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

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

The case history of seven children aged 1 5/12 to 5 9/12 years with non tuberculous bacterial pericarditis, observed in the last 8 years at the University children's hospitals of Basle, Berne and Zurich is reported. The history showed febrile illness of 3--14 days duration, which led to an admission diagnosis of pneumonia, angina or pseudocroup. From the signs of heart failure and cardiomegaly on chest X-ray the differential diagnosis of myocardial disease or pericardial effusion was made. The ECG-changes were uncharacteristic, and a friction rub and pulsus paradoxus was encountered once only. The effusion diagnosis should preferably be substantiated by a non-invasive method (scintigram, echocardiogram) as diagnostic pericardiocentesis does often not allow to aspirate the thick pus through the needle. Diagnostic and therapeutic surgical pericardiotomy with consecutive drainage is therefore mandatory. Halothane should be avoided as an anesthetic for this procedure of hemodynamic reasons. With surgery and antibiotics the recovery rate in our series was 100%, and no pericardial constriction was observed on follow-up 1 to 8 years later.
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PMID:Pericarditis purulenta in children. 61 70

In an attempt to assess cardiac risk in non-cardiac surgery, 1001 patients over 40 years of age who underwent major operative procedures were examined preoperatively, observed through surgery, studied with at least one postoperative electrocardiogram, and followed until hospital discharge or death. Documented postoperative myocardial infarction occurred in only 18 patients; though most of these patients had some pre-existing heart disease, there were few preoperative factors which were statistically correlated with postoperative infarction. Postoperative pulmonary edema was strongly correlated with preoperative heart failure, but 21 of the 36 patients who developed pulmonary edema did not have any prior history of heart failure. Nearly all of these 21 patients were elderly, had abnormal preoperative electrocardiograms, and had intraabdominal or intrathoracic surgery. In the absence of an acute infarction, bifascicular conduction defects, with or without PR interval prolongation, never progressed to complete heart block. Spinal anesthesia protected against postoperative heart failure but not against other cardiac complication. By multivariate regression analysis, postoperative cardiac death was significantly correlated with (a) myocardial infarction in the previous 6 months; (b) third heart sound or jugular venous distention immediately preoperatively; (c) more than five premature ventricular contractions per minute documented at any time preoperatively; (d) rhythm other than sinus, or premature atrial contractions on preoperative electrocardiogram; (e) age over 70 years; (f) significant valvular aortic stenosis; (g) emergency operation; (h) a 33% or greater fall in systolic blood pressure for more than 10 minutes intraoperatively. Notably unimportant factors included smoking, glucose intolerance, hyperlipidemia, hypertension, peripheral atherosclerotic vascular disease, angina, and distant myocardial infarction.
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PMID:Cardiac risk factors and complications in non-cardiac surgery. 66 58

Nineteen patients, aged 58-80 years, with severe isolated aortic valve stenosis, severely reduced ejection fraction and clinical heart failure underwent aortic valve replacement between January 1970 and April 1977. Ten had concomitant coronary artery disease (all underwent additional coronary bypass surgery), 17 had angina pectoris and four had syncope. Aortic valve area index was 0.32 +/- 0.03 cm2/m2 (mean +/- SEM); left ventricular (LV) end-diastolic volume index was 117 +/- 9 ml/m2 and LV ejection fraction was 0.37 +/- 0.02. There were four operative deaths and one late death. The follow-up time ranged from six to 74 months (38 +/- 6 months). Actuarially determined three-year survival is 74 +/- 10%; the expected five-year survival is the same. One patient had a serious cerebrovascular accident. Of the remaining survivors, seven were initially Functional Class IV and six Class III; currently, six are Class I and seven Class II (New York Heart Association classifications). The cardiothoracic ratio has decreased from 0.54 +/- 0.03 to 0.49 +/- 0.03. Repeat hemodynamic evaluation has been performed in 10 patients, 22 +/- 6 months after surgery. In these 10 patients, the aortic valve gradient decreased from 55 +/- 7 11 +/- 1.3 mm Hg; LV end-diastolic pressure from 22 +/- 2.4 to 9 +/- 1.9 mm Hg; LV end-diastolic volume index from 119 +/- 16 ml/m2 to 107 +/- 11 ml/m2. LV ejection fraction has increased dramatically from 0.34 +/- 0.03 to 0.63 +/- 0.05 and mean velocity of circumferential fiber shortening from 0.57 +/- 0.08 to 1.3 +/- 0.18 circ/sec. The encouraging long-term survival, improved functional class and the marked improvement in left ventricular function that occurred in our patients indicate that all patients with severe aortic stenosis in clinical heart failure should be offered aortic valve replacement.
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PMID:Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. 66 73

The incidence, circumstances, and mechanism of development of cardiac arrest in 786 patients with myocardial infarction treated at a coronary care unit within a five-year period were studied and clinical factors are analysed with respect to success of resuscitation. One or more episodes of cardiac arrest occurred in a total of 156 patients (19.8%). Of these, 25 (16.0%) were successfully resuscitated and 131 (84.0%) died. At the clinical ward where the patients had been transferred after the acute stage, cardiac arrest occurred in additional 22 patients, of whom two were successfully resuscitated. Thus, the total number of successfully resuscitated patients throughout the five-year period was twenty-seven. The results of resuscitation were poorer in elderly patients, in those with anterior infarction, and above all in patients with severe symptoms of mechanical heart failure. Anamnestic factors (chronic angina pectoris, previous myocardial infarction, hypertension, diabetes mellitus, ischaemic disease of the lower limbs) were not significantly associated with the results of resuscitation. Primary ventricular fibrillation was the principal mechanism of cardiac arrest in 24 of the 27 patients successfully resuscitated, and its total incidence in the investigated group was 3%. The prognosis of resuscitation in patients with primary ventricular fibrillation was very good, and in all of them the resuscitation was successful and permanent.
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PMID:Incidence of circulatory arrest in patients with acute myocardial infarction in coronary unit. Mechanism of their genesis and factors conditioning successful resuscitation. 67 95

519 patients with angina pectoris studied by selective coronary arteriography and left ventriculogram, were followed for a period ranging from 18 months to 7 years. The mean follow-up was 42.2 months. The patients showed a survival probability of 81% at the 7th year. After 5 years the survival probability was 83.2% for patients with typical stable angina, 70.3% for patients with unstable angina, 96.7% for patients with atypical angina. The survival probability was 78.8% for the male sex and 94.6% for the female (at the 5th year). Age, a long-lasting angina, the presence of: previous infarction, myocardial failure, cigarette smoking, hyperlipidemia, cardiomegaly and an ischemic resting EKG were factors with poor prognostic value. The prognostic value of significant coronary stenosis was confirmed. The survival probability at the 5th year of the patients without critical stenosis was 96.6%, of patients with stenosis of 1, 2 and 3 main coronary arteries was respectively: 87.6%, 79% 54.7%. Significative prognostic differences were observed in patients with normal left ventricle kinesia (survival probability at the 5th year: 90%), compared with patients with severe VS ipokinesia (62.7%) and with VS diskinesia (69%). In the follow-up period an incidence of 9% of myocardial infarctions was observed. The degree of each stenosis and the number of vessels involved, the type of angina, the presence of risk factors or previous myocardial infarction did not affect the clinical evolution of angina.
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PMID:[Natural history of angina pectoris: follow-up on 519 unoperated patients (author's transl)]. 71 Jul 62

To determine the effect of aneurysmectomy solely or combined with direct revascularization, 349 consecutive surgical patients treated between 1962 and 1972 were retrospectively reviewed. The minimum follow-up for survivors was 5 years (mean, 7 years). Single-vessel disease occurred in 171 (49%) and only ventricular aneurysmectomy was performed (Group 1). Multiple-vessel disease was found in 178 (51%), of whom 79 (44%) had resection of a ventricular aneurysm and revascularization of all major obstructed vessels (Group 2); 99 (56%) had aneurysm resection and incomplete revascularization (Group 3). Survival at 7 years was 69% for Group 1, 65% for Group 2, and 51% for Group 3. Actuarial survival at 7 years was 70% for patients operated on for angina; 55% for congestive heart failure; 57% for a combination of angina and heart failure; and 64% for ventricular tachycardia. Survival of patients with multiple-vessel disease who underwent aneurysmectomy and complete revascularization was similar to that of patients with single-vessel disease who underwent aneurysmectomy alone. Longevity is adversely influenced by incomplete revascularization (p less than 0.005) and preoperative congestive heart failure (p less than 0.005).
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PMID:Determinants of long-term survival after ventricular aneurysmectomy. 75 48

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.
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PMID:Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: lack of abolition of angina by infarction. 75 12

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.
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PMID:Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal. 77 91

The use of beta-adrenergic blocking drugs in angina pectoris was one of the original indications for these drugs suggested by Black. An anti-anginal effect was demonstrated with the first beta-adrenergic blocking drug, pronethalol, that was used clinically. This benefit in angina was confirmed in the early trials with propranolol in 1964-65. Although some definite anti-anginal effect can be demonstrated with low fixed dosage, evidence suggested that those trials which used a higher and a variable dose displayed a greater anti-anginal action of the drug. After a two dose trial (Gillam and Prichard, 1966,) demonstrated a dose dependent anti-anginal effect, a log-dose response study demonstrated a progressive reduction in angina attacks as dosage was increased (Prichard and Gillam, 1971). While a highly significant effect was found with an average dose of 52 mg a day a progressive reduction in angina attacks was found with logarithmic increases in dosage up to an average of 417 mg a day. Dosage in this trial was adjusted to produce a supine heart rate of 55-60 beats/minute provided this was not prevented by side effects. As the dosage of 417 mg a day was still on the straight line part of the dose response curve and therefore suboptimal, we not adjust dosage to produce a standing heart rate of 55-60. Fully meaningful comparative trials require that optimum dose of the drugs being compared are used. A variable dose comparative trial comparing propranolol and practolol, showed propranolol was the more effective agent. More recently a variable dose comparative trial of sotalol and propranolol indicated propranolol had greater anti-anginal action although sotalol, unlike practolol, was more effective than low dose propranolol. The use of beta-blocking agents in angina pectoris is relatively safe provided that the contraindications of asthma and cardiac insufficiency are observed and that treatment is commenced at a low dosage. The most dramatic change in the sympathetic environment of the heart takes place when treatment with a beta-blocking drug is commenced. The greatest danger of precipitating heart failure is therefore at the beginning of treatment even with a small starting dose. Once treatment has begun even an increase of 25% per dose represents a small pharmacological increment as there is no great change in the sympathetic drive to the heart. The larger dosage of beta-blocking drugs required for optimum treatment of angina may be gradually approached, but it has been my experience that heart failure is not likely to be precipitated at larger doses, provided they are not used initially. In other than mild angina pectoris the average optimum dosage of propranolol is 500-800 mg a day, similar, or perhaps more than the average dose in hypertension.
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PMID:Propranolol in the treatment of angina: a review. 78 54


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