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Coenzyme Q10 in dilated cardiomyopathy
U Manzoli1, E Rossi, G P Littarru
1Institute of Cardiology, Catholic University, Rome, Italy.
Insights
Coenzyme Q10 (CoQ10) supplementation improved symptoms and heart function in dilated cardiomyopathy patients. This suggests CoQ10 deficiency is reversible and supplementation aids heart failure treatment.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Dilated cardiomyopathy (DCM) is associated with reduced myocardial coenzyme Q10 (CoQ10) levels.
- CoQ10 deficiency may contribute to the pathophysiology of DCM.
Purpose of the Study:
- To evaluate the therapeutic efficacy of oral CoQ10 in patients with DCM.
- To assess the impact of CoQ10 on clinical symptoms, cardiac function, and CoQ10 levels in DCM patients.
Main Methods:
- Thirty DCM patients received oral CoQ10 (100 mg/day) for two months.
- Clinical (NYHA class) and echocardiographic (ejection fraction, ventricular volumes) assessments were performed before and after treatment.
- Plasma and myocardial CoQ10 levels were measured.
Main Results:
- 47% of patients showed symptom regression and improved NYHA class.
- Ejection fraction significantly increased (0.31 to 0.37, p<0.001).
- Plasma CoQ10 levels increased significantly (p<0.0001), with 95% of patients showing improvement.
Conclusions:
- CoQ10 deficiency in DCM appears reversible with oral supplementation.
- Therapeutic response correlates with baseline plasma and myocardial CoQ10 levels.
- CoQ10 may be a valuable adjunct therapy for chronic heart failure in DCM.
Abstract:
The authors have tried to study the therapeutic efficacy of coenzyme Q10 (CoQ10) in patients with dilated cardiomyopathy (DCM). In fact, CoQ10 has been shown to be deficient in myocardial tissue biopsies taken from DCM hearts, compared to normal hearts. Thirty patients with histological diagnosis of DCM were orally treated with CoQ10 (100 mg/die) for 2 months. Before and after treatment a clinical examination with determination of NYHA class and an echocardiographic examination with determination of ejection fraction (EF) and of telediastolic (TDV) and telesystolic (TSV) volumes were performed, and blood was drawn for plasma CoQ10 determination. In seven patients the pretreatment endomyocardial level of CoQ10 was also assayed. Seven patients left the study because of poor therapeutic compliance. In 47% of patients the clinical symptomatology regressed, with improvement of NYHA class. The EF improved from 0.31 +/- 0.09 to 0.37 +/- 0.11 (p less than 0.001). The TDV passed from 262.2 +/- 85 ml to 203.3 +/- 83 ml (p less than 0.05), and the TSV from 166.13 +/- 75 ml to 126.9 +/- 56 ml (ns). The CoQ10 plasmatic levels improved in 95% of the patients: from 0.74 +/- 0.37 micrograms/ml to 2.27 +/- 0.99 micrograms/ml (p +/- 0.0001). The CoQ10 myocardial levels did not show univocal values, but the patients with lower myocardial levels seemed to have a better therapeutic response. These data suggest that the CoQ10 deficiency in DCM may be reversible and that the therapeutic effects depend on the basal plasmatic and myocardial levels. Therapy with coenzyme Q10 may be considered to be an efficacious aid in the traditional treatment of chronic cardiac failure.