Extract

Aging of the population has a strong impact on the prevalence of heart failure (HF). Given our aging population, the number of patients with HF is expected to increase rapidly over the next decades.1 The clinical syndrome of HF consists of 2 largely distinct phenotypes, readily discerned by echocardiographic determination of the left ventricular ejection fraction (EF). While pharmacological inhibition of the renin–angiotensin–aldosterone system (RAAS) improves survival in patients with HF with reduced EF (left ventricular EF <50%; HFrEF), such therapy has little or no effect in patients with HF with preserved EF (left ventricular EF >50%; HFpEF).2 This may not be too surprising in view of the marginal RAAS parameter alterations in HFpEF vs. HFrEF.3 Indeed, in HFrEF, plasma renin activity is a strong predictor of mortality, even in patients taking renin-affecting drugs like RAAS inhibitors and β-adrenergic antagonists.4 Yet, neither renin nor aldosterone associates with diastolic dysfunction, a well-known characteristic of HFpEF.5 Nevertheless, both angiotensin II and aldosterone are established contributors to left ventricular hypertrophy and cardiac fibrosis, 2 important determinants of diastolic dysfunction.

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