Vitamin C fights cell death in heart failure patients

Related tags Blood vessel

Vitamin C can aid congestive heart failure patients by suppressing
the signal for cell death within blood vessel linings, French and
German scientists reveal this week.

Vitamin C can aid congestive heart failure patients by suppressing the signal for cell death within blood vessel linings, French and German scientists reveal this week. People with congestive heart failure (CHF) suffer from endothelial dysfunction, disturbances in the blood vessel function that restrict blood supply to the body. This is associated with the heart weakening and results in exhaustion and shortness of breath upon exertion. Scientists believe a loss of function of the endothelial cells, which make up the endothelium (inner lining of blood vessels), causes the malfunction. "Previous studies of our group suggested that these endothelial cells are lost by programmed cell death, also called apoptosis,"​ says study co-author Stefanie Dimmeler, Ph.D., professor of the experimental medicine division of molecular cardiology, University of Frankfurt, Frankfurt, Germany. "Increasing evidence suggests that oxidative stress regulates apoptosis of endothethial cells. Therefore, we questioned whether antioxidant treatment with vitamin C could reduce endothelial cell death in CHF patients."​ Oxidative stress is the tissue damaging process that can be spurred by factors such as smoking or fatty foods. Researchers conducted a randomised, placebo-controlled, double-blinded trial with 34 individuals to investigate the effects of vitamin C on apoptosis. They drew baseline blood samples, followed by a 10-minute infusion of 2.5 grams of vitamin C or sodium chloride solution (placebo), then took another blood sample 15 minutes later. For the next three days, patients received oral vitamin C supplements or placebo tablets twice daily. A third blood sample was taken the morning of the fifth day and blood levels of these apoptotic or death-causing microparticles were measured. Results showed that Vitamin C administration to CHF patients markedly reduced blood levels of circulating apoptotic microparticles to 32 per cent of baseline levels, while the placebo had no effect. "This study, for the first time, proves the relevance of these findings by demonstrating that antioxidant treatment inhibits apoptosis of endothelial cells in patients with CHF,"​ Dimmeler says. "The findings might contribute to our understanding of the mechanisms of heart failure progression and could add antioxidant treatment as a novel strategy to delay progression of heart failure."​ It is too early to make any conclusions about the inclusion of vitamin C in treating CHF patients because of the small number of patients studied, Dimmeler says. According to the American Heart Association, about 4.7 million Americans have CHF and are alive today. About 550,000 new cases of CHF occur each year and the incidence of CHF approaches 10 per 1,000 population after age 65. The five-year mortality rate for heart failure is about 50 per cent. Full findings are published in the October 30 issue of Circulation: Journal of the American Heart Association.

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