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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

In 59 digitalized and 3 non digitalized patients the effect of digitalis during the 1st to 4th days after transmural myocardial infarction was controlled. Rhythm disturbances in acute myocardial infarction may arise secondary to a complicating cardiac failure and may be influenced by digitalis. In 9 of 17 cases (53 p.c.) with ventricular or supraventricular extrasystoles daily doses of 0,4 mg beta-Methyldigoxin or 0,4 mg Digoxin i.v. resulted in undisturbed sinus rhythm. In two cases supraventricular tachycardia and extrasystoles with rapid ventricular rate were abolished by 1,2 mg beta-Methyldigoxin within 12 hours, in three other cases an improvement was recorded. Dysrhythmias or other complications did not occur in previously non digitalized patients. When the antiarrhythmic effect of digitalis cannot be obtained cardiodepressive complications by treatment with typical antiarrhythmic agents are diminished. In patients on digitalis and in cardiogenic shock, digitalization should be performed carefully. Intoxication leads to a diminution of cardiac output and to cardiac dysrhythmias.
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PMID:[The antiarrhythmic effect of digitalis in acute myocardial infarction with cardiac failure (author's transl)]. 5 51

Incidence and type of arrhythmia, using continuous ECG monitoring, were examined in 79 patients six weeks to 24 months after acute myocardial infarction, the findings being compared with arrhythmias at rest and on exercise, and correlated with signs of heart failure and coronary insufficiency. Arrhythmias were revealed in 16% (n = 13 at rest) and 19% (n = 10 of 52) on exercise. But continuous ECG monitoring revealed it in 86% (n = 68). On the other hand, arrhythmias may occur in the resting ECG but be rare on continuous monitoring. Ventricular extrasystoles were the most common arrhythmia, often multifocal and giving rise to bigeminy, only rarely as a result of exercise. Such extrasystoles usually showed right or right and left bundle conduction delays. Their frequency increased with increasing age of the patient. They were particularly frequent in patient who already had cardiac symptoms at rest, in patients with a large heart, and those who could not easily be exercised. Arrhythmias were more frequent a year after infarction than shortly before discharge from hospital or six months after infarction.
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PMID:[Cardiac arrhythmias in the chronic phase of myocardial infarction (author's transl)]. 5 49

Twenty-three patients with recurrent ventricular tachycardia or ventricular fibrillation, or both, were treated with aprindine, a new antiarrhythmic agent. It was found that: (1) no patient had a recurrence of ventricular fibrillation after aprindine therapy was begun, except as a terminal event subsequent to the development of acute myocardial infarction and cardiogenic shock or refractory congestive heart failure; (2) 6 patients experienced ventricular tachycardia after the loading dose, but with continued aprindine therapy the ventricular tachycardia was suppressed in 3 of these 6 patients, and a fourth patient was asymptomatic during brief paroxysms of ventricular tachycardia; (3) in 2 patients, aprindine was ineffective and was discontinued; (4) electrical cardioversion was not required in any patient receiving aprindine; (5) premature ventricular extrasystoles were decreased in 18 of the 23 patients treated with aprindine; (6) aprindine was discontinued in 1 patient because of intolerable side effects, although ventricular arrhythmias were suppressed in this patient; and (7) 5 patients died from acute myocardial infarction or severe heart failure while receiving aprindine.
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PMID:Treatment of recurrent ventricular tachycardia and fibrillation with aprindine. 6

Of 80 patients with acute myocardial infarction who had a cardiac arrest without shock 42 (52.5%) were resuscitated in a cardiological intensive care unit. Twenty-six were finally discharged from hospital. After an average of four years, 21 patients were still alive. Prognosis of primary ventricular fibrillation, the most frequent cause of circulatory arrest (51) was more favourable than that of primary asystole (23 patients). The younger the patient the better the prognosis: the average age of the 21 who survived for several years was 12 years less than those who had died. Follow-up examination indicated that 13 had signs of heart failure. Ventricular extrasystoles were demonstrated by ECG in 11. Eight had depressive episodes. It is likely that a further decrease in death-rate can be achieved only if the interval between onset of infarction and admission to an intensive care unit can be shortened.
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PMID:[Short- and long-term prognosis of cardiac arrest in acute myocardial infarction (author's transl)]. 6 61

75 patients aged under 70 years who had survived acute myocardial infarction complicated by both significant arrhythmias and cardiac failure were followed-up for 1 year in an attempt to identify features which suggest the likelihood of late death or reinfarction. Patients were carefully instructed in the identification and importance of possible prodromal symptoms and the availability of a mobile intensivecare ambulance service and a 24 h hospital control centre. Horizontal ST-segment depression or anginal pain on an exercise test done within 6 weeks of infarction was a useful predictor of late death. Routine twice weekly E.C.G. recordings taken by telephone transmitter at rest and after mild exertion resulted in the identification of significant arrhythmias in only 7 patients. 13 patients (17%) died, 5 of them instantaneously. 4 of the 13 patients and 22 of the 62 survivors reported "prodromal symptoms". Unreported prodromal symptoms were elicited retrospectively in 14 of the 62 survivors and from the relatives of 4 of the 13 patients who died. Thus, 35% of prodromal symptoms were not reported despite intensive patient education and counselling. The incidence of "prodromal symptoms" was no higher in patients who died than in those who did not die.
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PMID:Predictors of reinfarction and sudden death in a high-risk group of acute myocardial infarction survivors. 8 97

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

Sixty-three patients suffering from acute myocardial infarction were examined within the first 24 hours of the disease (27 within the first 6 hours) by means of catheterization of the right parts of the heart with a Swan-Ganz balloon catheter and thermodilution. Comparison between the cardiac output and the pressure of left ventricular filling allowed the following hemodynamic variants of myocardial infarction to be distinguished: normo-, hypokinetic, with increased pressure of left ventricular filling and normal cardiac output, hypovolemic, and hyperdynamic. The results of the tests with acute rheopolyglucin load (9 patients) showed that some of the patients with normal values of hemodynamics had latent cardiac insufficiency. Hemodynamic study and recognition of the variant of hemodynamic changes in the acute period of myocardial infarction made it possible to determine properly the indications for the use of vasodilators, active inotropic agents, and infusion therapy.
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PMID:[Variants of hemodynamic changes in acute period of myocardial infarct and the importance of their detection for treatment]. 10 48

The principal echocardiographic features of the main cardiovascular emergencies are discussed. After setting out a method of detailed analysis for echocardiography, the changes found in the main causes of severe chest pain, systemic embolisation and sudden heart failure are described. Special emphasis is laid on the signs of aortic root dissection, pericarditis and tamponade, ruptured valve, the mechanical complications of acute myocardial infarction and, in particular, on the assessment of residual myocardial function. Finally, the authors maintain that echocardiography should be a systematic complementary investigation for patients in the coronary care unit.
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PMID:[Echocardiographic aspects of left atrial thrombosis in 1 case of severe mitral stenosis]. 11 38

The principal echocardiographic features of the main cardiovascular emergencies are discussed. After setting out a method of detailed analysis for echocardiography, the changes found in the main causes of severe chest pain, systemic embolisation and sudden heart failure are described. Special emphasis is laid on the signs of aortic root dissection, pericarditis and tamponade, ruptured valve, the mechanical complications of acute myocardial infarction and, in particular, on the assessment of residual myocardial function. Finally, the authors maintain that echocardiography should be a systematic complementary investigation for patients in the coronary care unit.
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PMID:[Value of echocardiography in cardiovascular emergencies (not including congenital cardiopathies)]. 11 40


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