Background-aim Apelin is an endogenous peptide that binds the angiotensin-like 1 (APJ) receptor and increases cardiac contractility. The expression of apelin/APJ receptor system is differently modulated in healthy and failing heart. Although the levels of apelin pathway are increased in compensation for ischemic cardiomyopathy in animal models, its expression profile in human failing heart with similar function and different origin is still unclear. The aim of the study was to analyze the apelin/APJ mRNA profile in left ventricular (LV) tissue of patients affected by idiopathic (DCM) or ischemic (ICM) end-stage dilated cardiomyopathy undergoing cardiac transplantation. Methods Apelin/APJ mRNA expression was measured in LV myocardium of DCM (n = 8; age: <50 yrs.; LVEF% = 17.5 ± 3; LVEDV = 305.5 ± 110 ml) and ICM pts. (n = 8; age:<50 yrs.; LVEF% = 19.5 ± 5.2; LVEDV = 270 ± 97 ml) with similar cardiac function by Real-Time PCR analysis. All patients are affected by similar co-morbidities and received similar medications, and cardiac function was assessed by echocardiography. To understand if the difference of apelin/APJ mRNA expression depend on the origin of HF or on the magnitude of global cardiac function atrium cardiac tissue of 5 valvular disease patients (VLP), age matched, with LVEF % >50% and not pharmacologically treated were also used. Results Apelin mRNA expression resulted significantly higher in DCM with respect to ICM (DCM:38.7 ± 10.3; ICM:11.06 ± 6.0 p = .01) as well as APJ receptor mRNA expression (DCM:17.2 ± 3.3; ICM:11.3 ± 4.3) also if no significantly. A significant correlation was observed between Apelin and APJ receptor (r = 0.629, p = .0052). In addition, a significant increase of apelin (p = .05) and APJ receptor (p = .02) mRNA expression was observed in patients with LVEF<50% (apelin: 23.8 ± 6.08; APJ:13.8 ± 2.86) with respect to patients with LVEF>50% (apelin: 1.15 ± 0.23; APJ:1.39 ± 0.46). Conclusions LV apelin/APJ mRNA levels increase in patients with LVEF <50% probably due to a compensatory response to a loss of contractility. Noteworthy, LV apelin/APJ mRNA expression in DCM is higher than ICM hearts. Our results, for the first time, suggest that the induction of apelin gene expression in the failing ventricles may represent a new cardiac biomarker for an adaptative response to loss of inotropic strenght in the presence of coronary patency.

The apelinergic system cardiac expression in patients with idiopathic or ischemic end-stage dilated cardiomyopathy

B. Svezia;M. Matteucci;V. Lionetti
;
2019-01-01

Abstract

Background-aim Apelin is an endogenous peptide that binds the angiotensin-like 1 (APJ) receptor and increases cardiac contractility. The expression of apelin/APJ receptor system is differently modulated in healthy and failing heart. Although the levels of apelin pathway are increased in compensation for ischemic cardiomyopathy in animal models, its expression profile in human failing heart with similar function and different origin is still unclear. The aim of the study was to analyze the apelin/APJ mRNA profile in left ventricular (LV) tissue of patients affected by idiopathic (DCM) or ischemic (ICM) end-stage dilated cardiomyopathy undergoing cardiac transplantation. Methods Apelin/APJ mRNA expression was measured in LV myocardium of DCM (n = 8; age: <50 yrs.; LVEF% = 17.5 ± 3; LVEDV = 305.5 ± 110 ml) and ICM pts. (n = 8; age:<50 yrs.; LVEF% = 19.5 ± 5.2; LVEDV = 270 ± 97 ml) with similar cardiac function by Real-Time PCR analysis. All patients are affected by similar co-morbidities and received similar medications, and cardiac function was assessed by echocardiography. To understand if the difference of apelin/APJ mRNA expression depend on the origin of HF or on the magnitude of global cardiac function atrium cardiac tissue of 5 valvular disease patients (VLP), age matched, with LVEF % >50% and not pharmacologically treated were also used. Results Apelin mRNA expression resulted significantly higher in DCM with respect to ICM (DCM:38.7 ± 10.3; ICM:11.06 ± 6.0 p = .01) as well as APJ receptor mRNA expression (DCM:17.2 ± 3.3; ICM:11.3 ± 4.3) also if no significantly. A significant correlation was observed between Apelin and APJ receptor (r = 0.629, p = .0052). In addition, a significant increase of apelin (p = .05) and APJ receptor (p = .02) mRNA expression was observed in patients with LVEF<50% (apelin: 23.8 ± 6.08; APJ:13.8 ± 2.86) with respect to patients with LVEF>50% (apelin: 1.15 ± 0.23; APJ:1.39 ± 0.46). Conclusions LV apelin/APJ mRNA levels increase in patients with LVEF <50% probably due to a compensatory response to a loss of contractility. Noteworthy, LV apelin/APJ mRNA expression in DCM is higher than ICM hearts. Our results, for the first time, suggest that the induction of apelin gene expression in the failing ventricles may represent a new cardiac biomarker for an adaptative response to loss of inotropic strenght in the presence of coronary patency.
2019
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11382/528558
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