Assessment of myocardial fibrosis by late gadolinium enhancement imaging and biomarkers of collagen metabolism in chronic rheumatic mitral regurgitation.

Abstract

SummaryBackgroundIn chronic rheumatic mitral regurgitation (CRMR), involvement of the myocardium in the rheumatic process has been controversial. Therefore, we sought to study the presence of fibrosis using late gadolinium enhancement cardiac magnetic resonance imaging (LGE–CMR) and biomarkers of collagen turnover in CRMR. MethodsTwenty–two patients with CRMR underwent CMR and echocardiography. Serum concentrations of matrix metalloproteinase– 1 (MMP–1), tissue inhibitor of MMP–1 (TIMP– 1), MMP–1–to–TIMP–1 ratio, procollagen III N–terminal pro–peptide (PIIINP) and procollagen type IC peptide (PIP) were measured. ResultsFour patients had fibrosis on LGE–CMR. PIP and PIIINP concentrations were similar to those of the controls, however MMP–1 concentration was increased compared to that of the controls (log MMP–1 3.5 ± 0.7 vs 2.7 ± 0.9, p = 0.02). There was increased MMP–1 activity as the MMP–1–to– TIMP–1 ratio was higher in CRMR patients compared to the controls (–1.2 ± 0.6 vs –2.1 ± 0.89, p = 0.002). ConclusionMyocardial fibrosis was rare in CRMR patients. CRMR is likely a disease characterised by the predominance of collagen degradation rather than increased synthesis and myocardial fibrosis.