Abstract Title:

Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure.

Abstract Source:

Wien Klin Wochenschr. 2005 Aug;117(15-16):558-60. PMID: 3836876

Abstract Author(s):

S A Mortensen, S Vadhanavikit, U Baandrup, K Folkers


Coenzyme Q10 (CoQ10) treatment, orally administered as 100 mg daily dose, was initiated in a series of patients with advanced heart failure in an open, controlled design. They were all showing an insufficient response to classical therapy with diuretics and digitalis. Twelve patients with various causes of heart failure, classified clinically by echocardiography (ECHO), (12/12), and heart catheterization with endomyocardial biopsy, (10/12), were followed prospectively for a mean period of seven months. Serial assessments: Clinical examination (with questionnaire), ECG, chest X-ray, ECHO, systolic time intervals (STI) and blood levels of CoQ10 were performed. With a mean latency period of 30 days, eight out of 12 patients (67%) showed definite clinical improvement. Subjectively, the patients felt less tired, their general activity tolerance increased and dyspnoea at rest disappeared. There were obvious signs of decreased right-sided stasis (hepatic congestion). The heart rate fell significantly, and the heart volume (chest X-ray) decreased in the eight responders (although n.s.). A significant reduction in the left atrial size (ECHO) was registered, suggesting a reduced preload of the left ventricle, Furthermore, a significant decline in the PEP/LVET ratio (STI) was indicative of an improved myocardial performance. Preliminary CoQ10 withdrawal results showed severe clinical relapse with subsequent improvement on CoQ10 reinstatement, supporting the interpretation that treatment of these patients corrected a myocardial deficiency of CoQ10 and increased contractility. Hence CoQ10 appears to be an effective therapeutic agent in advanced cases of heart failure. This is an attractive circumvention of the traditional principles of therapy: supporting the myocardium directly by ameliorating a supposed underlying mitochondrial dysfunction (exhausted bioenergetics).

Study Type : Human Study

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