This review outlines the pathophysiological role of angiotensin II and aldosterone in diastolic heart failure, providing a mechanistic rationale for RAAS antagonism.
Offers mechanistic rationale for RAAS antagonists in diastolic dysfunction; leaves open need for outcome trials.
More than half of all persons with heart failure (HF) have diastolic HF. The prevalence of diastolic HF increases from 46% in persons younger than 45 years to 59% in those 85 years and older. The annual mortality rate associated with diastolic HF is >10%. Diagnosis is based on signs and symptoms of HF, elevated plasma B-type natriuretic peptide, preserved left ventricular systolic function, and evidence of diastolic dysfunction by Doppler examination on two-dimensional echocardiography. Approximately 80% of patients with diastolic HF have increased left ventricular mass and a history of hypertension. Neurohormonal activation is a key aspect of this condition. Studies suggest that activation of the renin-angiotensin-aldosterone system, specifically direct cardiac effects of angiotensin II and aldosterone, contributes to the pathogenesis and progression of diastolic dysfunction. Hence, there is a rationale for use of agents that antagonize the renin-angiotensin-aldosterone system, such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists, in patients with heart failure.
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Chinnaiyan et al. (2005) studied this question.
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