Long-term efficacy and safety of coenzyme Q 10 therapy for idiopathic dilated cardiomyopathy

Abstract

Coenzyme Q 10 (CoQ 10) occurs in the mitochondria of human cells. It is 2,3-dimethoxy-5-methyl-6-decaprenyl-l,4-benzoquinone and functions as a cofactor in several enzyme systems related to energy conversion. As such, it is essential for human life to exist. Since mitochondria are very abundant in myocardial cells and because of their huge energy needs, a deficiency of CoQ 10 could have a particularly severe effect on myocardial function. In 1981 we chose cardiomyopathy for clinical study because it has been a disease of unknown cause, which has been apparently limited to the myocardium and has been without effective treatment. A short-term doubleblind cross-over study of 19 patients with cardiomyopathy (New York Heart Association classes III and IV) was completed in 1982. Control subjects' CoQ 10 levels that were in the deficiency range were increased into the normal range by oral replacement therapy. This paralleled significant improvement in myocardial function and clinical status. There was no intolerance of the treatment. 1 A long-term open-label study was begun in November 1982 with the goal of determining if tolerance of CoQ 10 and clinical improvement were maintained over long periods of time. From our observations with untreated control subjects in the short-term study and those of Mortensen et al, 2 we thought it improper to use untreated control subjects in a long-term study. Myocardial function entails active energy input in both the contracting and relaxing phases, which may not be equally involved in clinical heart disease. Since precise measurement of each phase of myocardial function remains developmental, long-term survival figures could be finite and meaningful.