Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation

Author:

Pokorný Martin12,Mrázová Iveta23,Šochman Jan4,Melenovský Vojtěch4,Malý Jiří1,Pirk Jan1,Červenková Lenka3,Sadowski Janusz5,Čermák Zdeněk6,Volenec Karel6,Vacková Šárka3,Maxová Hana2,Červenka Luděk23,Netuka Ivan1

Affiliation:

1. Department of Cardiovascular Surgery, Institute for Clinical and Experimental Medicine, Prague, Czech Republic

2. Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic

3. Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic

4. Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic

5. Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

6. ELLA-CS, Ltd., Hradec Králové, Czech Republic

Abstract

Cardiac atrophy is the most common complication of prolonged application of the left ventricle (LV) assist device (LVAD) in patients with advanced heart failure (HF). Our aim was to evaluate the course of unloading-induced cardiac atrophy in rats with failing hearts, and to examine if increased isovolumic loading obtained by intraventricular implantation of an especially designed spring expander would attenuate this process. Heterotopic abdominal heart transplantation (HTx) was used as a rat model of heart unloading. HF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). The degree of cardiac atrophy was assessed as the weight ratio of the heterotopically transplanted heart (HW) to the control heart. Isovolumic loading was increased by intraventricular implantation of a stainless steel three-branch spring expander. The course of cardiac atrophy was evaluated on days 7, 14, 21, and 28 after HTx. Seven days unloading by HTx in failing hearts sufficed to substantially decrease the HW (−59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HTx. Implantation of the spring expander significantly reduced the decreases in whole HW at all the time points (−39 ± 3 compared with −59 ± 3, −52 ± 2 compared with −69 ± 3, −51 ± 2 compared with –71 ± 2, and −44 ± 2 compared with −71 ± 3%, respectively; P<0.05 in each case). We conclude that the enhanced isovolumic heart loading obtained by implantation of the spring expander attenuates the development of unloading-induced cardiac atrophy in the failing rat heart.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

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