Rationale for Treatment of Patients With Chronic Heart Failure With Adrenergic Blockade

Objectives-To examine clinical outcomes associated with optional blockade in a population of patients with evidence of heart failure after myocardial infarction. Design and patients-Data from the acute infarction ramipril eYcacy (AIRE) study were analysed retrospectively. At baseline 22.3% of the patients were receiving a blocker. To minimise confounding, blocker and diuretic treatments, presence of clinical signs of heart failure, left ventricular ejection fraction, and 16 other baseline clinical variables were simultaneously entered in a multivariate Cox regression model. In addition, the same analysis was repeated separately within a high and a low risk group of patients, as defined according to the need for diuretic treatment. Results-Blocker treatment was an independent predictor of reduced risk of total mortality (hazard ratio 0.66, 95% confidence interval (CI) 0.48 to 0.90) and progression to severe heart failure (0.58, 95% CI 0.40 to 0.83) for the entire study population. There were similar findings in high risk patients requiring diuretics (0.59, 95% CI 0.40 to 0.86; and 0.58, 95% CI 0.38 to 0.89). Conclusions-Blocker treatment is associated with improved outcomes in patients with clinical evidence of mild to moderate heart failure after myocardial infarction. Most importantly, high risk patients with persistent heart failure appear to benefit at least as much as lower risk patients with transient heart failure. (Heart 1999;81:25-32)

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“…45 46 Most of these actions would be particularly welcome when left ventricular dysfunction develops after myocardial infarction 47…”

Section: Discussionmentioning

confidence: 99%

beta Blocker treatment and other prognostic variables in patients with clinical evidence of heart failure after acute myocardial infarction: evidence from the AIRE study

Spargias

Hall²,

Greenwood³

et al. 1999

Heart

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“…10 Increased sympathetic tone can potentiate renin and angiotensin activity, leading to salt and water retention, arterial and venous constriction, and increased ventricular preload and afterload. 13 By increasing heart rate and promoting coronary vasoconstriction, catecholamine excess can also reduce myocardial blood flow. 14 Norepinephrine is potently cardiotoxic and results in cardiac myocyte injury in concentrations found in the failing heart.…”

Section: Pathophysiology Of Chfmentioning

confidence: 99%

Drug therapy in chronic heart failure

McKenzie

Cowley

2003

Postgraduate Medical Journal

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Chronic heart failure is widely recognised as a common and escalating problem that causes major disability and often shortens life. Diuretics and digoxin have formed the mainstay of treatment for many years. Clinical trials have demonstrated that angiotensin converting enzymes and β-blockers, in selected patients, improve symptoms and reduce mortality. Angiotensin-II antagonists and spironolactone may also have a role in certain individuals. Newer pharmacological approaches to the management of this complex disease are being developed, but await full evaluation.

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“…32,23 Therapy with angiotensinconverting-enzyme inhibitors has improved survival and decreased morbidity among patients with heart failure, 34 and there is growing evidence that modulation of the sympathetic nervous system by b -adrenoreceptor blockade can also favorably affect patients with heart failure. 35 Patients with heart failure have increased sympathetic activity that is associated with exercise intolerance, 36 hemodynamic abnormalities, 37 and increased mortality. 33 Increases in sympathetic tone can potentiate the activity of renin and angiotensin in such patients, leading to retention of salt and water, arterial and venous constriction, and increased ventricular preload and afterload.…”

Section: Congestive Heart Failurementioning

confidence: 99%

“…33 Increases in sympathetic tone can potentiate the activity of renin and angiotensin in such patients, leading to retention of salt and water, arterial and venous constriction, and increased ventricular preload and afterload. 35 Excess catecholamines can increase the heart rate and cause coronary vasoconstriction, thereby diminishing myocardial blood flow, 38 and they can decrease myocardial contractility on the cellular level. 39,40 Catecholamines can also stimulate growth and provoke oxidative stress in terminally differentiated cardiac-muscle cells; these two factors can trigger the process of programmed cell death (apoptosis).…”

Section: Congestive Heart Failurementioning

confidence: 99%