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

Left ventricular hypertrophy (LVH) has been studied as a condition predisposing to cardiovascular disease over a 34 year period in the Framingham study. Whether present on the electrocardiogramme, chest X-ray or echocardiography, LVH is a harbinger of cardiovascular disease. It increases the risks of coronary artery disease, cardiac failure, cerebral haemorrhage and peripheral arterial disease. Its contribution to global cardiovascular risk is three times greater than that of hypertension which is the principal cause of LVH. Age, blood pressure and obesity are the three essential factors predisposing to LVH. Each contributes independently to the development of electrocardiographic hypertrophy (ECG-LVH). Increased left ventricular mass detected by echocardiography is commoner with age but apparently as the consequence of an increased prevalence of hypertension, obesity, coronary artery and valvular heart disease with age. The increase of left ventricular mass with age seems largely to be due to fatty hypertrophy and to hypertension. The risk associated with ECG-LVH is particularly important when St-T wave changes are associated with increased voltage. The outcome and prognosis of ECG-LVH and of silent myocardial infarction are similar. When overt coronary artery disease is present, ECG-LVH further increases the risk of cardiovascular events. Electrocardiographic LVH carries a worse prognosis than radiographic LVH which corresponds to anatomic hypertrophy. As the two forms of LVH contribute independantly to the cardiovascular risk, it is probable that they result from different physiopathological mechanisms.
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PMID:[Prognostic implications of left ventricular hypertrophy in arterial hypertension]. 215 Apr 70

Causes of congestive heart failure include hypertension, coronary artery disease, alcohol abuse and valvular heart disease. Two-dimensional echocardiography with Doppler examination is excellent for identifying valvular heart disease. While noninvasive screening for coronary artery disease may seem cost-effective, the consequences of a missed diagnosis are such that coronary angiography should be strongly considered if there is any suggestion of ischemic heart disease. Medical management primarily consists of vasodilators, diuretics and inotropic agents. Vasodilator therapy may prolong the patient's life. Digoxin and diuretics improve symptoms and hemodynamic abnormalities. With advanced heart failure, adequate control of fluid retention and dyspnea may require diuretic doses associated with azotemia, and systolic blood pressure may have to be maintained at less than 100 mm Hg in spite of postural hypotension.
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PMID:Congestive heart failure. 220 40

A review of the clinical course of chronic heart failure demonstrates that current outcomes remain highly unsatisfactory both in mortality and perhaps more important in morbidity. The extraordinary satisfactory functional responses seen in patients who undergo cardiac transplantation clearly identify the primary cause as the status of the heart itself, whatever the pathophysiologic adjustments of the neuroendocrine system, and interventions of the wide variety of drugs. Since donor hearts are unlikely to be available even from younger sufferers of these clinical syndromes, prevention must be the hallmark. Protection of the viability of myocytes, such as in acute myocarditis and acute infarction, is essential. Myocardial collagen undergoes continual synthesis, and production is greatly stimulated in the presence of hypertrophy caused by increased wall stress. It is possible that excess collagen is intimately involved with diastolic ventricular dysfunction, but that this may be a reversible process if the collagen-producing stimulus is removed. Thus reduction in wall stress and reversibility of ventricular hypertrophy appear to be promising directions. However, to limit the catastrophic effects of chronic heart failure, early recognition of the precursors of these syndromes, prevention of progression, and surgical intervention in valvular heart disease at an optimal point in time are essential.
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PMID:Can heart failure be prevented, delayed, or reversed? 224 10

The purpose of this clinical study was to (1) evaluate mortality rates after surgical interventions for patients in cardiogenic shock (CS) secondary to acute coronary occlusion, acute ventricular septal defect (VSD) or acute valvular heart disease, (2) determine the pre-operative regional wall motion, and (3) ascertain the recovery of preoperative regional wall motion abnormalities after surgical intervention. The hospital records of twenty-five consecutive patients in CS were reviewed retrospectively. Regional wall motion was assessed preoperatively by ventriculography and postoperatively by 2D echocardiography (Sonotron Kardio VUE 60) after 1 and 3 days and at the day of discharge from the surgical ward (7-10 days). The left ventricle was divided in three segments according to the blood supply: LAD artery (antero-lateral wall), circumflex artery (lateral wall), and right coronary artery (inferior and basal wall). Regional wall motion was analyzed with the use of a scoring system in which grading was from 0 to 4 according to the following criteria: 0 = hyperkinesia, 1 = normokinesia, 2 = hypokinesia, 3 = dyskinesia, 4 = akinesia. Postmortem examination was performed in 8/9 patients. Data are presented as mean +/- SD. Significant differences were defined as probabilities for each test of p less than 0.05. The hospital mortality was higher for patients with acute coronary occlusion as compared to those with acute valvular disease or VSD (54.5%, 27.3%, 0%, resp.). The cause of death was cardiac in 7/9 patients. However, postmortem examination revealed loss by infarction of only moderate quantities of myocardium which could not explain the severe postoperative heart failure in those patients. Previous myocardial infarctions and preoperative cardiac arrest were significant risk factors for hospital mortality. In all patients with acute coronary occlusion (11/11) at least one region of the left ventricle was either a- or dyskinetic in the region supplied by the acute occluded vessel. In addition five patients had akinetic regions due to previous infarctions. The remaining remote myocardium was hypocontractile due to significant stenosis in coronary arteries supplying remote areas. Of 10 dyskinetic segments before surgical intervention, 5 were akinetic postoperatively, and only 5 developed slight hypokinetic contractions. The overall hypokinetic regions were not different as compared to the preoperative data (36.4% vs 39.4%). The normokinetic segments increased from 9.1% to 33.% (p less than 0.05).
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PMID:Prolonged abnormalities of LV regional wall motion after normal reperfusion in patients with preoperative cardiogenic shock. 237 33

We our department have performed tricuspid-tailoring annular constriction (T-TAC) as salvage operation for secondary tricuspid regurgitation (TR) with gratifying results. Of those cases undergoing MVR and T-TAC for mitral valve regurgitation (MR) and secondary TR with an associated severe cardiac cachexia, 2 autopsy cases in which an associated severe cardiac cachexia, 2 autopsy cases in which residual tricuspid regurgitation culminated in patient's death long after operation were investigated. In Case 1, the patient was discharged asymptomatic 2 months after operation, but later developed severe left heart failure and marked tricuspid regurgitation as precipitated by upper respiratory tract infection and died from exacerbation of LOS before undergoing a scheduled reoperation. T-TAC was found successful on autopsy. In Case 2, the patient died of long-persisting left heart failure and severe residual tricuspid regurgitation after following a similar postoperative course to that in Case 1. On autopsy stitches made through the tricuspid anterior leaflet, septum and posterior leaflet were found untied and loosened and the tricuspid annulus diameter increased. In severe valvular heart disease, even if T-TAC has proven successful, aggravation of cardiac failure may lead to the development of TR. Because of the fragility of myocardial tissue due to severe myocardial damage in such compromised patients, sophisticated operative techniques need to be devised. Cases illustrative of a limited long-term success of T-TAC used alone are presented.
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PMID:[A study of tricuspid-tailoring annular constriction in autopsy cases--cases which appear to embody limitation of tricuspid-tailoring annular constriction]. 239 87

Antiarrhythmic drugs occasionally facilitate, rather than prevent, ventricular tachycardia. The purpose of this study was to assess the incidence of procainamide facilitation of ventricular tachycardia initiation during programmed electrical stimulation in patients with no history of spontaneous sustained ventricular tachycardia but who are at high risk. Twenty patients with advanced heart failure (mean left ventricular ejection fraction 0.19 +/- 0.09) and nonsustained ventricular tachycardia and in whom sustained ventricular tachycardia was not inducible by programmed electrical stimulation in the basal state were studied. Six patients had coronary artery disease, 13 had idiopathic dilated cardiomyopathy, and 1 had valvular heart disease. All patients received programmed stimulation from the right ventricular apex with one to three extra-stimuli before and after the intravenous infusion of 10 mg/kg of procainamide (serum level 6.6 +/- 2.4 mcg/l). In two patients (10%) sustained monomorphic ventricular tachycardia was initiated only after the administration of procainamide. One of these patients later died in ventricular tachycardia during hyperkalemia. Of the noninducible patients, during a follow-up period of 6 +/- 5 months, two died suddenly and one developed symptomatic ventricular tachycardia. Thus, procainamide can unmask potential reentry circuits in some patients who have not had spontaneous sustained ventricular tachycardia. In patients with heart failure, this risk, as assessed by programmed stimulation after a single dose of procainamide, appears to be low.
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PMID:Facilitation of ventricular tachycardia initiation by procainamide during programmed ventricular stimulation in patients with heart failure. 240 61

The correlation between the plasma atrial natriuretic peptide (ANP) levels and echocardiographically measured atrial and ventricular dimensions was studied in various cardiovascular diseases. A total of 107 patients (valvular heart disease 27, cardiomyopathy 11, ischemic heart disease 17, hypertension 42, congenital heart disease 2, and normal 8) were studied. None of the patients had overt signs of heart failure, though 22 of them had atrial fibrillation. Left ventricular end-diastolic and end-systolic diameters, ejection rate and end-diastolic posterior wall thickness were measured by M-mode echocardiography. Maximal left and right atrial diameters and right ventricular end-diastolic diameter were measured by the apical four-chamber view. Following echocardiographic evaluation and blood pressure measurement, blood sampling was performed via the antecubital vein into a tube containing aprotinin and the samples were analyzed by radioimmunoassay. There was no significant correlation between ANP level and heart rate, systemic blood pressure, left ventricular end-diastolic and end-systolic diameters, ejection fraction, posterior wall thickness or right ventricular end-diastolic diameter. The most probable reason for the insignificant relationships was that the correlation varied according to the underlying cardiovascular diseases; e.g., correlation between ANP level and left ventricular diameter was significantly positive in mitral regurgitation, while it was significantly negative in hypertrophic cardiomyopathy. There was a significant correlation between ANP level and the maximal right (r = 0.40, p less than 0.001) or left atrial diameter (r = 0.57, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relations of intracardiac dimensions as measured by echocardiography and plasma atrial natriuretic peptide levels in various cardiovascular diseases]. 253 Mar 34

The authors analysed a series of 557 consecutive patients who suffered cardiorespiratory arrest at the Dante Pazzanese Institute of Cardiology (DPIC) during a period of 5 years in order to examine factors predicting successful resuscitation and long-term survival. Cardiopulmonary resuscitation (CPR) maneuvers were tried in 536 patients, with the following results: 284 patients (53%) died immediately, another 102 (19%) died within the first 24 h after the cardiac arrest and 150 patients (28%) survived more than 24 h. Among these, 65 (12.1%) died in the first month after cardiac arrest and other 29 (5.4%) died after that period. There were 43 late survivors (8%). Thirteen patients (2.4%) were lost to follow-up. After 9 years, the accumulative life expectancy was 8.7%. Coronary heart disease, cardiomyopathy and valvular heart disease were the most frequent underlying diseases. None of the 49 patients with cyanotic congenital heart disease survived. The heart arrest was mostly caused by heart failure (55.8%) and primary arrhythmia (17.2%) in the whole group, whereas the survivor group showed primary arrhythmia in 81.7% and heart failure in 7.3%. In those patients where the initial mechanism of cardiac arrest was ventricular fibrillation, 33.2% survived more than 1 month, while among those on ventricular asystole, only 3.4% survived more than 1 month.
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PMID:Results of cardiopulmonary resuscitation in a cardiology hospital. 255 49

Polysomnography was carried out in 11 adult outpatients with stable chronic heart failure (CHF) due to valvular heart disease in order to investigate respiratory abnormalities during sleep. The subjects consisted of 6 males and 5 females and their ages ranged from 54 to 76 years. A coexisting central dominant sleep apnea syndrome (SAS) was found in 4 males, 3 of whom had evidence of nasal obstruction. A successful mitral valve replacement in one patient with central dominant SAS was associated with a reduction in the frequency of sleep apnea. The results suggest complications caused by respiratory abnormalities during sleep are common and should be considered in the management of patients with CHF.
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PMID:Breathing abnormalities during sleep in patients with chronic heart failure. 263 19

Patients with very poor ventricular function have been thought to be highly vulnerable to elective myocardial revascularization. Ischemic cardiomyopathy is now the major indication for cardiac transplantation. The 2-year survival of medically treated patients with ejection fractions less than 20%, but who are not sufficiently symptomatic for cardiac transplantation, is less than 25%. At our institution we have taken an aggressive approach by using myocardial revascularization for chronic ischemic cardiomyopathy. Between 1983 and 1988, 39 patients with preoperative ejection fractions less than 20% underwent coronary artery bypass. Patients were excluded if they had valvular heart disease other than mild to moderate mitral regurgitation, required resection of a left ventricular aneurysm, or required emergency operation for acute coronary occlusion. Mean age was 63.3 years (range, 43 to 80 years) and 31 were men. Mean preoperative ejection fraction was 18.3% (range, 10% to 20%) and the mean preoperative left ventricular end diastolic pressure was 22 mm Hg (range, 8 mm Hg to 38 mm Hg). There was one operative death (2.6%). Mean follow-up was 21 months (range, 3 to 60 months) with eight late deaths (a total mortality rate of 21%). Seven deaths were due to arrhythmias. Three patients continued to have severe heart failure, one of whom underwent successful cardiac transplantation. By life table analysis, there was a 3-year survival rate of 83%. With the present shortage of cardiac transplant donors, myocardial revascularization for ischemic cardiomyopathy is a reasonably effective means for preserving residual ventricular function.
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PMID:Coronary revascularization rather than cardiac transplantation for chronic ischemic cardiomyopathy. 267 84


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