Statin drugs, known primarily for their ability to lower cholesterol, also may reduce the overactive sympathetic nervous system response that contributes to the worsening of heart failure and increases the risk of sudden cardiac death, two University of Missouri-Columbia researchers have found. Heart failure is the leading cause of morbidity and mortality in the United States.
James Fisher, a postdoctoral fellow at MU, and Paul Fadel, an assistant professor of medical pharmacology and physiology in the MU School of Medicine, reported their findings of the effect of the popular statin drugs at Experimental Biology 2007 in Washington, D.C., part of the scientific program of The American Physiological Society.
Heart failure, sometimes called congestive heart failure, is a chronic condition in which the heart can no longer pump enough blood to the rest of the body, causing damage and negatively impacting the quality and duration of life.
In several large clinical trials, cholesterol-lowering statin medications improved survival and other health outcomes in patients with heart failure, an effect that appeared not to be solely due to lowering these patients' cholesterol levels. In the search for a possible mechanism to explain this observation, scientists have turned to measures of sympathetic nervous system activity.
The sympathetic nervous system controls blood pressure and heart rate. When a heart begins to fail, the sympathetic nervous system works harder to compensate by helping to maintain heart function, blood pressure and the delivery of needed blood to vital organs and peripheral muscles. While this increased activity is beneficial in the early stages of heart failure, prolonged full-tilt sympathetic nervous system overactivity soon becomes harmful, causing damage to the heart and kidneys.
The largest difference in sympathetic nervous system activity between individuals with and without heart failure can be seen when they are resting, when the body is placing no unusual demands on the heart. An earlier University of Nebraska study found that animals with heart failure characteristics experience a return to normal sympathetic nervous system activity after being treated with statin drugs.
Fisher and Fadel continued the study with humans, treating those with longstanding mild-to-moderate heart failure. The researchers measured sympathetic nervous system activity by placing an electrode in a nerve of the lower leg.
After one month of treatment, all patients had reduced sympathetic nerve activity while resting. Although none of the patients had experienced cholesterol or blood pressure levels elevated enough to require treatment, significant decreases in cholesterol and diastolic blood pressure also were absorbed and considered beneficial for the patients' overall health.
Fadel said that the preliminary results are promising and exciting. The findings indicate that short-term treatment with a low level of statin medication significantly lowered resting sympathetic nerve activity, thus lowering a factor known to be associated with increased mortality in heart failure patients, Fadel said.
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