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

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.
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PMID:Secondary and tertiary prevention with calcium antagonists in coronary artery disease. 137 87

As the myocardial carnitine content, a key control factor in myocardial oxidative metabolism and energy transfer, is reduced in heart failure, administration of L-propionylcarnitine (LPC), a potent analogue of L-carnitine, potentially may improve cardiac function, possibly through a positive inotropic effect. As its hemodynamic profile is unknown in humans, 32 fasting normotensive patients with coronary artery disease received either 15 mg/kg of LPC (n = 16) or vehicle (mannitol/acetate, n = 16) infused over 5 min. Hemodynamic, radionuclide [peak ejection and filling rates (PER and PFR, respectively)], and metabolic variables (myocardial O2, lactate, and carnitine uptake) were studied at baseline and 1, 3, 5, 10, 15, and 45 min postdrug. The baseline ejection fraction was depressed in LPC patients (40 +/- 3% vs. 48 +/- 4% in the vehicle group, p less than 0.05) as a result of a significant high incidence of previous infarctions. Immediately following LPC, the cardiac total carnitine uptake changed from 102 +/- 181 to 5,335 +/- 1,761 mumol/L (p less than 0.05). In both groups, left ventricular systolic and end-diastolic pressures increased significantly by 5 and 20%, respectively, during the first 5 min. In the vehicle group, contractility decreased by 5%, accompanied by a significant 11% fall in the stroke volume. In contrast, following LPC, isovolumetric contractility indices remained unaltered. Instead, both the PER and PFR improved by 16% at 45 min. Moreover, the cardiac output increased by 8%. LPC did not affect systemic or coronary hemodynamics. Lactate uptake increased by 42%, but myocardial O2 consumption did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute improvement of cardiac function with intravenous L-propionylcarnitine in humans. 138 25

Congestive heart failure is a syndrome common in the United States, especially in elderly patients. The most common etiology is coronary artery disease. A number of general factors contribute to the heart failure syndrome, including loss of muscle, decreased myocardial contractility, pressure or volume overload, or restricted filling. All of these factors may play a role in a given patient as, for example, with coronary artery disease. Although systolic dysfunction with a reduced ejection fraction is the most common heart failure syndrome, up to 40% of patients may have a relatively preserved ejection fraction with diastolic dysfunction. As the heart begins to fail, a number of compensatory mechanisms are activated. These include increased heart rate, the Frank-Starling mechanism, increased catecholamines, activation of the renin-angiotensin system, and release of atrial natriuretic peptides. Although these mechanisms are initially helpful to the cardiovascular system, they frequently overshoot, initiating a vicious cycle. For example, with a decrease in cardiac output, there is a reflex increase in systemic vascular resistance in order to maintain perfusion pressure. This increase in resistance, however, acts as a load on the left ventricle and further reduces cardiac output. The best evidence for the existence of this vicious cycle is the beneficial change in hemodynamics produced by vasodilator drugs and the ACE inhibitors. Thus, an understanding of pathophysiology allows for the selection of rational therapy. An unresolved problem in heart failure patients is how best to reduce the high incidence of sudden death, which is one of the major challenges for the future.
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PMID:Pathophysiology of congestive heart failure. 139 15

The efficacy of beta-blockers was tested in 11 patients who avoided sudden death as a result of ventricular tachycardia or fibrillation due to coronary artery disease or non-ischaemic underlying heart disease, after implantation of an automatic defibrillator. Ten patients initially tolerated acebutolol despite prior class III or IV heart failure in six cases; nadolol replaced acebutolol in nine cases for long-term therapy. In these 10 patients, periods of treatment with and without beta-blocking agent were available, making possible a crossover comparison, during a follow-up lasting 31.6 +/- 17.8 months. One hundred and ten shocks were delivered: 14 were considered as probably inappropriate and ruled out, leaving the remaining 96 shocks to be analysed. The monthly rate of shocks was lower during beta-blocking treatment: 0.12 +/- 0.24 vs. 1.09 +/- 1.41 (P = 0.03). While taking beta-blockers, only four patients received shocks, compared to 10 (i.e. all cases) not administered beta-blockers (P less than 0.01). Despite the technical limitations of the study, since only a few spontaneous shocks could be documented on ECG recordings, the efficacy of beta-blockers in preventing occurrence of severe ventricular tachyarrhythmias seems likely, and deserves further investigations using new implanted devices with improved memory functions.
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PMID:Efficacy of beta-blocking agents in reducing the number of shocks in patients implanted with first-generation automatic defibrillators. 139 26

During the past years, several large trials (Consensus, VHEFT I and II, SOLVD) have shown a significant reduction of mortality in patients with moderate and severe heart failure. However, despite effective treatment with vasodilators, digitalis and diuretics mortality in these patients remains unacceptable high. It seems logic, to state treatment at an earlier stage of the disease to achieve more benefit. The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. On the long run, LVH may lead to diastolic and systolic heart failure, myocardial ischemia, arrhythmias and sudden death. With ACE-inhibitors LVH can be reduced within 1 month of treatment. The large SAVE- and SOLVD-prevention trials will show, whether this early intervention will improve proposis in patients with asymptomatic heart failure.
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PMID:[Early therapeutic intervention in heart failure]. 141 67

Echocardiographic predictors of clinical outcome were examined in subjects from the Framingham Heart Study with overt coronary artery disease. The study population consisted of 185 men and 147 women with coronary artery disease who underwent M-mode echocardiography and were followed for a mean of 3.90 years. At baseline, 37 men (18.4%) and 16 women (10.9%) had reduced fractional shortening, 43 men (23.2%) and 28 women (19%) had left ventricular (LV) dilatation, and 76 men (41%) and 76 women (51.7%) had LV hypertrophy. During the follow-up period new cardiovascular disease events (coronary disease, stroke, transient ischemic attack, claudication, heart failure and deaths from cardiovascular disease) occurred in 60 men (32%) and 58 women (39%). With use of age-adjusted proportional hazards analyses, LV mass/height in men (relative risk [RR] = 1.25/50 g/m increment, 95% confidence interval [CI] 1.01 to 1.55) and LV end-diastolic diameter in women (RR = 1.36/5 mm increment, 95% CI 1.05 to 1.76) were predictors of new cardiovascular disease events. Cardiovascular risk was also associated with LV end-systolic diameter in both sexes (in men RR = 1.28/1 SD increment, 95% CI 1.02 to 1.63; in women RR = 1.40/1 standard deviation increment, 95% CI 1.09 to 1.82). Reduced fractional shortening alone (RR = 1.91, 95% CI 1.11 to 3.31) and in combination with LV dilatation (RR = 2.13, 95% CI 1.13 to 4.02) was associated with the incidence of new cardiovascular disease outcomes in men.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Echocardiographic determinants of clinical outcome in subjects with coronary artery disease (the Framingham Heart Study). 141 14

In this study, independent contribution of age, HR, BMI, casual and ambulatory blood pressure, LVM and LVEF in evaluating diastolic filling have been investigated in 34 never-treated hypertensive patients and in 15 healthy normotensive subjects. All the subjects were free from coronary artery disease, valvular disease, heart failure, renal disease and psychiatric problems. All the hypertensive subjects (never treated) were subgrouped according to presence or absence of LVH. The PFR decreased significantly and tPFR increased significantly in hypertensive patients in comparison with normotensive subjects and they did not change in the presence vs absence of LVH. The PFR was inversely correlated with BMI, age, 24-h mean SBP and with 24-h DBP. In multiple regression analysis, PFR decreased with BMI, age, 24-h mean SBP and DBP but not with LVMI. These results suggest that BMI, age and 24-h mean blood pressure were the major determinants of PFR abnormalities in hypertensive patients.
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PMID:Rapid left ventricular filling in untreated hypertensive subjects with or without left ventricular hypertrophy. 142 72

Sudden cardiac death (SCD) is usually due to monomorphic ventricular tachycardia and/or ventricular fibrillation. However, in the vast majority of patients these arrhythmias are associated with advanced structural disease. In our society, this is usually due to coronary artery disease (CAD). The implantable cardioverter--defibrillator is the logical approach to management in survivors of SCD. Its rational use must be guided by electrophysiology study. However, a realistic and cost-effective approach to the prevention of a first cardiac arrest must be multifaceted and take cognisance of other aspects including primary prevention. Limitation of the size of myocardial infarction (MI) is vital. Trials already suggests that effective thrombolysis may impinge long-term on arrhythmic end-points. Following infarction, ventricular arrhythmias and sudden death may also be decreased by aspirin, beta-blockers, and possibly angiotensin converting enzyme inhibitors and amiodarone. Many post-infarction studies employ a combined end-point of death and clinical arrhythmias. However, death is usually confined to those with an ejection fraction < 35%. In them, treatment of associated heart failure is often a consideration and if the ejection fraction < 15-20%, depending on donor availability, transplantation may even be the preferred therapeutic option to the cardioverter-defibrillator.
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PMID:Prevention of sudden cardiac death: the ICD, or an electrical end-point with preceding opportunities for intervention? 144 53

Twenty patients (two female, 18 male, mean age 57 +/- 11 years) with severe heart failure NYHA IV (7 coronary artery disease, 13 congestive cardiomyopathy) were treated with 8.8 +/- 1.7 micrograms.kg-1 x min-1 of dobutamine. Pulmonary gas exchange was analysed by withdrawal of blood samples from a central venous catheter and a radial artery cannula. Dobutamine increased SvO2 from 58.7 +/- 11.2% to 72.2 +/- 6.3% (P = 0.0001) and decreased avDO2 from 7.7 +/- 2.45 Vol% to 4.97 +/- 1.34 Vol% (P = 0.0001). PaO2 and PaCO2 were not changed. Qs/Qt increased slightly from 9.1 +/- 8.3% to 11.3 +/- 6.4% (P = 0.035). Cardiac index increased by 51% (P = 0.0001), pulmonary capillary wedge pressure decreased by 28% (P = 0.0001). In patients with severe heart failure, dobutamine improved haemodynamics without detrimental effects on arterial oxygen concentration.
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PMID:Effect of dobutamine on pulmonary gas exchange in patients with severe heart failure. 146 44

During the last decades heart failure has become a syndrome of major concern. Despite a decline in the occurrence of coronary artery disease and improved treatment of systemic hypertension, its primary aetiologic factors, the incidence of heart failure has been ever increasing. It is estimated that in the U.S.A. and most of western Europe approximately 1% of the population suffers from congestive heart failure. Its importance is directly related to its very adverse prognosis with an annual mortality rate as high as 50-60% in the advanced stages of failure. Although treatment with certain vasodilators or converting enzyme inhibitors may improve survival to some extent, the remaining mortality rate still remains high. As it is also extremely difficult to improve the clinical well-being of heart failure patients, emphasis is now on the early phase of failure and in particular on the preceding stage of asymptomatic ventricular dysfunction. Recent animal and human data indicate the significance of myocardial hypertrophy as a first step towards progressive myocardial muscle dysfunction superimposed on the initial cardiac event which leads to asymptomatic ventricular dysfunction. Moreover, there is evidence that neurohumoral activation occurs before heart failure has developed. Although available data only relate to circulating neurohormones, early alterations in local paracrine or autocrine acting systems may well be at issue. Also, whereas heart failure is generally considered a cardiac disorder, there is accumulating evidence that peripheral systems such as the skeletal musculature and the kidney are markedly involved. Changes in peripheral tissue function are not necessarily related to a reduction in cardiac pump function and tissue perfusion, but may be intrinsic of nature. Thus, significant abnormalities in skeletal muscle oxidative metabolism occur which are not secondary to regional flow disturbances. The recognition of cardiac and peripheral changes before or during the early phases of heart failure are likely to alter the current strategies in the treatment of this syndrome.
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PMID:Pathophysiology and therapy of heart failure, new insights and developments. Part I. 147 Feb 89


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