Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy

Biomarkers in patients with myocardial fibrosis

“…In a study of 54 hypertrophic cardiomyopathy (HCM) patients, MMP-9 was associated with fibrosis and with cardiac events in women, increased MMP-2 levels were associated with lower fibrosis in women and MMP-3 levels were positively related to cardiac events. These findings suggest MMP-9 as a useful biomarker for fibrosis in female HCM patients [18]. Regulation of myocardial collagen turnover and deposition by MMP-9 is thought to be related to periostin, connective tissue growth factor (CTGF) and TGF-β/Smad signaling in cardiac ageing.…”

Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

“…Many researchers studied the role of MMP-9 in cardiac fibrosis in senescent hearts without any other cardiac injury, which is associated with the higher possibility of HFpEF in aging individuals. Munch et al found that serum MMP-9 is a useful biomarker for myocardial fibrosis and sudden cardiac death (SCD) in female patients with HCM, whereas MMP-3 is associated with a higher rate of cardiac events independent of factors such as fibrosis or sex (Munch et al, 2016). MMP-14, the membrane-type MMP, is involved in many different pathogeneses of LV remodeling.…”

Biomarkers of Myocardial Fibrosis: Revealing the Natural History of Fibrogenesis in Fabry Disease Cardiomyopathy

“…As an index of degree of coupling between the synthesis and degradation of collagen type I, the PICP:ICTP ratio, after adjustment to bone turnover, was significantly higher in the subgroup of patients with established LV hypertrophy and inversely correlated with MMP1 activity. Thus, as reported in HCM, we can hypothesize that in incipient FD cardiomyopathy, increased collagen synthesis is balanced by degradation (limiting fibrogenesis), but when collagen type I synthesis exceeds the degradation, there is deposition of collagen in the myocardium and LV hypertrophy; the suppression of MMPs may be another mechanism of myocardial collagen type I buildup.…”

“…The suppression of MMPs as a pathophysiological mechanism for cardiac fibrosis has been described previously in HCM . The multiple pathways involved in MMP suppression are not well understood, but recent studies imply aldosterone‐induced expression of TIMP1 (tissue inhibitor of metallopeptidase 1), acting mainly through MMP1 inhibition increasing net cardiac collagen content .…”