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)

Increased activation of polymorphonuclear neutrophils in the wideness of irreversible myocardial injury was described by many authors. Released proteolytic enzymes may cause deliquescence of necrotic muscle tissue and attenuate collagenic structure of myocardium, lead to endothelium damage and generate free oxygen radicals. Eosinophilic leucocytes reveal also enhanced proinflammatory activation. They take participation in inflammatory and immunologic reactions, among others, by producing and releasing many biologic mediators. One of the most important and powerful mediators is eosinophil cationic protein (ECP), the specific marker of eosinophil activation in vivo. We studied 17 patients (pts) with acute myocardial infarction (MI) and 21 pts with angina pectoris (AP). The plasma concentrations of ECP and the number of eosinophils in peripheral blood were measured 3 times-near before beginning of the treatment, and on the 4-th and 8-th day of MI. During the first 4 days measurements of CK-MB every 6 hours were made. We observed the significant increase of eosinophils and ECP correspondingly on the 8-th and 4-th day, when compared to the first day of MI (p < 0.05) and the patients with AP (p < 0.01). Despite tendency, the significant correlation of eosinophils and ECP values was not obtained (r = 0.36). In the group of patients with AP the eosinophil and ECP values were significantly higher at the pts with unstable angina, when compared to pts with stable angina (p < 0.001).
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PMID:[Eosinophilic activation based on measurements of eosinophil cationic protein in patients with acute myocardial infarction and patients with angina pectoris]. 1022 63

The Food and Drug Administration held a Circulatory System Devices Advisory Panel meeting, December 5 and 6, 2012, to review the classification or potential reclassification of the following device types: external counterpulsation, intra-aortic balloon pump (IABP), and non-roller-type cardiopulmonary bypass blood pumps. These 3 devices are preamendment (Medical Device Amendments of 1976) class III devices. The advisory panel discussed the data and provided recommendations for reclassification of these devices. The panel recommended reclassification of ECP to class II for stable angina pectoris and to retain a class III for all other indications. For IABP, the recommendation was to reclassify IABP to class II for several indications (acute coronary syndrome, cardiac and noncardiac surgery, and heart failure complications) and remain class III for all other indications. As for non-roller type, the panel recommended that for cardiopulmonary bypass and temporary circulatory bypass, these devices should be reclassified to class II while retaining a class III device status for all other indications, including ventricular support both for hemodynamically unstable patients and for prophylactic support in high-risk percutaneous interventions.
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PMID:Overview of the 2012 Food and Drug Administration circulatory system devices panel meeting on the reclassification of external counterpulsation, intra-aortic balloon pump, and non-roller-type cardiopulmonary bypass blood pump devices. 2401 88