The Role of Erythropoietin Upon Myocardial Fibrosis

Abstract

IntroductionRegarding the process of myocardial remodeling occurs myocyte hypertrophy and inappropriate collagen deposition in the interstitium developing an overall process of structural and geometric remodeling of the heart. Erythropoietin (EPO) has been studied because exerts cardioprotective effects including inflammatory and oxidative stress modulation.HypothesisThe aim of this study was to assess the role of EPO upon structural, geometric and functional remodeling.Materials and Methods75 Wistar rats were divided into 5 groups: Control, Control+EPO, Sham, Infarcted, Infarcted+EPO. Interstitial collagen volume fraction in the left (LV-ICVF) and right ventricle (RV-ICVF) was quantified by videomorphometry using a Quantimet 520 Image Analyses System (LEICA Microsystems). The analyzed echocardiographic parameters were the left ventricle ejection fraction (LVEF) and diastolic diameter (LVDD, cm).ResultsLV-ICVF (%) was greater in the infarcted groups compared to controls (p<0.001), and attenuated by EPO (p<0.001, MI vs MI+EPO) (CT= 0.76±0.21; CT+EPO= 0.63±0.15; MI+EPO= 1.43±0.92; MI= 3.47±2.5 and Sham= 0.37±0.04). The RV-ICVF (%) was also greater in the infarcted groups compared to controls (CT=0.60±0.2; CT+EPO= 0.83±0.3; MI+EPO= 1.01±0.55; IAM= 1.60±1.15 and Sham= 0.53±0.11) (p<0.001) but without statistical difference between MI vs MI+EPO. The infarcted groups had a worsening ejection fraction compared to controls (CT= 81%±6.5; CT+EPO=77%±5; MI+EPO= 40%±12 and MI= 38%±11.5) (p<0,001) but without EPO protection. The infarcted groups also showed increased LV dilation (p<0.001) (CT= 0.73±0.06; CT+EPO= 0.74±0.05; MI+EPO= 0.81±0.09; MI= 0.87±0.11) without EPO attenuation.ConclusionsEPO significantly attenuated the accumulation of interstitial collagen, but it did not reflected in the protection of the heart dilation or dysfunction in this model.Grant Fapesp: 2010/06834-2 IntroductionRegarding the process of myocardial remodeling occurs myocyte hypertrophy and inappropriate collagen deposition in the interstitium developing an overall process of structural and geometric remodeling of the heart. Erythropoietin (EPO) has been studied because exerts cardioprotective effects including inflammatory and oxidative stress modulation. Regarding the process of myocardial remodeling occurs myocyte hypertrophy and inappropriate collagen deposition in the interstitium developing an overall process of structural and geometric remodeling of the heart. Erythropoietin (EPO) has been studied because exerts cardioprotective effects including inflammatory and oxidative stress modulation. HypothesisThe aim of this study was to assess the role of EPO upon structural, geometric and functional remodeling. The aim of this study was to assess the role of EPO upon structural, geometric and functional remodeling. Materials and Methods75 Wistar rats were divided into 5 groups: Control, Control+EPO, Sham, Infarcted, Infarcted+EPO. Interstitial collagen volume fraction in the left (LV-ICVF) and right ventricle (RV-ICVF) was quantified by videomorphometry using a Quantimet 520 Image Analyses System (LEICA Microsystems). The analyzed echocardiographic parameters were the left ventricle ejection fraction (LVEF) and diastolic diameter (LVDD, cm). 75 Wistar rats were divided into 5 groups: Control, Control+EPO, Sham, Infarcted, Infarcted+EPO. Interstitial collagen volume fraction in the left (LV-ICVF) and right ventricle (RV-ICVF) was quantified by videomorphometry using a Quantimet 520 Image Analyses System (LEICA Microsystems). The analyzed echocardiographic parameters were the left ventricle ejection fraction (LVEF) and diastolic diameter (LVDD, cm). ResultsLV-ICVF (%) was greater in the infarcted groups compared to controls (p<0.001), and attenuated by EPO (p<0.001, MI vs MI+EPO) (CT= 0.76±0.21; CT+EPO= 0.63±0.15; MI+EPO= 1.43±0.92; MI= 3.47±2.5 and Sham= 0.37±0.04). The RV-ICVF (%) was also greater in the infarcted groups compared to controls (CT=0.60±0.2; CT+EPO= 0.83±0.3; MI+EPO= 1.01±0.55; IAM= 1.60±1.15 and Sham= 0.53±0.11) (p<0.001) but without statistical difference between MI vs MI+EPO. The infarcted groups had a worsening ejection fraction compared to controls (CT= 81%±6.5; CT+EPO=77%±5; MI+EPO= 40%±12 and MI= 38%±11.5) (p<0,001) but without EPO protection. The infarcted groups also showed increased LV dilation (p<0.001) (CT= 0.73±0.06; CT+EPO= 0.74±0.05; MI+EPO= 0.81±0.09; MI= 0.87±0.11) without EPO attenuation. LV-ICVF (%) was greater in the infarcted groups compared to controls (p<0.001), and attenuated by EPO (p<0.001, MI vs MI+EPO) (CT= 0.76±0.21; CT+EPO= 0.63±0.15; MI+EPO= 1.43±0.92; MI= 3.47±2.5 and Sham= 0.37±0.04). The RV-ICVF (%) was also greater in the infarcted groups compared to controls (CT=0.60±0.2; CT+EPO= 0.83±0.3; MI+EPO= 1.01±0.55; IAM= 1.60±1.15 and Sham= 0.53±0.11) (p<0.001) but without statistical difference between MI vs MI+EPO. The infarcted groups had a worsening ejection fraction compared to controls (CT= 81%±6.5; CT+EPO=77%±5; MI+EPO= 40%±12 and MI= 38%±11.5) (p<0,001) but without EPO protection. The infarcted groups also showed increased LV dilation (p<0.001) (CT= 0.73±0.06; CT+EPO= 0.74±0.05; MI+EPO= 0.81±0.09; MI= 0.87±0.11) without EPO attenuation. ConclusionsEPO significantly attenuated the accumulation of interstitial collagen, but it did not reflected in the protection of the heart dilation or dysfunction in this model.Grant Fapesp: 2010/06834-2 EPO significantly attenuated the accumulation of interstitial collagen, but it did not reflected in the protection of the heart dilation or dysfunction in this model.