Abstract: Described herein are polypeptides that home to developing microvasculature, (also referred to as developing microvessels), such as newly developing microvasculature in mammals, particularly in humans, and to DNA that encodes such polypeptides. These polypeptides are referred to herein as developing microvasculature homing polypeptides. In a specific embodiment, the homing peptides are collateral vessel endothelia (CVE) homing polypeptides, which have been shown to home to collateral vessel endothelia after ischemia.

Abstract: An association between the Ala allele of the P12A variant of the human PPAR? gene and development of CAD, particularly premature CAD, in individuals, and specifically in women, particularly Caucasian women, is described, as are methods of assessing or predicting the likelihood or risk that an individual, such as a woman, will develop premature CAD. Single nucleotide polymorphisms in the human resistin gene, human resistin gene variants, gender-related increase in premature coronary artery disease, methods of assessing or aiding in assessing the risk that an individual will develop premature CAD, and methods of predicting the likelihood or aiding in predicting the likelihood that an individual will develop premature CAD are described.

Abstract: An individual's risk profile for developing a cardiovascular disorder or for experiencing a cardiovascular event is determined by 1) measuring levels of certain stress-evoked proteins including heat shock proteins (HSPs), cytokines, adhesion molecules, chemokines, and the like, or titers of the antibodies targeted to them, or 2) determining the number of seropositive responses to a group of pathogens that have been associated with the presence of atherosclerosis and/or clinical events related to atherosclerosis. The measured levels are compared with clinically derived standards that define the association of these markers with cardiovascular disease. These markers are independent of traditionally recognized risk factors.

Abstract: The invention is directed to methods for angiotyping individual patients to predict the likelihood of whether a given individual will develop good vs. poor collaterals naturally. Accordingly, this can involve obtaining and providing a list of genes involved in collateral development. In particular, angiotyping individual patients can be used to predict the likelihood of whether a given individual will develop good vs. poor collaterals in response to specific angiogenesis therapy. From an array of genes that have been determined through experimental studies as being differentially expressed in tissues in which collaterals are developing in response to arterial occlusion, single nucleotide polymorphisms (SNPs), or other epigenetic changes, such as DNA methylation patterns, can be identified. SNPs and DNA methylation patterns are detected using microchips or similar technology assaying for all, or most, of the genes determined to play a role in collateral development.

Abstract: The invention relates to predicting which individuals are at risk of developing atherosclerotic vascular disease, and once having disease, which individuals are at risk of experiencing plaque rupture which, depending on the site of the plaque, could produce myocardial infarction, stroke, critical limb ischemia, or other vascular event. The invention further relates to methods of diagnosing and aiding in the diagnosis of vascular conditions such as atherosclerosis, premature coronary artery disease and coronary artery disease, by detecting a resistin gene product in an individual. The invention further relates to methods of predicting, and aiding in predicting, the likelihood that an individual will experience a vascular event, such as but not limited to, a myocardial infarction, acute coronary syndrome, stroke, transient ischemic attack (TIA), or critical limb ischemia.

Abstract: Methods are provided for assessing the risk of developing restenosis in an individual, by detecting the presence of biologically important polymorphisms in genes involved in the formation of the elastin fiber network. In particular, detection of polymorphorphisms in the elastin, fibrillin, fibrillin-1, fibrillin-2, lysyl oxidase, microfibril-associated glycoprotein, biglycan, osteopontin, and/or decorin genes allows the rapid and objective prediction of the risk of developing restenosis. Methods for treating restenosis and for reducing its recurrence also are provided.