Effects of cardiac support device on reverse remodeling: molecular, biochemical, and structural mechanisms.
Progressive left ventricular (LV) dilation is a characteristic feature of heart failure and is invariably associated with poor long-term prognosis. This review discusses observations made in dogs with chronic heart failure using a passive mechanical containment device, the Acorn Cardiac Support Device (CSD), which is designed to prevent progressive LV enlargement. Studies have shown that, in addition to preventing LV dilation, long-term therapy with the CSD also improved LV ejection fraction, tended to normalize LV shape, reduced LV wall stress, and reduced or eliminated functional mitral regurgitation. At the cellular level, the CSD attenuates cardiomyocyte hypertrophy, reduced oxygen diffusion distance and downregulated stretch response proteins. The CSD also improved calcium cycling within the sarcoplasmic reticulum and upregulated mRNA gene expression for alpha-myosin heavy chain. These findings, when viewed in concert, provide an explanation for mechanisms that may be responsible for the improvement in LV function seen in dogs with heart after long-term CSD therapy.
Sabbah
Hani N
HN
Department of Medicine, Division of Cardiovascular Medicine, Henry Ford Health System, Detroit, Michigan 48202, USA.
D000818:Animals; D020013:Calcium Signaling / Q000502:physiology; D004285:Dogs; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D006353:Heart-Assist Devices; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
D018995:Myosin Heavy Chains