NEW YORK (Reuters Health) – In patients with chronic stable heart failure (HF) due to nonischemic dilated cardiomyopathy, a year’s treatment with n-3 polyunsaturated fatty acids (n-3 PUFAs) increases left ventricular ejection fraction and functional capacity, new research shows.

Although these are surrogate markers, the authors suggest that these effects “may favorably affect cardiac remodeling and the decline of myocardial function in patients with HF and may (reduce) cardiovascular hospitalizations.”

In the expedited study released online January 5th by the Journal of the American College of Cardiology, n-3 PUFA treatment led to a 10% increase in left ventricular ejection fraction, a 6% rise in peak oxygen uptake, and an increase in exercise duration of 7.5%. By contrast, placebo treatment was associated with declines in all three measures.

In addition, HF hospitalizations fell from 30% with placebo to 6% with n-3 PUFAs, Dr. Mihai Gheorghiade at the Center for Cardiovascular Innovation at Northwestern University Feinberg School of Medicine, Chicago, and colleagues report.

The 133 trial subjects (mean age 63), had an ejection fraction no higher than 45%, and were on maximal tolerated evidence-based therapy. All were in New York Heart Association functional class I or II.

In the double-blinded study, researchers randomly assigned them to n-3 PUFAs (n = 67) supplied as capsules containing about 850 mg of EPA and DHA ethyl esters, or identical placebo (n = 66). Treatment dose was 5 capsules daily for the first month followed by two capsules daily for the remaining 11 months.

Echocardiography showed a significant increase in left ventricular ejection fraction from baseline in the n-3 PUFAs group (from 36 to 39%), and a significant decrease in the placebo group (from 37 to 35%, p < 0.001 between groups).

During exercise testing, duration rose from 10.4 to 11.2 minutes in the active treatment group while falling from 114 to 108 minutes in the placebo group (p = 0.0013). Peak oxygen uptake followed a similar pattern, going from 19.5 to 20..7 mL/kg/min after n-3 PUFA treatment and from 18.3 to 17.4 ml/kg/min after placebo treatment.

According to the report, active treatment reduced inflammation, as indicated by significant decreases in circulating levels of inflammatory cytokines.

During 12 months follow-up, 14.9% of patients given n-3 PUFAs required cardiovascular hospitalization, vs 39.4% of placebo patients (p = 0.0029); corresponding percentages of HF hospitalizations were 5.9% and 30.3% (p = 0.0002).

Dr. Gheorghiade and associates note that their study was a relatively small, single-center trial, and that their results cannot be generalized to patients with HF due to other etiologies, at more advanced stages, or who are not received evidence-based therapies.

Dr. Gheorghiade reports consulting for a number of pharmaceutical and device manufacturers.

In an editorial, Dr. W. H. Wilson Tang, from the Cleveland Clinic in Ohio, can’t decide whether physicians should “prescribe an otherwise safe and well-tolerated (but not inexpensive) drug to a broad heart failure population (without) large-scale pivotal studies…, or whether future clinical effectiveness studies are warranted to justify such indications?”

J Am Coll Cardiol 2011.