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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 necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.
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PMID:Hypertrophic cardiomyopathy in the dog. 15 45

A 58-year-old man had sudden and progressive heart failure after a severe myocardial infarction. Aggressive medical treatment consisting of diuretics, vasopressors, and digitalis failed to improve his condition significantly. Cardiac catheterization disclosed a critical stenosis in the left anterior descending branch of the left coronary artery, a large posterior left ventricul aneurysm, and severe mitral insufficiency. Intermittent third degree heart block developed after admission. Surgical correction resulted in a dramatic recovery, and three years after operation he is fully recovered and asymptomatic.
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PMID:Resection of posterior ventricular aneurysm, replacement of mitral valve, and coronary bypass. 31 60

1. Coronary insufficiency is a pathophysiologic state that can initiate lethal cardiac arrhythmias in the absence of myocardial necrosis. Patients with suspected coronary insufficiency should be monitored until they are stabilized and a diagnosis is confirmed. 2. Early and adequate intravenous antiarrhythmic prophylaxis with lidocaine to raise the fibrillation threshold in the setting of coronary insufficiency can prevent primary ventricular fibrillation. Classic "warning arrhythmias" are not predictive of ventricular fibrillation. Their persistence during adequate antifibrillatory prophylaxis does not indicate therapeutic failure. 3. The isoenzyme of creatine phosphokinase, CPK-MB, is an extremely sensitive and specific indicator of myocardial necrosis if measured serially during the 24 hours following the onset of symptoms suggesting coronary insufficiency. It may prove most useful in eliminating the false positive diagnosis of myocardial infarction in difficult clinical cases. 4. The management of heart failure in myocardial infarction requires an understanding of the relationship between ventricular preload and the cardiac output. The treatment of clinical manifestations of an elevated ventricular preload in asymptomatic patients is not justified and may be detrimental. In symptomatic patients, however, judicious manipulation of ventricular preload should be the first therapeutic consideration, and an optimal filling pressure should be achieved and maintained when other determinants of the cardiac output are manipulated. 5. Indications for the prophylactic insertion of a temporary transvenous pacing electrode for heart block associated with myocardial infarction must be individualized. Most authorities agree that prophylactic pacing may be justified in patients with evidence of new infranodal block involving two of the three fascicles. Patients with bifascicular block who progress to complete heart block transiently may benefit from permanent transvenous pacemaker insertion before discharge. 6. Hospitalized patients with persistent pain of suspected cardiac origin but without evidence of myocardial infarction can be studied safely with coronary angiography. A small percentage will be normal or have diffuse disease that is inoperable. Of those with operable disease, short-term mortality appears to be similar for medical and surgical therapy. 7. Patients with an uncomplicated myocardial infarction may be safely discharged from thehospital by day 7-10. 8. Experimental evidence indicates that modification of infarct size is possible. Application of these concepts to human subjects presently is limited by the absence of a proved method of measuring infarct size in vivo in humans.
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PMID:The management of acute coronary insufficiency. 32 38

Disopyramide is a new antiarrhythmic drug with a pharmacological profile of action similar to that of quinidine and procainamide. In a few controlled therapeutic trails and a large number of uncontrolled studies in patients with arrhythmias, often following a myocardial infarction, disopyramide has been relatively effective (more so in ventricular than in atrial arrhythmias) and usually well tolerated. In treating premature atrial and ventricular contractions, the best-studied area of its therapeutic use, disopyramide was superior to a placebo and of similar efficacy to but better tolerated than quinidine; the drop-out rate due to adverse effects of the disopyramide group (10%) being less than one-third that of the quinidine group (36%). In an open ward setting, disopyramide used prophylactically after myocardial infarction appeared to reduce both the incidence of reinfarction and the mortality rate, while in patients treated in coronary care units although the incidence of reinfarction was lower with disopyramide than with a placebo, the mortality rate was not significantly different. Further well-designed trials with adequate numbers of patients are needed before the routine use of disopyramide in infarct patients treated in either setting can be justified. Comparative studies are also required to determine if disopyramide has advantages over other antiarrhythmic agents in this area of use. Side-effects with disopyramide are usually a result of its anticholinergic activity, a dry mouth and difficulty in urination being the most common. Like other antiarrhythmic agents, disopyramide exerts a negative inotropic action on cardiac muscle, and development of acute heart failure has been reported. Development of worsening of heart block and hypotension have also occurred. Disopyramide is largely excreted unchanged and dosage should be reduced in patients with impaired renal function, in accordance with creatinine clearance values.
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PMID:Disopyramide: a review of its pharmacological properties and therapeutic use in treating cardiac arrhythmias. 35 May 55

Four babies with complete heart block associated with maternal systemic lupus erythematosus (SLE) are described, together with a 5th baby whose mother had serological abnormalities only. One baby had a rapidly fatal outcome, one has required digoxin for heart failure, and the remaining 3 are asymptomatic but remain in complete heart block. Additional manifestations were present in 2 of them. The spectrum of neonatal abnormalities that may occur in association with maternal SLE and related connective tissue disorders is discussed, together with the possible causes and the prognosis. We conclude that congenital heart block is more common than had previously been appreciated.
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PMID:Congenital complete heart block in the newborn associated with maternal systemic lupus erythematosus and other connective tissue disorders. 42 May 26

In 18 patients who presented in less than 2 years with heart disease characterized by arrhythmias (including atrial fibrillation, ventricular arrhythmias and heart block), atypical chest pain, pericarditis and cardiac failure, extensive investigation revealed no cause for the disease except for evidence of toxoplasmic infection. One patient had acute toxoplasmosis; the other 17 patients had chronically increased titers, higher than the expected level in the community and also higher than in a control series of patients with well defined heart disease. Toxoplasmosis is probably a fairly common cause of heart disease in this community. The source of infection appeared to be cats, uncooked meat and congenital infection. Patients received chemotherapy with either pyrimethamine and sulfadiazine or tetracycline. Serious relapse occurrred in three patients and embolic complications in two. Experimental myocarditis occurs when toxoplasmic cysts rupture within the heart; therefore clinical symptoms may occur sporadically during a chronic infection.
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PMID:Toxoplasmic infection in cardiac disease. 42 23

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.
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PMID:Canine hypertrophic cardiomyopathy. 42 33

Controversy persists concerning the role of early surgical intervention in severe infective endocarditis (IE). We therefore reviewed 163 episodes of well-documented IE in which 32 cardiac operations were performed during the active phase of IE. Congestive heart failure (CHF) was the principal indication for surgery in 88% (28/32); systemic emboli, 1/32; and persisting sepsis, 3/32. Staphylococcus and enterococcus were the most common infecting organisms in the operative group (44% and 16% respectively). Surgical mortality (11/32,37%) did not differ (p greater than 0.05) from medical mortality (26/131,20%). All 11 operative deaths occurred in patients moribund prior to surgery, including three with preoperative cardiac arrest. Surgical patients undergoing preoperative cardiac catheterization demonstrated marked CHF: a mean left ventricular end-diastolic pressure of 25.3 mm Hg. The mean cardiac index in 8/11 surgical deaths was lower (p less than 0.05) vs surgical survivors: 2.21/min/m2 vs. 3.21/min/m2. Postoperative complications were rare in the 21 surgical survivors. There were no episodes of continued infection, prosthetic dehiscence, or advanced heart block; only one paravalvular leak; and one systemic embolus. These findings emphasize the high medical and surgical mortality in patients with IE, suggest that delayed operative intervention may be a major causative factor resulting in a high surgical mortality, and justify an aggressive surgical approach in patients with valve dysfunction and heart failure. These data indicate that survivors of surgical intervention during active IE have eradication of infection and few postoperative complications.
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PMID:Surgery in active infective endocarditis. 44 78

The hospital mortality in 1,246 consecutive acute myocardial infarction patients treated in a large community hospital coronary care unit was 14.4%. Of the total, 52.3% showed no evidence of heart failure, 25.8% had mild to moderate failure, 9.9% had pulmonary edema, and 12% developed cardiogenic shock; the mortality in these groups was 2.2%, 7.4%, 8.9%, and 87.2%, respectively. The mortalitiy in the 1,097 patints who did not have cardiogenic shock was 4.5%. Only one patient died as a result of primary ventricular fibrillation (0.08%). The mortality of complete heart block in the absence of cardiogenic shock (8.3%) was not significantly different from that of comparable patients who did not have complete heart block (4.3%). These results are lower than those generally reported.
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PMID:Treatment of myocardial infarction in a community hospital coronary care unit. Experience with 1,246 patients. 62 50

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


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