Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and pathological findings in 15 autopsy cases, 13 males and 2 females, confirming cardiac free wall rupture after AMI were reported. The incidence is 30.6% of all autopsy cases of AMI in Chinese PLA General Hospital from 1958 to 1979. The ages ranged from 46 to 79 years, 10 being above 60 years. For 73.3% it was the first AMI and 66.7% of the patients had a history of hypertension. Thirteen of the 15 patients died within 5 days after the onset of AMI and another 2 within 7 days. When the cardiac rupture occurred, the ECG generally showed bradycardia, AV-junctional rhythm, III degrees AV block or isorhythmic ventricular rhythm and cardiac arrest. Both the gross and microscopic AMI were examined in 13 cases. All of them had a septal infarct, but only 2 had an ECG diagnosis. Of the 6 patients with inferior MI on ECG, 5 had right and left coronary lesions worse than grade III. The effective prevention of cardiac rupture consists of early diagnosis, control of chest pain and vomiting, prevention or treatment of hypertension or hypotension and 1 to 2 weeks of bed rest after the onset of AMI.
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PMID:Cardiac free wall rupture after acute myocardial infarction. Clinical and pathological analysis. 383 11

Myocardial infarction results from a platelet-rich occlusive coronary thrombus. Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet adhesion and aggregation. Two polymorphisms of the gene encoding the IIIa subunit. PLA1 and PLA2, have been identified. We investigated the frequency of these polymorphisms in 114 consecutive patients with a history of angina-like chest pain admitted for coronary arteriography. Forty-three of these patients had previously suffered a myocardial infarction. The PLA2 polymorphism was found in 21% of the patients with previous myocardial infarction and in 27% of the patients with angina-like chest pain but no previous myocardial infarction (p = 0.634). There was also no significant association with the extent of coronary disease. There is no evidence, therefore, from this study of an association between the PLA polymorphisms and the occurrence of myocardial infarction.
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PMID:Coronary thrombosis and the platelet glycoprotein IIIA gene PLA2 polymorphism. 971 40

C-reactive protein (CRP) is a marker of arterial inflammation while lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is related to plaque instability. The aim of this study was to evaluate the correlation between the risk of unstable plaque presenting as acute coronary syndrome (ACS) and Lp-PLA(2), and to assess the influence of statins on interpretation of Lp-PLA(2). A total of 362 consecutive patients presenting to the emergency department (ED) with acute chest pain suggestive of ACS were evaluated by cardiologists as STEMI, NSTEMI, or unstable angina, and non-ACS. Serum biomarkers measured on admission: troponin I, C-reactive protein (Abbott), and Lp-PLA(2) (DiaDexus). Four groups were defined according to the final diagnosis and history of statin medication: ACS/statin-; ACS/statin+; non-ACS/statin-; non-ACS/statin+. Lp-PLA(2) was highest in ACS/statin- group; statins decreased Lp-PLA(2) both in ACS and non-ACS of about 20 %. Lp-PLA(2) was higher in ACS patients in comparison with non-ACS patients group without respect to statin therapy (p<0.001). Lp-PLA(2) predicted worse outcome (in terms of acute coronary syndrome) effectively in patients up to 62 years; limited prediction was found in older patients. C-reactive protein (CRP) failed to discriminate four groups of patients. Statin therapy and age should be taken into consideration while interpreting Lp-PLA(2) concentrations and lower cut-off values should be used for statin-treated persons.
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PMID:The importance of age and statin therapy in the interpretation of Lp-PLA(2) in ACS patients, and relation to CRP. 2531 78