Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 microM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thromboglobulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.
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PMID:Platelet reactivity in unstable coronary artery disease. 295 54

A patient with systemic lupus erythematosus and anticardiolipin antibodies and antibodies to platelet factor 4/heparin complexes suffered an acute myocardial infarction caused by delayed heparin-induced thrombocytopenia after heparin administration given to treat pulmonary hypertension. Furthermore, additional heparin administration for emergency coronary angiography appeared to have led to an acute immunoreaction, which might have resulted in acute coronary occlusion during coronary angiography and to a decreased platelet count. The present findings suggest that one must suspect delayed-type HIT in rare cases of induction of thrombosis after the cessation of heparin treatment, and avoid re-exposure to heparin in such cases.
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PMID:Acute myocardial infarction caused by delayed heparin-induced thrombocytopenia and acute immunoreaction due to re-exposure to heparin in a systemic lupus erythematosus patient with HIT antibodies. 1465 45