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

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

A retrospective analysis of the informativeness of certain methods of examination for ascertaining the possibility of cardiac failure developing in the subacute period of penetrating, predominantly primary transmural myocardial infarction with no clinical signs of cardiac failure in the first three days after the onset of the disease. In 60 patients circulation time in the "arm--ear" area and in 25 of them the stroke and minute volumes by the dye dilution method were studied. The state of the fluid spaces was investigated in 18 patients and daily natriuresis in 23. In 36 patients the condition of the pulmonary circulation was judged by means of roentgenogram. The high value of the information gained from study of circulation time and natriuresis and X-ray examination in the prognostication of the development of cardiac failure is shown.
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PMID:[Retrospective evaluation of various methods of examination for prognosis of cardiac insufficiency in the subacute period of myocardial infarct]. 33 63

Lignocaine is widely used as a local anaesthetic and antiarrhythmic drug. It is commonly administered to patients with acute myocardial infarction as prophylaxis for ventricular fibrillation, although its efficacy in preventing primary ventricular fibrillation is still debated. Toxicity, sometimes with serious clinical consequence, is not uncommom and is usually related to overdosage. Blood lignocaine concentrations correlate roughly with antiarrhythmic and toxic effects and might be useful as an end point for monitoring prophylactic therapy. Administration of lignocaine as a local anaesthetic may result in blood lignocaine concentration in the antiarrhythmic or even toxic ranges. Expected peak levels for various routes of local anaesthesia are tabulated so that 'safe' total doses can be calculated. Intramuscular injection of high doses results in sustained therapeutic levels but is often associated with early minor toxicity. Lignocaine is eliminated primarily by hepatic metabolism, which appears to be limited by liver perfusion. Active metabolites may contribute to therapeutic and/or toxic effects. Disease states such as cardiac failure or drugs that alter hepatic blood flow may significantly affect lignocaine clearance. Pharmacokinetic studies in man show wide variability in drug disposition between patients, even when cardiac and hepatic status is considered, making specific dosing recommendations a problem. With intravenous injection, multicompartment kinetics is observed, with an initial rapid decline phase and initial decline in antiarrhythmic activity due to redistribution. With constant infusion, steady state concentrations of lignocaine are seen after 3 to 4 hours in normal subjects and after 8 to 10 hours in patients with myocardial infarction without circulatory insufficiency. In patients with cardiac failure, blood lignocaine concentration may continue to rise for 24 to 48 hours. In the presence of cardiac failure, decreased volumes of distribution and clearance require reduction in loading and maintenance doses. Lignocaine clearance is reduced in patients with liver disease and appears to be a sensitive index of liver dysfunction. A dosing algorithm for treatment of patients with myocardial infarction is presented.
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PMID:Clinical pharmacokinetics of lignocaine. 35 Apr 70

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

Clinical applications involve heart failure during the acute phase of myocardial infarction, with the possibility of reducing the degree and extent of the perinecrotic ischaemic zone of the infarction. Treatment of this type would seem also to be particularly valuable in the provisional management of acute or sub-acute regurgitating valvular lesions: mitral insufficiency and interventricular communication secondary to an acute infarction, mitral and/or aortic regurgitation due the endocarditis. Finally, the results of oral vasodilators in the context of chronic refractory heart failure would seem ot be encouraging in the short term but their influence on long term prognosis is not known.
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PMID:[The treatment of cardiac insufficiency using vasodilators (author's transl)]. 35 54

160 consecutive CCU-treated AMI patients below 66 yr were investigated for ventricular ectopic beats (VEB) by 6-h telemetry prior to discharge and after 1 yr. During the follow-up year 11 patients died suddenly and 20 suffered reinfarction. By stepwise discriminant analysis three independent prognostic parameters were found: (1) radiologic cardiomegaly; (2) severe VEBs prior to discharge; (3) diabetes mellitus. Previous infarct, angina, functional class II to IV, smoking, higher age and radiologic cardiomegaly were significantly more frequent in patients with VEBs prior to discharge. History of heart failure, functional class deterioration, higher age, male sex, large first infarct, VT or VF in CCU, transmural infarction, radiologic cardiomegaly were more frequent in patients with severe VEBs prior to discharge. VEB severity increased significantly during the follow-up year in survivors without reinfarction. This increase occurred in patients with previous infarction, angina pectoris, higher age and heart failure.
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PMID:Ventricular arrhythmias after an acute myocardial infarction. Prognostic weight and natural history. 35 1

Hemodynamic measurements before and during graded leg-up tilt were performed in 20 patients on the 1st and 3rd day following myocardial infarction. In those with an elevated pulmonary capillary pressure (greater than 11 mm Hg), independent of the cardiac index, the tilt-test (i.e. an additional increase in preload) unmasked heart failure. When applied to test drug responses, furosemide (n = 7) reduced the tilt-stimulated cardiac index with an attendant fall in pulmonary capillary pressure; nitroglycerine (n = 7) did not change cardiac index but reduced the pulmonary capillary pressure.
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PMID:[Stress hemodynamics in fresh myocardial infarct]. 41 90

A retrospective study of 100 case notes of patients who died from a recent myocardial infarction (less than one month before death) has established the causes of death: cardiac failure (52), rupture of the heart (40), major pulmonary emboli (3), primary irreversible ventricular fibrillation (2), unexplained death (3). Study of the extent of the necrosis by the technique of segmentation of the ventricular mass has allowed us to clarify the correlation between the "index of extent" ("i"), an the clinico-pathological findings. It has been noted in particular that those infarctions complicated by cardiogenic shock and/or by bilateral bundle branch block were those with the highest value of index of extent (i = 8.91, i = 9.40); also that cardiac failure and ventricular tachycardia were found in the extensive infarctions (i = 7,33, i = 9.52); also that rupture of the outer wall and pulmonary thromboses complicated infarctions of very small extent (i = 4,80, i = 5,67). It would not seem possible to reduce the hospital mortality of infarctions significantly, since it is essentially linked with circulatory failure caused by extensive necrosis, and with ruptures of the heart which are unpredictable and untreatable.
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PMID:[Cause of death in recent myocardial infarct. Correlation between extent of necrosis and clinical, electrocardiographic and anatomical findings]. 41 79

In a series of 51 clinico-pathological examinations on patients who died during the first 15 days after the onset of clinical symptoms of their first and only transmural myocardial infarction (anterior: 29 cases; posterior: 22 cases) the causes of death were divided into: heart failure -- 26 cases (53 p. 100); rupture of the heart -- 22 cases (43 p. 100); disorders of ventricular rhythm -- 2 cases (4 p. 100). The anatomical basis of fatal cardiac failure is twofold: either a very extensive area of necrosed muscle, of poor quality of the mass of muscle not involved in the infarction. In the anterior infarctions (16 cases, representing 55 p. 100 of deaths in this group) the first factor was foremost, the mean extent of necrosed muscle constituting 42 p. 100 of the total left and septal ventricular mass; stenotic coronary lesions, which were commonly found on the anterior descending artery, were confined to this artery alone in 10 cases 62 (p. 100). In posterior infarctions (11 cases, representing 50 p. 100 of deaths in this group), the mass of muscle destroyed was less (mean 36 p. 100), but the stenotic coronary lesions were diffuse, involving the three main trunks in 9 cases, which also explains the poor quality of the muscle not involved by necrosis. Thus there is a clear difference between anterior and posterior infarctions followed by deaths from cardiac failure: in the first group, the remaining muscular mass is quantitatively insufficient to maintain the haemodynamics, while in the second it is qualitatively insufficient, because of poor blood supply, to maintain an adequate cardiac output.
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PMID:[Fatal cardiac insufficiency in the course of an initial acute myocardial infarct. Anatomical-clinical data]. 41 80

Myocardial infarction (MI), (and especially anteriorly situated necrosis) was complicated by complete branch block (CBB) in 9.7% of cases (45 patients out of 462). A comparison of the short- and long-term outcome in two groups of patients (group A: 45 cases of MI complicated by CBB; group B: 45 cases of MI with no atrio-ventricular or intra-ventricular conduction defects) showed that there was a much bigger immediate mortality in group A, which was not changed by temporary cardiac pacemaking, and depended on the extent of myocardial destruction. A study of the long-term outcome showed that there were more deaths in group A (recurrence of MI, intractable cardiac failure). However, the incidence of sudden death was equal in the two groups (group A 15%, group B 13%), and there was no obvious explanation in the absence of electrocardiographic tracings. Therefore this study lends no support to the argument which favours prophylactic implantation of a cardiac pacemaker during the course of MI complicated by CBB.
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PMID:[Complete bundle-branch block and myocardial infarct. Natural history. Comparative study]. 41 72


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