a medically effective manner to structurally enlarge an existing blood vessel. A distal portion of a catheter can be advanced to an existing blood vessel to deliver the arteriogenic factor.

Compositions and method for stimulating and controlling arteriogenesis and lymphatic vasculature by preventing and / or reducing the cellular interaction between RAF1 and AKT have been developed. The compositions include molecules that increase the bioavailability of non-phosphorylated RAF1, for example, the RAF1 Ser259 to Ala259 mutant in (RAF1 S259A), and AKT1 inhibitory molecules. Defects, disorders or diseases of insufficient blood or lymphatic vasculature are treated by administering to a patient in need thereof, a pharmaceutical composition comprising a molecule specifically blocking RAF1-AKT crosstalk in a pharmaceutically acceptable carrier or excipient in an amount effective to enhance the growth of blood or lymphatic vasculature in the patient. Compositions can be administered by injection or by controlled or sustained release devices, coating on devices or implants, microparticles, bulking agents or depots, or other techniques providing controlled or sustain release over a period of time effective to induce blood or lymphatic vasculature growth as desired.

A method and system for non-invasive assessment of coronary artery stenosis is disclosed. A patient-specific real anatomical model of a diseased coronary artery of a patient is generated from medical image data of the patient. A hypothetical normal anatomical model is generated for the diseased coronary artery of the patient. Blood flow is simulated in each of the patient-specific real anatomical model of the diseased coronary and the hypothetical normal anatomical model for the diseased coronary artery. A hemodynamic index is calculated using simulated blood flow rates in the patient-specific real anatomical model of the diseased coronary and the hypothetical normal anatomical model for the diseased coronary artery. In particular, fractional flow reserve (FFR) for the diseased coronary artery is calculated as the ratio of the simulated blood flow rate in the patient-specific real anatomical model of the diseased coronary artery and the simulated blood flow rate in the hypothetical normal anatomical model for the diseased coronary artery.

The present invention inter alia relates to a method of treating or preventing an arterial insufficiency, wherein an NO donor is administered in an intermitting manner to a subject in an amount effective for the induction of arteriogenesis, and wherein the NO donor is a solid pharmaceutical preparation with the active substance glyceryl trinitrate for oromucosal or oral administration characterized in that it contains between 0.05 and 2 weight % glyceryl trinitrate (GTN), at least one diluent, one carrier material, and at least one substance that reduces the volatility of GTN, whereby this substance is a non-volatile ester stabilizer whose melting point is not higher than 60° C.

The present invention relates to bradykinin receptor modulators and pharmaceutical compositions thereof for use as a medicament for modulating collateral blood vessel growth of collateral arteries and / or other blood vessels of pre-existing arterial networks. The bradykinin receptor modulators of arteriogenesis are applicable in the treatment and / or prevention of disorders associated with defective blood flow or blood vessel malformation. A preferred aspect of the invention relates to bradykinin receptor agonists for use as a medicament for the prevention of cardiovascular ischemic disease in a patient at risk thereof. Further, the invention relates to a bradykinin receptor agonist for use in a method for treating a cardiovascular ischemic disease in a patient in need thereof, wherein said cardiovascular ischemic disease is a peripheral limb disease.

The present invention inter alia relates to a method of promoting collateral circulation comprising the step of exposing a subject to a therapeutically effective amount of an NO donor wherein the therapeutically effective amount of the NO donor promotes arteriogenesis sufficient to augment collateral circulation in a physiological or pathological condition.

The disclosure relates to the field of ischemia and how to increase tissue perfusion in ischemic tissue by cellular therapy. Specifically, the beneficial effects of myeloid (bone marrow-derived) cells with a particular arteriogenic gene expression profile are shown, and it is shown that increased arteriogenesis and perfusion is specifically due to the effects of combined PDGFB and SDF-1. The arteriogenic gene profile of the myeloid cells used for therapy can, for instance, be obtained by inhibition of PHD2.

A method for determining an arteriovascular condition of a subject having an arterial blood flow is shown. The method involves determining a temporal progression of an instantaneous blood flow condition of the arterial blood flow as well as deriving a slew rate of the temporal progression during an increase of the temporal progression. In addition, an arteriovascular condition indicator device is shown, which comprises: an input for receiving an input signal representing an instantaneous arterial blood flow condition of a subject and a slew rate monitor connected to the input. A corresponding control device for providing an activation signal is also shown. The control device comprises a maximum detector connected to the slew rate monitor. A method for stimulation of arteriogenesis is also shown, wherein a temporal progression of an instantaneous blood flow condition is monitored, a slew rate of the temporal progression is derived, and the maximum of the slew rate is determined. An external pressure is applied repeatedly to the arteriovascular section in synchronization with the occurrence of the determined maximum.

The present invention relates to nucleic acids and polypeptides encoded thereby, whose expression is modulated in a subject suffering from insufficient arteriogenic capacity. These nucleic acids are among other useful in methods for diagnosing insufficient arteriogenic capacity, treating a subject suffering from insufficient arteriogenic capacity and / or stimulating arteriogenic capacity and / or stimulating arteriogenesis.