Microsoft word - j11-025.doc

COENZYME Q10 IN ISOLATED DIASTOLIC HEART Govt Medical College / GND Hospital, Amritsar, India *Correspondence Contact: [email protected] Introduction: - It is well known that by improving mitochondrial bioenergetics and oxidative phosphorylation, Coenzyme Q-10 improves systolic function in heart failure. The patients of HCM on the other hand have heart failure due to Diastolic LV dysfunction (due to and increased stiffness), the systolic function being normal. Diastolic relaxation like systolic contraction requires energy. Co Q-10 is a key substance which affects the common bioenergetics process in contraction and relaxation to keep these functions normal. The filling phase of the cardiac cycle involves the ATP-dependent clearance of calcium which in turn is required for the breaking of the actin-myosin binding. CoQ10 stabilizes Ca channels and decreases Ca overload. It prevents QT prolongation by improving sodium potassium ATPase function, thereby optimizing the membrane repolarization. Due to this effect, addition of Coenzyme Q-10 to the conventional therapy in HCM cases may reduce dangerous arrhythmias like VT & might decrease incidence of SCD. It also has anti- oxidant properties. Isolated Diastolic LV dysfunction is reported to be associated with low CoQ10 blood levels in some studies. Material and Methods:- With this background , 46 cases of HCM (Group I) aged 24.4-77.5 years (mean of 48.5yrs) with M/F ratio 32/14 (69.5% / 30.5%) and ≥ NYHA II class of HF with symptoms of palpitation/dyspnea /chest pain and /or presyncope /syncope were taken up for the study. The diagnosis was established by detailed M-Mode /Color Doppler echocardiography (with evidence of LV Hypertrophy - Asymmetrical Septal Hypertrophy or Concentric LVH type; Absence of Regional wall motion abnormality; EF ≥55% and presence of ≥ 2 markers of Diastolic dysfunction viz abnormal E/A ratio; deceleration time and isovolumetric relaxation time and reverse pulmonary venous flow exceeding transmitral A wave in duration or peak reverse flow velocity ≥ 35cms/sec.). Out of 46 cases, 34 (73.9%) were of non-obstructive type and 12 (26.1%) were of obstructive type with ≥ 20mm Hg LVOT gradient. All patients had ≥ Grade I Mitral Regurgitation . 41 age and sex matched cases of HCM (30/41-73.1% non obstructive and 11/41-26.9% of obstructive type) were taken as controls (Group II). Patients in Gp I were given CoQ10 -100mg BD in addition to betablockers /Calcium channel blockers and ACE inhibitors etc . 14 cases with palpitation / presyncope / syncope with ECG/ Holter evidence of VT were on Amiodarone therapy. Control Gp II cases were given conventional treatment only without Coenzyme Q10. 2 patients in Gp I and 1 pt in Gp II had associated Friedreichs Ataxia. The follow up period ranged from 9.4 months -27.5 months (mean of 14.5 months). End points of the study were improvement in NYHA class ≥ I ; improvement in QOL on detailed questionnaire and on 6 minutes walk test ; improvement in Diastolic dysfunction by ≥ I parameter ; significant reduction in LVOT gradient ≥ 15mm Hg in obstructive cases and mortality pattern etc. Results and Discussion- Clinical parameters on detailed questionnaire & on 6 minutes walk test Improvement in Diastolic dysfunction by ≥ 1 parameter Improvement in MR ≥ 1 LVOT gradient ≥ 15 mm Hg in obstructive cases No of Deaths In addition, mean IVS thickness decreased from 1.54 ± 0.22 cms to 1.19 ± 0.18cms, a 22.4 % reduction (p < 0.005). Mean LV posterior wall thickness decreased from 1.34 ± 0.16 cms to 1.06± 0.18 cms, a 23.1% reduction (p< 0.005). Out of 14 cases with presyncope/ syncope with ECG /Holter documentation of VT & also on Amiodarone therapy in addition, 1 patient had SCD most likely arrhythmogenic in nature. 1 similar death occurred in the control Gp. No other patient had any VT episode in the treatment Gp I whereas 4 cases in the control Gp II had VT during the study period . Conclusion: - Coenzyme Q-10 produced significant clinical and haemodynamic improvement in Isolated Diastolic Heart failure cases of HCM and is an important adjuvant therapy in these cases. References:- 1. Langsjoen PH, Langsjoen A, Willis R, Folkers K. : Mol Aspects Med. 2. A.O. Hausse et al ; Heart 2002; 87; 346-349.

Source: http://www.senpu.jp/coq10/pdf/j11-025.pdf