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

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.
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PMID:Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction. 4 3

Of 945 patients hospitalised for myocardial infarction between January 1st 1972 and December 31st 1975, 40 with anterior myocardial infarction (Group I-A) and 53 with posterior myocardial infarction (Group II-A) were complicated by atrioventricular and/or intraventricular arrhythmias. The average follow up period is now of 48 months (range 24 to 78 months). Their outcome was compared to two control groups of 50 anterior myocardial infarctions (Group I-B) and 50 posterior myocardial infarctions (Group II-B) uncomplicated by arrhythmias in the acute phase. The immediate (10%) and secondary (30%) mortality was identical in the two groups II-A and II-B with posterior wall necrosis. The immediate (32%) and secondary (40%) mortality in Group I-A was much higher than in Group I-B (22% and 28% respectively). Sudden death was the most frequent form of demise in all groups (I-A, II-A, II-B) except Group I-B in which heart failure predominated. Death occured earlier in Group I-A than in the control Group II-B. These results pose the problem of the indication of prophylactic permanent pacing to decrease the incidence of sudden death.
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PMID:[Outcome of myocardial infarctions complicated by heart conduction disorders in the acute phase]. 11 18

Two patients were hospitalised with severe heart failure and hypotension thought initially to be due to acute anterior myocardial infarction because of very suggestive electrocardiographic appearances. Heart failure rapidly regressed in both cases. The young age of these two patients, the pyrexia, rapid and total regression of the ECG appearances, the absence of atheromatous lesions at coronary angiography and clinical cure with a follow-up of 10 years in one of the cases, were factors in favour of the diagnosis of acute myocarditis.
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PMID:[Acute myocarditis simulating myocardial infarct with regressive heart failure]. 12 32

We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.
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PMID:Large ventricular aneurysms occurring after myocardial infarction. 65 17

Mortality during the hospitalization period was analyzed in a sample of 786 patients with acute myocardial infarction [AMI], admitted to the coronary care unit within a five-year period from a catchment area of 200 000 urban inhabitants. The total mortality during the hospitalization period amounted to 19.2%. The prognostic significance of certain clinically meaningful phenomena was appraised on the basis of their association to the mortality. It was demonstrated that the factors decisive for the prognosis of a patient with AMI are age, previous myocardial infarction, extent and localization of the ischaemic lesion apparent from the ECG tracing, and, in addition, presence of the atrioventricular and intraventricular conduction defects, especially if combined with anterior myocardial infarction. Patients with a high cumulation of these prognostic factors exhibited severe signs of mechanical heart failure, which is the mechanism of death in practically all of the deceased patients under the present possibilities of treatment.
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PMID:Hospital mortality in patients with acute myocardial infarction: five-year experience. 102 1

To assess the effects of nisoldipine on chronically underperfused myocardial areas ("hibernating myocardium"), the global and regional left ventricular (LV) function was analyzed before and after 2 months of double-blind monotherapy with nisoldipine (10 mg twice daily) or placebo in 17 patients with a previous anterior myocardial infarction. The baseline LV ejection fraction ranged from 34 to 51%, and no patient had heart failure. Compared to placebo, nisoldipine significantly lowered the LV systolic pressure and end-diastolic pressure (-3 vs. +6 mmHg with placebo; p < 0.01) and the LV pressure at the time of mitral valve opening (-2.0 +/- 3.4 vs. +3.5 +/- 3.0 mm Hg; p < 0.01). Despite this reduction in driving pressure, the global LV early peak filling rate improved only with nisoldipine and this improvement was related to a selective increase in the expansion rate of the anterior areas, from 1,010 +/- 360 to 1,339 +/- 496 mm2/s (p < 0.001). The time to regional peak filling rate (-8%; p < 0.01), the asynchrony of diastolic wall motion, and the regional ejection fraction (33 +/- 10 to 38 +/- 12%; p < 0.001) also improved in the anterior areas with nisoldipine but not with placebo. In contrast, in the inferior control zones, the regional ejection fraction and filling rate remained unchanged, both when compared to baseline and to placebo. In conclusion, prolonged nisoldipine therapy had no significant effect on the normal myocardium but improved systolic and diastolic function in hypokinetic areas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of prolonged nisoldipine administration on the "hibernating" myocardium. 128 19

The prevailing wisdom generally has been that the failing heart hypertrophies in response to increased wall stress. The increase in myocardial mass observed in heart failure is therefore a relatively late compensatory event geared to normalize wall stress. Although this is undoubtedly true, especially for heart failure resulting from a large anterior myocardial infarction accompanied by rapid left ventricular expansion, it is possible that an important form of hypertrophy occurs much earlier as an initial response to myocardial injury. One can hypothesize that the initial response to injury is a nonspecific phenotypic alteration of the cardiac myocyte to one of growth and development. Such changes may be driven by both trophic and mechanical forces and may be important in altering the architecture of the myocardial cell and surrounding cardiac interstitium. Preliminary data from a variety of models support the concept that neuroendocrine activity is an important component in the ventricular remodeling process, and that pharmacologic interventions designed to block systemic and tissue neuroendocrine activity may prevent excessive cardiac enlargement and its ultimate consequences. Because this concept has important implications for preventive cardiology, the results of several prevention trials, including the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS), Studies of Left Ventricular Dysfunction (SOLVD), and Survival and Ventricular Enlargement (SAVE) are awaited eagerly.
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PMID:Left ventricular hypertrophy: an initial response to myocardial injury. 138 70

The aim of this study was to clarify the mechanisms responsible for the increase in early filling rate observed during oral nisoldipine therapy in patients with ischaemic left ventricular (LV) dysfunction. For that purpose, the global and regional LV function was analysed before and after 2 months of double-blind monotherapy with nisoldipine (10 mg twice daily) or a placebo, in 17 patients with a previous anterior myocardial infarction. The baseline LV ejection fraction ranged from 34-51% and no patient had heart failure. Compared to the placebo, nisoldipine significantly lowered LV systolic pressure and end-diastolic pressure (-3 mmHg vs +6 with the placebo; P less than 0.01) and the LV pressure at the time of mitral opening (-2.0 +/- 3.4 mmHg vs +3.5 +/- 3.0; P less than 0.01). Despite this reduction in driving pressure, the global LV early peak filling rate improved with nisoldipine only and this improvement was related to a selective increase in expansion rate of the anterior areas, from 1010 +/- 360 to 1339 +/- 496 mm2.s-1 (P less than 0.001). The time to regional peak filling rate (-8%; P less than 0.01), the asynchrony of diastolic wall motion and the regional ejection fraction (33 +/- 10 to 38 +/- 12%; P less than 0.001) also improved in the anterior areas with nisoldipine but not with the placebo. In contrast, in the inferior, control zones, the regional ejection fraction and filling rate remained unchanged, both when compared to baseline and to the placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of the mechanisms underlying the changes in left ventricular filling dynamics during oral nisoldipine therapy in patients with anterior myocardial infarction. 164 87

Five-year survival amongst 485 consecutive patients with their first acute myocardial infarction (AMI) was 78.2%. Univariate survival analysis showed that the following variables during the acute stage were of prognostic significance for survival: signs of left ventricular heart failure, enlarged cardiac volume, pulmonary congestion on chest X-ray, anterior myocardial infarction on ECG, and low left ventricular ejection fraction (LVEF), whereas enzyme analysis and Q/non-Q signs on ECG were not. In the multivariate analysis two equivalent models were found. The first pinpointed age and LVEF as independent predictors of mortality, and the second age and left ventricular heart failure. Finally, our subcohort of patients aged less than the mean 63 years and with normal LVEF values of greater than or equal to 50%, or no left ventricular failure had an observed survival for 5 years close to an age- and sex-matched group from the Norwegian population.
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PMID:First myocardial infarction: 5-year survival predicted from routine clinical, laboratory, and radionuclide findings during the acute stage. 193 10

Elderly patients with acute myocardial infarction (AMI) have a higher subsequent mortality than younger ones, yet the reasons for this adverse prognosis are poorly understood. We compared the clinical course and the prognosis of 163 patients aged 40 to 69 years with 112 patients older than 70 years. During hospitalization period 15.9% of younger and 37.5% of older patients died; at 1 year follow-up the cardiac mortality rate was 8.7% in younger and 12.9% in older patients. In elderly patients a greater prevalence of female gender, diabetes mellitus, anterior myocardial infarction, atrial fibrillation and a greater incidence of heart failure and shock were observed. Multivariate stepwise analysis identified shock and heart rate greater than or equal to 90 bpm at the time of admission as the most important prognostic variables for in-hospital mortality in both groups; heart failure (Killip class II and III) was significant in younger patients, while non Q wave myocardial infarction correlated with a better prognosis in elderly. In elderly patients who survived AMI, predischarge Holter monitoring showed higher frequency and complexity of ventricular arrhythmias, and radionuclide angiography lower left ventricular ejection fraction (E.F.) values. In these patients no difference was found in E.F. values despite myocardial infarction sites. At 1 year follow-up E.F. less than 40% and ventricular arrhythmias (3-4 Moss grading system) were significantly related to prognosis in younger patients, while E.F. less than 40% and clinical signs of heart failure in elderly. Therefore, low E.F. and heart failure account for a worse prognosis in elderly patients, while ventricular arrhythmias in younger ones. The results of this study support aggressive management even in elderly patients following AMI to preserve left ventricular function. In elderly patients a large use of antiarrhythmic drugs is not recommended because of low prognostic value of ventricular arrhythmias.
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PMID:[Influence of age on the short- and medium-term prognosis in patients with acute myocardial infarct]. 193 43


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