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Background: The hallmark of Chagas disease (CD) is multifocal myocarditis and extensive fibrosis. We investigated the potential effect of colchicine on myocardial remodeling in experimental CD., Methods and Results: One hundred Syrian hamsters were randomly divided into noninfected untreated control (CG), noninfected control treated with colchicine (COLG 0.4 mg kg(-1) d(-1) by gavage), infected (IG), and infected treated with colchicine (ICOLG, 0.4 mg kg(-1) d(-1)) groups. The interstitial collagen volume fraction (ICVF) was evaluated by videomorphometry with picrosirius red staining. The gelatinolytic activities of matrix metalloproteinase (MMP) 2 were examined with the use of zymography. Myocarditis was described according to the Dallas criteria. Statistical comparisons were performed with parametric analysis of variance and Tukey test. ICVF (%) accumulation was attenuated in infected colchicine-treated animals in the left (CG 0.81 ± 0.13, COLG 0.85 ± 0.13, IG: 1.35 ± 0.31,* ICOLG 1.06 ± 0.19; *P < .05 compared with ICOLG) and right ventricles (CG 1.4 ± 0.36, COLG 1.26 ± 0.14, IG 1.97 ± 0.058,* ICOLG: 1.52 ± 0.23; *P < .05 compared with ICOLG). A significant increase in MMP-2 enzymatic activity (UA) was observed in ICOLG (17,432.8*) compared with GC (3731.6), COLG (2,792.6), and IG (4,286.3; *P < .001). In IG, 66% of animals had myocarditis compared with only 49% in ICOLG., Conclusions: Colchicine had a protective effect on myocardium, indicated by decreased interstitial myocardial fibrosis, increased intensity of MMP-2, and attenuated myocardial inflammation., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Systemic sclerosis (SSc) is a disease characterized by the fibrosis of the skin and internal organs. The nature and functional significance of myocardial damage is controversial. Systematic endomyocardial biopsy in this disease has not yet been performed., Methods: The hypothesis that increased myocardial fibrous tissue deposition occurs in patients with systemic sclerosis with no signs or symptoms of heart failure and normal left systolic ventricle function was tested in 16 SSc patients and 10 controls. Endomyocardial biopsy specimens were obtained from the right ventricular septum in SSc patients. Myocardial specimens were obtained from the same area in controls. Masson's trichrome staining was used for collagen fiber identification. Interstitial (ICVF) and perivascular collagen volume fraction (PCVF) was quantified by videomorphometry. There was a significant increase in the ICVF in patients with SSc compared with the controls, in spite of normal systolic left ventricular function. However, it was not observed in the PCVF., Conclusions: It is possible to identify cardiac remodeling, characterized by myocardial fibrosis deposits, particularly within the interstitium in SSc patients before the any signs or symptoms of heart failure appear.

Background: Endothelins are associated with cardiac remodeling. These peptides are the most powerful vasoconstrictor described-whether this remodeling is a direct effect of this hormone or indirect response to a relative ischemia promoted by vasoconstrictor effect. We evaluated the role of endothelin upon myocardial fibrosis despite of its hemodynamic effects and the benefits of its antagonism., Methods and Results: We used 40 Wistar rats: control, sham operated, rats had undergone myocardial infarction (MI) and MI rats treated with SB209670 which is an ET(A)/ET(B) endothelin antagonist. We evaluated tail systolic blood pressure (BP) and left ventricular end diastolic pressure (LVED) before surgery, just after, and at the end of the study. Remodeling was studied based on interstitial collagen and MI size by an image system analysis. BP decreased in MI groups after surgery, but did not differ between treated and untreated animals. LVED had increased levels in MI groups after surgery and did not differ between them. However, ICVF had an increase in MI group but significantly less in MI+SB209670. MI size was similar in both groups., Conclusions: Endothelin may have a pivotal role in the myocardial fibrosis by direct stimulation of collagen accumulation despite of its hemodynamic effects.