Abstract 3159: Relation Between Left Ventricular Chamber Stiffness Constant and Turnover of Type I Collagen in Heart Failure
Objectives: Myocardial fibrosis is one of the determinants of left ventricular (LV) systolic and diastolic function in patients with heart failure (HF). The carboxy-terminal propeptide of procollagen type I (PICP) is a serum marker of type I collagen synthesis and the carboxy-terminal telopeptide of collagen type I (CITP) reflects degradation of type I collagen. We examined the effects of synthesis and degradation of collagen type I on LV chamber stiffness constant in HF.
Methods: We studied 50 HF patients who were admitted to our hospital with acute exacerbation (NYHA functional class of III or IV). 19 were female and mean age was 70 years. Serum P1CP and C1TP concentrations were assayed with ELISA in addition to measurement of plasma brain natriuretic peptide (BNP) concentration and echo Doppler studies of the mitral flow velocity pattern on admission and after treatment. The deceleration of early diastolic filling wave (Dct) was measured to provide for the calculation of LV chamber stiffness constant (KLV) using the following equation, KLV = (0.08/Dct )2. All patients were divided into 2 groups according to changes in KLV. The patients in whom KLV decreased after treatment were designated as KLV (−). LV chamber stiffness was supposed to have improved after treatment in this group. The patients in whom KLV increased after treatment were designated as KLV (+). LV chamber stiffness was supposed to be deteriorated after treatment in this group.
Results: After treatment, serum concentration of PICP significantly decreased in both groups (KLV (−): 67 ± 4 vs.101 ± 7 ug/L, p < 0.01; KLV (+): 58 ± 8 vs. 97 ± 12 ug/L, p < 0.05). Plasma BNP concentration significantly decreased in both groups (KLV (−): 512 ± 184 vs. 1183 ± 286 pg/ml, p < 0.01; KLV (+): 411 ± 147 vs. 784 ± 175 pg/ml, p < 0.01). Serum concentration of C1TP significantly increased after treatment in the KLV (−) group (9.6 ± 0.8 ug/L vs. 7.8 ± 0.6 ug/L, p < 0.01), while it was constant in the KLV (+) group (7.8 ± 0.5 ug/L vs. 7.0 ± 0.6 ug/L, p = 0.22).
Conclusions: Synthesis of type I collagen increased in HF with acute exacerbation and it uniformly settled down after treatment. Not only a decrease in the synthesis but also an increase in the degradation of type I collagen are required for improvement of LV chamber stiffness constant.