Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A common mutation in coagulation factor V gene gives rise to factor V Leiden, which is resistant to the proteolytic activity of activated protein C. This mutation is known to be a major inherited risk factor for venous thrombosis. In order to investigate the possible pathogenetic role of factor V Leiden in coronary thrombosis, we screened patients with acute ischemic heart disease for this genetic mutation. We conducted a case-control study on 114 unrelated patients referred to the Cardiology Department of a University Hospital for coronary angiography. Fifty-three case patients with myocardial infarction or unstable angina were compared with 61 control patients seen for a different coronary syndrome or for stable angina pectoris. The two groups did not differ with respect to the well established risk factors for ischemic heart disease. For each patient genomic DNA was extracted from whole blood by standard techniques; the DNA region carrying the mutation was amplified by polymerase chain reaction, and the allele-specific restriction digestion was used in order to detect the mutation itself. The frequency of factor V Leiden was 0.028 among cases and 0.008 among controls (p = 0.5). According to the data presented, factor V Leiden cannot be considered as a risk factor for acute coronary events.
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PMID:Factor V Leiden in patients with acute coronary syndromes. 1052 20

Upon activation, platelets release a host of soluble and vesicular signals, collectively termed the "platelet releasate" (PR). The contents of this PR play a significant role in haemostasis, inflammation, and pathologic sequelae. Despite this, proteomic studies investigating the PR in coronary artery disease have not been performed. Here, we undertook a comparative label-free quantitative (LFQ) proteomic profiling of the 1 U/ml thrombin-induced PR from 13 acute coronary syndrome vs. 14 stable angina pectoris patients using a tandem mass spectrometry approach. Data are available via ProteomeXchange with identifier PXD009356. 318 PR proteins were identified across both cohorts with 9 proteins found to be differentially released, including tetranectin (CLEC3B), protein disulfide-isomerase-A3 (PDIA3), coagulation factor V (F5), and fibronectin (FN1). Strikingly, these 9 differential proteins were all associated with the gene ontology cellular component term "extracellular vesicle" and reduced levels of EVs were detected in the corresponding plasma of ST-segment elevation myocardial infarction (STEMI) patients. Network analysis revealed 3 proteins either reduced (F5; FN1) or absent (CLEC3B) in the PR of STEMI patients that are strongly connected to both the clotting cascade and major druggable targets on platelets. This moderated proteomic signature may prove useful for non-invasive risk assessment of the progression of coronary artery disease. These data further contribute to the growing evidence-base of using the platelet releasate as a predictor of pathological state and disease severity.
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PMID:Comparative Platelet Releasate Proteomic Profiling of Acute Coronary Syndrome versus Stable Coronary Artery Disease. 3267 Oct 99