Crestor Omega 3 and Heart Failure


1.) A simple, safe, one-a-day capsule of omega-3 polyunsaturated fatty acids (PUFA) can reduce mortality and admission to hospital for cardiovascular reasons in patients with heart failure.

These are the conclusions of an Italian study published online and soon to be in the Lancet. This study looked at patients with chronic heart failure from 357 cardiology sites in Italy. Patients received either omega-3  in a capsule once daily (3494 patients) or a placebo (3481).

955 patients in the Omega 3 group (27%) died, compared with 1014 (29%) in the placebo group, meaning a relative risk reduction of 9% in the Omega 3 group. A higher proportion of patients in the placebo group (2053 / 59%) died or were admitted to hospital for cardiovascular reasons than in the Omega 3 group (1981 / 57%) a relative reduction of 8% in the Omega group.

In absolute terms, 56 patients needed to be treated with Omega for just under four years to avoid one death The authors concluded: "Our study shows that the long-term administration of 1g per day omega-3 was effective in reducing both all-cause mortality and admissions to hospital for cardiovascular reasons."

As I have mentioned previously, the potential of omega 3 in suppressing arterial inflammation is now well known. Lee and his group at the Thrombosis and Vascular Biology Unit of Birmingham's City Hospital in the U.K., strongly recommend omega-3 in the long-term treatment plan of myocardial infarction patients. There is no longer any doubt as to the vital role of this polyunsaturated fatty acid in reducing cardiovascular disease risk. Not only has it been firmly documented to stabilize the myocardium electrically, resulting in reduced ventricular arrhythmias and sudden death but also it has been found to have potent anti-inflammatory effects quite comparable to those of the statin drugs. This is one of the first studies to document the role of Omega 3 in heart failure.

2.) Statin treatment with Crestor does not affect clinical outcomes in patients with chronic heart failure.

The same authors compared the effect of the statin drug, Crestor, on the same patient population looking at possible benefit for heart failure.  Patients received either Crestor 10 mg daily (2285 patients) or placebo (2289), and were followed up for a median of nearly four years. The researchers found that 657 patients (29%) died from any cause in the rosuvastatin group, compared with 644 (28%) in the placebo group. The authors conclude: "Rosuvastatin 10 mg daily did not affect clinical outcomes in patients with chronic heart failure of any cause."

These results will no doubt be challenged by physicians convinced of statin benefit generally in cardiovascular disease. Yet this outcome is a predictable result of the inevitable statin inhibition of CoQ10, integral to ATP energy production. When our cardiac mitochondria are deficient in CoQ10, heart failure is the consequence. Dr. Perter Langsjoen has reported this on multiple occasions and has also shown the benefit of supplemental CoQ10 in statin users.

I submit that the effects of statin use on this patient population was to produce an additional energy deficit in hearts already burdened with failure and am surprised only that the Crestor group did not show greater mortality.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor


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