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Treating diastolic heart failure
  1. Adriaan A Voors,
  2. Richard M de Jong
  1. Department of Cardiology, University Medical Centre Groningen, Groningen, The Netherlands
  1. Dr A A Voors, Department of Cardiology, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, The Netherlands; a.a.voors{at}

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In around half of patients diagnosed with heart failure, a relatively preserved systolic function (left ventricular ejection fraction (LVEF) >0.40–0.50) is found. These patients are generally diagnosed with diastolic heart failure or heart failure with preserved ejection fraction. Owing to an ageing population and an increased incidence of hypertension and diabetes, this percentage is expected to increase in the near future.

The diagnosis of diastolic heart failure is challenging. In a consensus statement of the European Society of Cardiology, the definition of diastolic heart failure is based on signs and symptoms of heart failure, a relatively preserved left ventricular systolic function (LVEF >0.40–0.50), evidence of diastolic dysfunction on echocardiography and raised natriuretic peptides.1

Treatment of diastolic heart failure is hampered by the absence of evidence for a specific drug that can reduce mortality and morbidity in these patients. Theoretically, a number of treatments might benefit patients with diastolic heart failure. First, in symptomatic patients, diuretics will reduce fluid overload and symptoms. Second, heart rate lowering and negative inotropic agents, such as (some) calcium channel blockers and β blockers, will increase left ventricular filling time and might improve relaxation. Third, every agent that will decrease blood pressure is expected to reduce left ventricular hypertrophy and therefore improve relaxation. Of particular interest are blockers of the renin–angiotensin system, such as ACE inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists. Their potential benefit can be explained by a reduction in both pre- and afterload, a reduction in left ventricular hypertrophy, a reduction in interstitial collagen deposition and fibrosis and, possibly, a favourable effect …

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  • Competing interests: AAV has been (partly) reimbursed for attending conferences, received speaking and/or consultancy fees by/from Sanofi-Synthelabo (irbesartan), Astra Zeneca (candesartan), Novartis (valsartan), Aventis (ramipril), Servier (perindopril). Also, AAV is the principal investigator of a phase II trial with alagebrium, which is sponsored by its manufacturer Synvista. RMJ has been (partly) reimbursed for attending a conference by Astra Zeneca (candesartan).