Meel Ruchika, Nethononda Richard, Libhaber Elena, Dix-Peek Therese, Peters Ferande, Essop Mohammed
Division of Cardiology, Chris Hani Baragwanath Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa. Email:
Division of Cardiology, Chris Hani Baragwanath Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa.
Cardiovasc J Afr. 2018;29(3):150-154. doi: 10.5830/CVJA-2018-002. Epub 2018 Feb 6.
In 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.
Twenty-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.
Four patients had fibrosis on LGE-CMR. PICP 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).
Myocardial 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.
在慢性风湿性二尖瓣反流（CRMR）中，心肌是否参与风湿过程一直存在争议。因此，我们试图利用延迟钆增强心脏磁共振成像（LGE-CMR）和胶原代谢生物标志物来研究CRMR中纤维化的存在情况。
22例CRMR患者接受了CMR和超声心动图检查。测量了血清基质金属蛋白酶-1（MMP-1）、MMP-1组织抑制剂（TIMP-1）、MMP-1与TIMP-1的比值、前胶原III N端前肽（PIIINP）和I型前胶原C端肽（PICP）的浓度。
4例患者在LGE-CMR上出现纤维化。PICP和PIIINP浓度与对照组相似，然而MMP-1浓度与对照组相比有所升高（log MMP-1 3.5±0.7对2.7±0.9，p=0.02）。由于CRMR患者的MMP-1与TIMP-1比值高于对照组，MMP-1活性增加（-1.2±0.6对-2.1±0.89，p=0.002）。
CRMR患者中心肌纤维化罕见。CRMR可能是一种以胶原降解为主而非合成增加和心肌纤维化的疾病。
