We investigated whether modification of collagen type I turnover is related to the long-term response to cardiac resynchronization therapy (CRT).
Methods and Results: Serum carboxy-terminal propeptide of procollagen type I or PICP (a marker of collagen type I synthesis), carboxy-terminal telopeptide of collagen type I or CITP (a marker of collagen type I degradation), matrix metalloproteinase (MMP)-1, -2, -9 and tissue inhibitor of MMP (TIMP)-1, were measured in 54 patients (35 responders) at baseline and after 1 year of CRT. At baseline, PICP and the ratio PICP: CITP were higher (p < 0.01) in responders than in nonresponders. At 1-year, both PICP (p < 0.005) and the ratio PICP:CITP (p < 0.05) decreased in responders, while increased in nonresponders (p < 0.005 and p < 0.05, respectively). MMP-1 (p < 0.05), MMP-9 (p < 0.005), and the ratio MMP-1:TIMP-1 (p < 0.01) increased, while TIMP-1 decreased (p < 0.005) in responders, but remained unchanged in nonresponders. The ratio PICP:CITP correlated inversely with ejection fraction (r = -0.501, p < 0.01) and directly with left ventricular end-diastolic diameter (r = 0.376, p < 0.05) in responders after CRT. Direct correlations were found between MMP-1, and -9 and ejection fraction (r = 0.315, p < 0.05, r = 0.516, p < 0.01) in responders after CRT.
Conclusions The ability of CRT to modify collagen type I turnover (i.e. decreasing synthesis and increasing degradation) is associated with its long-term response.
Impact of collagen type I turnover on the long-term response to cardiac resynchronization therapy
