Heart Failure With Better Ejection Fraction
A Modern Diagnosis
The emerging population of heart failure with improved ejection fraction, characterized in this issue of Circulation by Basuray et al1for 3 heart failure centers, testifies to the cumulative benefit of therapeutic advances during the past 30 years. The initial triage for referral to heart failure centers, many of which were launched with the approval of cyclosporine in 1984, was an assumed “less than six months to live,” derived from the classic Stanford experience in which most waiting transplant candidates who did not receive transplantation were dead within 6 months.2 Although the prognosis was not uniformly grim, most patients referred to transplant centers were dead within 1 to 2 years on the limited medical therapy of that time.
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The direct vasodilators hydralazine and nitrates were the first proven in a randomized trial to improve outcomes in any heart failure population.3 Angiotensin-converting enzyme inhibitors then were shown to improve outcomes in patients with myocardial infarction,4 asymptomatic and symptomatic chronic heart failure,5 and acute decompensated heart failure in hospital.6 In comparison with the hydralazine/nitrate regimens, the angiotensin-converting enzyme inhibitors offered superior survival benefit for New York Heart Association class I to II ambulatory patients, but outcomes were equivalent for class III.7 Benefit was subsequently shown in hospitalized class IV patients for captopril over hydralazine, when both were titrated to the same hemodynamic goals achieved on intravenous nitroprusside and diuretics, usually requiring the addition of oral nitrates to both.8 Increasing survival for the heart failure center referral population could soon be attributed to both the increasing use of angiotensin-converting enzyme inhibitors (ACEIs) and the diminished use of type I antiarrhythmic therapy,9 which was being replaced by amiodarone.
During this time, experience was growing with β-blocker therapy, first used in Sweden …