This is the typical pathophysiology of both-side HF, named passive-caused “cardiopulmonary failure/syndrome”. Ultimately, the pulmonary, right ventricular, right atrial and systemic venous blood pressure elevations are clearly identified. The pathophysiological, hemodynamic and clinical studies have clearly established that HF caused by HCM/DCM associated with elevation of LV end-diastolic pressure that undoubtedly elicit elevations of left atrial and pulmonary capillary wedge pressures. Ĭopious etiologies can cause cardiopulmonary failure. Accordingly, this kind of DCM is the end stage of HCM. The HCM can elicit (1) heart failure (HF) in early stage without left ventricular (LV) chamber dilatation (i.e., HF in stage of LV preservation with diastolic dysfunction and poor compliance) and (2) late stage (i.e., end stage) of HF with LV dilatation and remodeling (i.e., decompensated HF in stage of LV dysfunction), that accounts for one of the most popular reasons of dilated cardiomyopathy (DCM). Hypertrophic cardiomyopathy (HCM) can be categorized into two casual etiologies, i.e., (1) due to a normal physiological stimulation, such as marathon running, weightlifting and (2) due to pathological stimulation, for examples: HCM resulted from primary disease (i.e., genetic mutation), hypertension without treatment, aortic or supra-aortic valvular stenosis, or coarctation of aorta, etc. In conclusion, Entresto is non-inferior to enalapril for protecting the heart-lung against CPS. The protein expressions of pressure/volume overload (BNP/MHC-β) mitochondrial-damaged (cytosolic cytochrome-C) of LV myocardium exhibited an identical pattern of SL (all P<0.001). The protein expressions of fibrotic (Smad3/TGF-β), apoptotic (mitochondrial-Bax/cleaved-caspase3/PARP) and DNA-damaged (γ-H2AX) markers in lung and LV myocardium as well as oxidative (NOX-1/NOX2/oxidized protein) in LV myocardium exhibited an identical pattern of SL (all P<0.0001). The sarcomere-length (SL), LV fibrotic area, cardiomyocyte size, and lung injury score were highest in group 4, lowest in groups 1 to 3 and significantly lower in group 6 than in group 5 (all P<0.0001). By day 60, the left-ventricular (LV) ejection fraction was significantly lower in group 4 than in other groups and significantly lower in groups 5 and 6 than in groups 1 to 3, whereas the ratios of heart and lung weights to tibial-length as well as the right-ventricular-systolic blood pressure exhibited an opposite pattern among the groups (all P<0.001). Adult-Male SD rats (n = 36) were equally categorized into group 1, group 2, group 3, group 4 (TAC only), group 5 (TAC + enalapril) and group 6 (TAC + entresto) and euthanized at day 60 after TAC induction. This study tested the hypothesis that entresto therapy effectively protected heart and lung against cardiopulmonary syndrome (CPS) caused by transverse aortic constriction (TAC) in rat.

Kid3 cardiomyocyte