Evaluation of the relationship between dyssynchrony and myocardial fibrosis markers in patients with biventricular pace maker

ABSTRACT Evaluation of The Relationship Between Dyssynchrony and Myocardial Fibrosis Markers in Patients with Biventricular Pace Maker Aim: Dyssynchrony seen in some patients with heart failure causes severe myocardial loading and remodeling in left ventricle. Myocardial fibrosis caused by these effects is thought to be responsible for the progression of heart failure. The goal of cardiac resynchronization therapy (CRT) is the correction of dyssynchrony. Consequently, the correction of myocardial loading and remodeling is thought to be able to prevent development of the myocardial fibrosis. The aim of this study is to evaluate myocardial fibrosis markers in patients with heart failure CRT applied and to assess the relationship between these markers and dyssynchrony. Method: Fifty one patients (27 male, 24 female, mean age 63.3±10.5, ejection fraction (EF) ≤%45, QRS duration ≥120 msec, despite the optimal medical theraphy NYHA functional class II-IV) were included into the study. Electrocardiography (ECG), 6 minute walk test, and echocardiography by using M-mode, B-mode and Coloured Doppler techniques were applied before and 6 months after CRT to all patients. Furthermore, Type I Collagen C-Terminal Propeptide (PICP), Type I Collagen C-Terminal Telopeptide (ICTT) levels and PICP/ICTT ratio were studied as myocardial fibrosis markers in blood samples. The relationship between myocardial fibrosis markers and QRS duration on ECG and dyssynchrony parameters in echocardiography is evaluated. Results: It is observed that QRS duration which is one of dyssynchrony parameters was shortened (p=0.0001) while 6 minute walk distance was increased (p=0.0001) 6 months after CRT. PICP level which is collagen turnover's synthesis product measured before CRT as 560.2±300.4 µg/L while it is measured as 476.9±285.8 µg/L (p=0.004) 6 months after CRT. ICTT level which is collagen turnover's degradation product measured before CRT as 15.0±11.5 µg/L while it is measured as 16.6±9.0 µg/L (p=0.173) 6 months after CRT. PICP/ICTT ratio before and 6 months after CRT was 9.7±10 and 37.1±32.8 (p=0.0001) respectively. In addition, significant improvement was observed in the echocardiographic dyssynchrony parameters (septum-posterior wall motion delay (SPWMD), interventricular mechanical delay (IVMD) and aortic pre ejection time) after CRT. At the same time it is determined that mitral regurgitation (MR), left ventricular end diastolic diameter (LVEDD) and left ventricular end sistolic diameter (LVESD) were decreased while ejection fraction (EF) was significantly increased. It is determined a negativ relationship between EF and PICP level and PICP/ICTT ratio (p=0.008, r = -0.37). A positive correlation was found between PICP level and SPWMD which is one of the intraventricular dyssynchrony parameters (p =0.039, r = 0.29). However, no significant association was determined between ICTT level and PICP/ICTT ratio and other dyssynchrony parameters. Conclusion: Our results show that CRT reduces the left ventricular dyssynchrony and consequently leads to positive changes in myocardial fibrosis markers. Reducing the mechanical stresses on left ventricle and returning of consequent remodeling may be one of the important mechanisms in the prevention of cardiac fibrosis. Key words: Cardiac resynchronization thraphy, dyssynchrony, myocardial fibrosis