Investigation of left ventricular dysfunction in acute dyspnoea. Echocardiography is important in the management of heart failure.
Explore the source record for details and available documents.
Acute Disease↗
Biomedical subjects
R N Doughty
Publications and source records attributed to R N Doughty.
Left ventricular remodeling with carvedilol in patients with congestive heart failure due to ischemic heart disease. Australia-New Zealand Heart Failure Research Collaborative Group.
OBJECTIVES: The aim of this study, a substudy of the Australia-New Zealand trial of carvedilol in patients with heart failure due to ischemic heart disease, was to determine the effects of this treatment on left ventricular size and function with the use of quantitative two-dimensional (2D) echocardiography. BACKGROUND: Beta-adrenergic blocking drugs have been shown to improve left ventricular ejection fraction in patients with heart failure due to either ischemic heart disease or idiopathic dilated cardiomyopathy. However, the effects of such treatment on left ventricular size remain uncertain. METHODS: One hundred twenty-three patients from 10 centers in New Zealand and Australia participated in the 2D echocardiographic substudy. Echocardiography was performed before randomization and was repeated after 6 and 12 months of treatment. Left ventricular end-diastolic and end-systolic volumes were measured from apical four- and two-chamber views with the use of a modified Simpson's rule method. RESULTS: After 12 months, heart rate was 8 beats/min lower in the carvedilol than in the placebo group, whereas left ventricular end-diastolic and end-systolic volumes were increased in the placebo group but reduced in the carvedilol group. At 12 months, left ventricular end-diastolic volume index was 14 ml/m2 less in the carvedilol than in the placebo group (p = 0.0015); left ventricular end-systolic volume index was 15.3 ml/m2 less (p = 0.0001), and left ventricular ejection fraction was 5.8% greater (p = 0.0015). CONCLUSIONS: In patients with heart failure due to ischemic heart disease, carvedilol therapy for 12 months reduced left ventricular volumes, increased left ventricular ejection fraction and prevented progressive left ventricular dilation. These changes demonstrate a beneficial effect of carvedilol on left ventricular remodeling in heart failure. The observed changes may explain in part the improved clinical outcomes produced by treatment with carvedilol.
Adrenergic beta-Antagonists↗
Immunoreactive amino-terminal pro-brain natriuretic peptide (NT-PROBNP): a new marker of cardiac impairment.
OBJECTIVE: Human brain natriuretic peptide-32 (BNP) (i.e. proBNP(77-108)), the mature form of BNP and secreted predominantly by the cardiac ventricle, is formed from a high molecular weight precursor, proBNP(1-108). We have recently identified the aminoterminal form proBNP(1-76) (NT-proBNP) in human plasma but its source, metabolism and production in circulatory disorders are unknown. We have investigated the relationship between immunoreactive (IR) NT-proBNP and BNP-32 in normal and hypertensive subjects and in patients with cardiac impairment, as well as the regional plasma concentrations in patients undergoing routine cardiac catheterization. DESIGN AND PATIENTS: Plasma hormone measurements were made in 26 normal subjects, 20 subjects with untreated mild hypertension and 111 treated patients with a history of coronary heart disease and documented cardiac impairment (left ventricular election fraction (LVEF) < 45% (mean 29%); 25 NYHA Class I, 65 Class II and 21 Class III). Regional blood sampling from the femoral artery, femoral vein, renal vein and coronary sinus was undertaken in 14 patients presenting for left and right cardiac catheterization studies in the course of standard investigation for a range of cardiac disorders. MEASUREMENTS: Plasma samples were assayed for IR NT-proBNP and IR BNP-32 (and atrial natriuretic peptide (ANP) in the regional blood samples). In the patients with cardiac impairment, LVEF was determined by gated radionuclide ventriculography, exercise capacity was measured using a modified Naughton multistage protocol and creatinine clearance was calculated from plasma creatinine, age and weight. In the regional study, extraction ratios across the kidney and lower limb (and step-ups across the heart) were calculated from plasma peptide concentrations. RESULTS: In normal subjects mean IR NT-proBNP levels (10.8 +/- 1.3 pmol/L) were similar to levels of IR BNP-32 (9.7 +/- 0.5 pmol/L). In hypertensive patients the levels of IR NT-proBNP and IR BNP-32 tended to be higher than but were not significantly different from normal subjects. Both IR NT-proBNP and IR BNP-32 were raised in NYHA Classes I, II and III compared with normals (P < 0.001 for all) with higher levels of both BNP forms seen with increasing cardiac impairment. The levels of IR NT-proBNP were greater than IR BNP-32 in all NYHA Classes (P < 0.001) for all). Overall, the levels of IR NT-proBNP (129 +/- 12 pmol/L) were 4-fold higher than concomitant BNP-32 levels (29 +/- 2 pmol/L). Multivariate analysis showed that LVEF, exercise test time and creatinine clearance were independent predictors of IR NT-proBNP. In all study groups, the levels of IR NT-proBNP and IR BNP-32 levels were highly correlated. Regional plasma sampling showed similar step-ups in IR NT-proBNP and IR BNP-32 levels across the heart, together with similar extraction of both BNP forms across the kidney and lower limb. For both BNP forms, these changes across tissues were significantly less than for ANP. CONCLUSIONS: Plasma levels of immunoreactive amino terminal-proBNP are raised in cardiac impairment, including NYHA Class I, and rise with increasing cardiac decompensation. Metabolism and tissue uptake of immunoreactive amino terminal-proBNP and immunoreactive BNP-32 appear similar. In cardiac impairment the proportional and absolute increment above normal levels of the aminoterminal BNP peptide exceeds that for BNP-32 and suggest that amino terminal-proBNP may be a more discerning marker of early cardiac dysfunction than BNP-32.
Adult↗
Effects of beta-blocker therapy on mortality in patients with heart failure. A systematic overview of randomized controlled trials.
AIMS: Several randomized trials have reported that beta-blocker therapy improves left ventricular function and reduces the rate of hospitalization in patients with congestive heart failure. However, most trials were individually too small to assess reliably the effects of treatment on mortality. In these circumstances a systematic overview of all trials of beta-blocker therapy in patients with congestive heart failure may provide the most reliable guide to treatment effects. METHODS AND RESULTS: Details were sought from all completed randomized trials of oral beta-blocker therapy in patients with heart failure of any aetiology. In particular, data on mortality were sought from all randomized patients for the scheduled treatment period. The typical effect of treatment on mortality was estimated from an overview in which the results of all individual trials were combined using standard statistical methods. Twenty-four randomized trials, involving 3141 patients with stable congestive heart failure were identified. Complete data on mortality were obtained from all studies, and a total of 297 deaths were documented during an average of 13 months of follow-up. Overall, there was a 31% reduction in the odds of death among patients assigned a beta-blocker (95% confidence interval 11 to 46%, 2P = 0.0035), representing an absolute reduction in mean annual mortality from 9.7% to 7.5%. The effects on mortality of vasodilating beta-blockers (47% reduction SD 15), principally carvedilol, were non-significantly greater (2P = 0.09) than those of standard agents (18% reduction SD 15), principally metoprolol. CONCLUSIONS: Beta-blocker therapy is likely to reduce mortality in patients with heart failure. However, large-scale, long-term randomized trials are still required to confirm and quantify more precisely the benefit suggested by this overview.
Administration, Oral↗
Beta-adrenergic blocking agents in the treatment of congestive heart failure: mechanisms and clinical results.
Congestive heart failure is a major public health problem in Western countries. Despite current treatment including angiotensin converting enzyme inhibitors, mortality and morbidity remain high. The sympathetic nervous system is markedly activated in heart failure, and inhibition of this system with the beta-adrenergic blocking agents may provide further benefit. Several clinical trials involving over 3,000 patients have shown that beta-blocker therapy improves left ventricular function in patients with heart failure. However, the effects of such therapy on symptoms and exercise tolerance have been variable. Recent reports have suggested that survival is improved with the beta-blocker carvedilol. Large-scale, long-term clinical trials are required to confirm these findings and to clearly define the role of this promising therapy for patients with heart failure.
Adrenergic beta-Antagonists↗
Left ventricular function in scleroderma.
Scleroderma affects the left heart directly and indirectly via the effects of systemic hypertension. Using transthoracic echocardiography, we evaluated 35 patients with scleroderma and compared them with matched control subjects. Compared with controls, there were no differences between left ventricular dimensions, wall thickness, calculated mass or fractional shortening. However, the left atrium was enlarged (P = 0.006) and the mitral deceleration time was prolonged (P = 0.0005) in patients with scleroderma; suggesting abnormal diastolic function. After adjusting for potential confounders, duration of Raynaud's was found to be an independent predictor of deceleration time (P = 0.04), E/A peak velocity ratio (P = 0.04), A peak velocity (P = 0.004) and A velocity time integral (P = 0.0001), all measures of diastolic function. This group of individuals with scleroderma have evidence of abnormal diastolic function of the left ventricle despite normal left ventricular size and systolic function, and in the absence of hypertrophy. This finding is independent of the use of vasoactive medications and history of systemic hypertension, and thus may be due to primary myocardial involvement by scleroderma. The tendency to abnormal diastolic function of the left ventricle correlated with the duration of Raynaud's phenomenon.
Adolescent↗
Optimal treatment of angina in older patients.
Ischaemic heart disease is a major problem in the elderly. Compared with younger patients, coexisting medical conditions are more common and the patients are more likely to be receiving multiple drugs. In addition, drug pharmacodynamics are altered in the elderly and this needs to be carefully considered when commencing treatment for angina. In practice, the general principles of management of elderly patients with angina are similar to that of younger patients. However, particular care needs to be taken with the therapeutic regimens used. This article reviews the approach to the treatment of stable exertional angina in the elderly.
Adrenergic beta-Antagonists↗
Beta-blockers in heart failure: promising or proved?
Despite recent improvements in the management of congestive heart failure, the prognosis of many patients with this condition remains poor. The level of neurohormonal activation appears to be predictive of survival, and clinical studies indicate that inhibition of overactivated neurohormonal systems may be beneficial. Activation of the renin-angiotensin-aldosterone system is well documented in heart failure, and angiotensin-converting enzyme inhibition now has an established role in treatment based on evidence of hemodynamic, symptomatic and mortality benefit. Sympathetic nervous system activation also occurs as a compensatory mechanism in heart failure but with long-term deleterious effects. Increasing evidence suggests that beta-adrenergic blockade can produce hemodynamic and symptomatic improvement in heart failure of idiopathic or ischemic etiology. Trials of beta-adrenergic blocking agents in patients after myocardial infarction suggest a beneficial effect on mortality, even among those with heart failure. However, there remains uncertainty as to how generalizable are the results from the postinfarction trials, particularly in the current therapeutic environment with routine angiotensin-converting enzyme inhibitor therapy. Appropriately powered randomized, controlled trials are required to determine precisely the balance of benefit and risk resulting from long-term beta-blocker therapy in patients with heart failure of ischemic and other etiology.
Adrenergic beta-Antagonists↗
Current management of congestive heart failure.
Congestive heart failure is a major public health problem in developed countries. There have been significant advances in the management of this condition over the last few decades. However, many patients are still not receiving adequate therapy. Optimal management requires appropriate investigation, education, counselling, medical treatment and planned follow-up. This review outlines the recommended approach for optimal management of patients with heart failure.
Cardiovascular Diseases↗