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Sildenafil falls short for heart failure with preserved ejection fraction


 

AT ACC 13

SAN FRANCISCO – Sildenafil was no better than placebo for improving exercise capacity or clinical status in patients with heart failure and preserved ejection fraction, based on the results of a 24-week randomized trial published online in JAMA Mar. 11 and presented simultaneously at the annual meeting of the American College of Cardiology.

Sildenafil (Viagra), a phosphodiesterase-5 inhibitor, was shown beneficial in a previous single-center study of patients with heart failure and preserved ejection fraction (HFPEF). In the randomized trial, however, sildenafil had no significant effect "on maximal or submaximal exercise capacity, clinical status, quality of life, left ventricular remodeling, diastolic function parameters, or pulmonary artery systolic pressure," wrote lead investigator Dr. Margaret Redfield, professor of medicine at the Mayo Clinic in Rochester, Minn., and her colleagues (JAMA 2013 Mar. 11 [doi:10.1001/jama.2013.2024]).

Further, sildenafil appeared to be associated with poorer outcomes as "renal function worsened more and NT-proBNP [N-terminal fragment of the precursor to brain-type natriuretic peptide], endothelin-1, and uric acid levels increased more in patients treated with sildenafil," the researchers wrote. There was a trend, though not significant, for more patients in the sildenafil group to withdraw consent, die, or be too ill to perform the cardiopulmonary exercise test.

The researchers randomized 113 HFPEF patients to 20 mg of sildenafil three times daily for 12 weeks, followed by 60 mg three times daily for 12 weeks; 103 others were randomized to placebo in the multicenter trial.

At week 24, there were no statistically significant differences between the placebo and sildenafil groups in median changes in peak oxygen consumption (P = 0.90); median clinical status rank score—a composite of quality of life changes and times to death or hospitalization (P = 0.85); or changes in 6-minute walk distance (placebo 15.0 m, sildenafil 5.0 m; P = 0.92).

The median age in the trial was 69 years, 48% of the patients were women, and patients were under treatment for diabetes, atrial fibrillation, kidney disease, and other comorbidities. They were stable at baseline with ejection fractions equal to or greater than 50%, but had reduced exercise capacity, median peak oxygen consumption, and 6-minute walk distances. Their left atrial volumes and other measurements were consistent with chronically elevated left ventricular filling pressures.

A higher incidence of vascular adverse events was seen in the sildenafil group and included headache, flushing, and hypotension. Arterial elasticity and systemic vascular resistance tended to decrease more in sildenafil patients, but there were no significant changes in mean arterial pressure between the two groups.

Cardiac, respiratory, or other serious adverse events occurred in 16 placebo patients (16%) and 25 sildenafil patients (22%). Three people died in the sildenafil arm, but none in the placebo arm.

The "modest but statistically significant worsening of renal function" in sildenafil patients has not been reported before in studies of pulmonary arterial hypertension and erectile dysfunction, the investigators noted.

A previous single-center study found a benefit for sildenafil over placebo in HFPEF for left ventricular diastolic function, right ventricular systolic function, and left ventricular hypertrophy; the effect on exercise capacity was not tested (Circulation 2011;124:164-74).

"In that study, patients with HFPEF had fewer comorbidities and significantly higher blood pressure, left ventricular mass, and pulmonary artery systolic pressure ... [plus] catheterization-documented pulmonary arterial hypertension, profound right ventricular systolic dysfunction, and right ventricular failure. [The] profile [was] somewhat atypical for HFPEF cohorts," the investigators wrote.

"It may be that the primary therapeutic effects of PDE-5 inhibitors in heart failure involve the drugs’ ability to dilate the pulmonary vascular bed, enhance right ventricular contractility, and reduce ventricular interdependence, and that pulmonary arterial hypertension and right ventricular failure must be significant in order to observe clinical benefit in HFPEF," they wrote.

"Although left ventricular hypertrophy was common in participants in this study, it was far less severe than among participants in the [previous] study. ... Conceivably, activation of PDE-5 or of cyclic guanosine monophosphate–sensitive downstream pathways in the left ventricle or other organs may occur only in heart failure associated with advanced left ventricular remodeling," they wrote.

The study was funded by the National Institutes of Health. Pfizer donated the sildenafil and matched placebo. The investigators reported commercial relationships with many companies, including Amgen, Bristol-Myers Squibb, Eli Lilly, GlaxoSmithKline, Merck, Novartis, Pfizer, and Roche.

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