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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical variables and the results of non-invasive tests (exercise test, echocardiogram, gated equilibrium radionuclide ventriculography and 24 h ECG) were recorded in a series of 202 patients who left the hospital alive after an acute myocardial infarction. The short term (two months) predictive value of all these data was prospectively assessed by uni- and multi-variate analysis. The best correlation with early death was observed with the variables related to the extent of infarction and left ventricular dysfunction, namely: early clinical signs of heart failure, high peak CK-MB level, complete bundle branch block, increased cardiothoracic ratio on chest X-Ray, number of Mets reached during the stress test, echocardiographic dyskinesia index, and decreased left ventricular ejection fraction as measured by radionuclide ventriculography. Using multi-variate stepwise discriminant analysis, the following independent prognostic factors appeared by order of entry: early clinical signs of heart failure, peak CK-MB level and cardiothoracic ratio on chest X-Ray. These results highlight the short-term predictive value of the data related to left ventricular dysfunction and especially of simple clinical data for patients surviving an acute myocardial infarction.
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PMID:Predictors of early death after acute myocardial infarction: two months follow-up. 372 Jul 58

The influence of myocardial infarction size, as indicated by the maximum elevation of creatine kinase (CK) and its iso-enzyme CK-MB, on the exercise training response and resting left ventricular function was studied in 15 male patients who underwent exercise training for 8 weeks. Patients were found to divide themselves into two subgroups; those with maximum CK less than or equal to 200 IU/l (n = 7) and greater than or equal to 400 IU/l (n = 8). All were evaluated by treadmill exercise testing (Bruce Protocol), M-mode echocardiography and radionuclide ventriculography before training, immediately after, 3 and 6 months after training. Both of the subgroups showed statistically significant improvements in exercise duration, heart rates for doing equal workloads, energy expenditure and functional aerobic impairment immediately after training which were maintained 3 and 6 months later, with no inter-group differences. Resting left ventricular function, both by radionuclide and echocardiography, did not demonstrate significant changes throughout the study period, again with no inter-group differences. It is suggested that myocardial infarction size in the absence of heart failure does not appear to have a significant influence on the exercise training response and resting left ventricular function in those patients who recovered sufficiently to participate in exercise training.
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PMID:Myocardial infarction size; effect on the training response. 373 67

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

A 56-year-old woman with no history of cardiac disease developed acute pulmonary edema following a subarachnoid hemorrhage. A constellation of findings, including elevated creatine kinase MB isoenzyme activity in the absence of electrocardiographic or scintigraphic evidence of acute myocardial infarction, elevated pulmonary artery wedge pressure, segmental wall motion abnormalities, and depressed ejection fraction of the left ventricle demonstrated by two-dimensional echocardiography and radionuclear ventriculography, pointed to a direct myocardial injury leading to cardiac failure. The evidence for cardiogenic origin of pulmonary edema provided by this case is in contrast to the belief that "neurogenic" pulmonary edema is of noncardiac origin.
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PMID:Pulmonary edema associated with subarachnoid hemorrhage. Evidence for a cardiogenic origin. 382 38

Incidence and significance of pericardial effusion in patients with acute myocardial infarction (AMI) have not been established. To evaluate these issues, we studied prospectively 138 consecutive patients with AMI. An echocardiogram was obtained in each 1, 3, and 10 days and 3 and 6 months after admission. Fifty four patients with unstable angina and 57 without heart disease were studied as controls. Echocardiographic diagnostic criteria of pericardial effusion were established from 33 additional patients undergoing surgery. Pericardial effusion was found in 28% of patients with AMI. Twenty-five percent of patients with AMI had pericardial effusion on the third day, vs 8% of patients with unstable angina (p less than .02) and 5% of patients without heart disease (p less than .01). At 1, 3, and 10 days and 3 and 6 months prevalence of pericardial effusion was 17%, 25%, 21%, 11%, and 8%, respectively. There was no case of tamponade. Pericardial effusion was more common in anterior AMI (p less than .02) and in patients with heart failure (p less than .05) but it was not significantly associated with early pericarditis, peak creatine kinase-MB, the level of anticoagulation, or mortality. Thus, pericardial effusion is a common event in patients with AMI (incidence of 28%), but does not result in specific complications. The reabsorption rate of pericardial effusion is slow and, in our experience, mild or moderate pericardial effusion does not preclude heparin therapy.
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PMID:Pericardial effusion in the course of myocardial infarction: incidence, natural history, and clinical relevance. 394 64

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 +/- 1,004 versus 1,357 +/- 1,036). Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p less than 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p less than 0.0001) and ventricular gallop at the time of discharge (p less than 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p less than 0.0001) and peripheral edema (p less than 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction. 403 Dec 86

Sustained ventricular tachycardia or fibrillation that develops during the early recovery period after acute myocardial infarction is a common clinical problem whose management remains controversial. Fifty-three patients who survived an initial episode of sustained ventricular tachycardia or fibrillation occurring between 3 and 60 days (mean +/- SD 21 +/- 16) after myocardial infarction were evaluated. Most of these patients had had a large (peak creatine kinase = 1,729 +/- 882 IU) complicated infarction. Forty-two (79%) of the 53 patients had had repetitive sustained ventricular arrhythmias and the condition of 19 of these could not be stabilized with drug therapy. Twenty-eight patients received medical therapy only. Twenty-four survived and were discharged from the hospital. Twenty-five patients underwent infarctectomy or aneurysmectomy either on an emergency basis (16 patients) or electively because of coexistent heart failure or angina (9 patients). Intraoperative mapping was attempted in these patients but was completely successful in only 13 (52%). Operative mortality was 16% with all deaths occurring in patients who were in shock before surgery. Five of 21 surgically treated survivors required long-term antiarrhythmic therapy. Twenty-one of 24 patients medically treated remain alive and well after 15 +/- 10 months of follow-up. Nineteen of 21 surgically treated patients remain alive and well after 17.9 +/- 11 months. One of these patients required reoperation for severe mitral regurgitation. These results confirm the poor medical prognosis of sustained ventricular tachyarrhythmias that present during the first 2 months after myocardial infarction but demonstrate that an acceptable rate of survival can be achieved with a combined medical and surgical approach to therapy.
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PMID:Sustained ventricular tachyarrhythmias within 2 months of acute myocardial infarction: results of medical and surgical therapy in patients resuscitated from the initial episode. 403 Dec 90

The mortality rate from myocardial infarction is disproportionately high in diabetic patients. One explanation for this may be that diabetic patients incur more extensive myocardial necrosis. This possibility was examined in a three part study. Firstly, peak serum aspartate aminotransferase concentrations of all diabetic and non-diabetic patients admitted with myocardial infarction over a 16 year period were compared retrospectively. Secondly, peak aspartate aminotransferase concentrations in a series of diabetic patients and controls matched by age and sex were examined retrospectively. Thirdly, creatine kinase MB release and electrocardiographic measures of infarct size were investigated prospectively in a case/control study. Although cardiac failure and death were more common in the diabetic groups, there were no significant differences in estimates of infarct size between diabetic and non-diabetic patients in any of the studies. Therefore, the high case fatality rate amongst diabetic patients is not caused by increased myocardial damage. Presumably survival is prejudiced by factors operating before the infarction.
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PMID:Myocardial infarct size and mortality in diabetic patients. 405 87

Rabbits receiving adriamycin (ADR) on a chronic schedule developed significant histopathologic, ultrastructural and tissue electrolyte alterations of the ventricular myocardium. Rabbits that developed clinicopathologic evidence of cardiomyopathy with ADR had histologic lesions of the myocardium, including perivascular fibrosis, interstitial fibrosis and edema and myocytolysis. Ultrastructurally, large vacuoles resembling distended sarcoplasmic reticulum displaced the contractile elements and mitochondria, which were diminished in number within affected myocytes. Frequently, mitochondria appeared as electron-dense structures surrounded by layers of membranes resembling myelin figures. In addition, rabbits with cardiomyopathy had marked elevations in ventricular Ca, Na and H(2)O concentrations. Serum electrolytes were not significantly elevated, but lactic dehydrogenase (LDH) and creatine phosphokinase (CPK) were significantly increased, indicative of a cardiomyopathy. Rabbits receiving ADR but not developing clinicopathologic evidence of heart failure also had significant elevations in ventricular Ca, Na and H(2)O. Rabbits with no cardiomyopathy had no increases either in serum electrolyte concentrations or CPK and LDH levels. These studies indicate that marked increases in ventricular tissue Ca precede and accompany morphologic evidence of chronic myocardial degeneration and may be instrumental in the development of the ADR-induced cardiomyopathy.
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PMID:Electrolyte and morphologic alterations of myocardium in adriamycin-treated rabbits. 443 14

The effect of several phenothiazines on the extent of cellular damage resulting from the calcium paradox was examined. Hearts treated with trifluoperazine, a potent calmodulin inhibitor, exhibited less cellular damage than untreated myocardium as reflected by light microscopy, high-energy phosphate content and the loss of protein and creatine phosphokinase into the perfusate. A dose response of this effect revealed a maximal response at about 1 microM trifluoperazine, a concentration which lies well within the range generally attributed to calmodulin inhibition. Several other lines of evidence were also obtained suggesting a possible role for calmodulin in calcium-overload induced necrosis. First, the phenothiazines had little influence on membrane changes believed responsible for altered calcium permeability. Second, trifluoperazine was without major effect unless included in the reperfusion buffer, indicating that the drug is only effective during the phase associated with calcium overload. Finally, less protection was afforded hearts exposed to phenothiazines such as chlorpromazine and promethazine, which are weaker inhibitors of calmodulin, than those treated with the potent inhibitor trifluoperazine. While other interpretations are possible, these studies are consistent with a role for calmodulin in calcium overload-induced heart failure.
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PMID:Phenothiazine protection in calcium overload-induced heart failure: a possible role for calmodulin. 613 9


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