Coenzyme Q10 (CoQ10) in isolated diastolic heart failure in hypertrophic cardiomyopathy (HCM)

被引:36
作者
Adarsh, K. [1 ]
Kaur, H. [1 ]
Mohan, V. [1 ]
机构
[1] GND Hosp, Govt Med Coll, Amritsar, Punjab, India
关键词
Coenzyme Q(10); HCM; diastolic dysfunction; energy;
D O I
10.1002/biof.5520320117
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It is well known that by improving mitochondrial bioenergetics, Coenzyme Q(10) improves the systolic function in heart failure. The aim of this study was to see whether it benefits the diastolic dysfunction in hypertrophic cardiomyopathy (HCM) cases since diastolic relaxation also requires energy like the systole. 200 mg/day of CoQ(10) was added to the conventional treatment in 46 patients with HCM diagnosed clinically and by echocardiography and by excluding cases of long standing hypertension. A comparable group of 41 age/sex matched cases received only conventional therapy. There was a significant improvement in the parameters like NYHA class >= 1, in quality of life (QOL) on 6 minutes walk test, in diastolic dysfunction by >= 1 parameter and in MR >= 1 grade. Post treatment echocardiogram showed significant reduction in left ventricular outflow tract (LVOT) gradient >= 15 mm Hg in obstructive cases (12 out of 46) in the treatment group. The mean interventricular septal thickness (IVS) showed a 22.4% reduction (p < 0.005). The mean posterior wall thickness showed a 23.1% reduction (p < 0.005). No patient in the treatment Group had ventricular tachycardia (VT) whereas 4 cases in the control group had VT. In both groups I patient was lost due to sudden cardiac death (SCD).
引用
收藏
页码:145 / 149
页数:5
相关论文
共 10 条
[1]   Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy [J].
Crilley, JG ;
Boehm, EA ;
Blair, E ;
Rajagopalan, B ;
Blamire, AM ;
Styles, P ;
McKenna, WJ ;
Östman-Smith, I ;
Clarke, K ;
Watkins, H .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2003, 41 (10) :1776-1782
[2]   Idebenone and reduced cardiac hypertrophy in Friedreich's ataxia [J].
Hausse, AO ;
Aggoun, Y ;
Bonnet, D ;
Sidi, D ;
Munnich, A ;
Rötig, A ;
Rustin, P .
HEART, 2002, 87 (04) :346-349
[3]  
LANGSJOEN PH, 1993, CLIN INVESTIGATOR, V71, pS140
[4]  
Langsjoen PH, 1997, MOL ASPECTS MED, V18, pS145
[5]   The molecular genetic basis for hypertrophic cardiomyopathy [J].
Marian, AJ ;
Roberts, R .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2001, 33 (04) :655-670
[6]   Pathogenesis of diverse clinical and pathological phenotypes in hypertrophic cardiomyopathy [J].
Marian, AJ .
LANCET, 2000, 355 (9197) :58-60
[7]   Myocardial Energy Transport and Heart Failure [J].
Portman, Michael A. ;
Zhang, Jianyi .
CURRENT CARDIOLOGY REVIEWS, 2005, 1 (01) :17-27
[8]   Effect of atorvastatin on left ventricular, diastolic function and ability of coenzyme Q10 to reverse that dysfunction [J].
Silver, MA ;
Langsjoen, PH ;
Szabo, S ;
Patil, H ;
Zelinger, A .
AMERICAN JOURNAL OF CARDIOLOGY, 2004, 94 (10) :1306-1310
[9]   Diastolic dysfunction and altered energetics in the αMHC403/+ mouse model of familial hypertrophic cardiomyopathy [J].
Spindler, M ;
Saupe, KW ;
Christe, ME ;
Sweeney, HL ;
Seidman, CE ;
Seidman, JG ;
Ingwall, JS .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (08) :1775-1783
[10]   Effect of coenzyme Q10 administration on endothelial function and extracellular superoxide dismutase in patients with ischaemic heart disease:: a double-blind, randomized controlled study [J].
Tiano, Luca ;
Belardinelli, Romualdo ;
Carnevali, Paola ;
Principi, Federica ;
Seddaiu, Giovanna ;
Littarru, Gian Paolo .
EUROPEAN HEART JOURNAL, 2007, 28 (18) :2249-2255