Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The systolic murmur of papillary muscle dysfunction is a well-recognized feature of acute myocardial infarction (AMI), but no large prospective studies have determined its incidence, associated variables, and prognostic implications. Of 1653 patients who entered our data base with MI, 283 (17%) were classified as having a systolic murmur suggesting mitral regurgitation. At hospital discharge, there was a 5% incidence. There was a higher incidence of systolic murmur in non-Q wave AMI than in inferior or anterior Q wave MI (24% vs 13% and 15%, p less than 0.001). Advanced age, previous MI, and heart failure were all associated with systolic murmur (p less than 0.01). Persistent pain in the coronary care unit occurred more often in those with systolic murmur (45% vs 26%, p less than 0.0001). Systolic murmur was associated with an S3 and bibasilar rales (p less than 0.001) in the hospital; however, it was inversely related to peak creatine kinase and unrelated to heart failure or ejection fraction at discharge. Univariate predictors of mortality associated with systolic murmur included complex premature ventricular contractions at discharge and a non-Q wave location. Patients with systolic murmur had higher hospital and 1-year mortalities than those without systolic murmurs (p less than 0.01). When systolic murmur was present during hospitalization, the average time to reinfarction was 2.5 times earlier than when no systolic murmur was present (84 vs 214 days, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The murmur of papillary muscle dysfunction in acute myocardial infarction: clinical features and prognostic implications. 376 69

The dynamics of circulating platelet aggregates (CPA) in acute myocardial infarction (MI) was correlated to its extent, localization and clinical outcome. Creatine kinase (CK) and CPA were measured in 30 patients with acute MI 24 hours after its onset, and on the third, fifth and eighth day following the accident. Twelve patients had anteroseptal MI, another 12 had inferior, and the remaining 6 had non-Q wave MI. 24 hours after the accident CPA values differed significantly between the three groups (p < 0.05). The values of CPA increased with increasing CK. In all the patients CPA and CK returned to normal or almost normal values on days 8 and 5 following MI, respectively. Eleven patients (37%) had heart failure: 8 of them (73%) had anteroseptal MI and 3 had inferior MI (27%). In 10 patients with heart failure (91%) and only in 2 out of 19 patients without heart failure (10.5%), CPA peaked on days 3 or 5 after MI (p < 0.05). In all other patients CPA declined steadily from the initial value. These results suggest that platelet aggregability is significantly associated with the severity of MI and with heart failure.
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PMID:[Dynamic aggregation of thrombocytes in acute myocardial infarct]. 901 39