Electrophysiologic Remodeling of the Left Ventricle in Pressure Overload-Induced Right Ventricular Failure

Abstract

Pressure-induced RVF is associated with electrophysiologic remodeling of the atrophic LV.

Diastolic Dysfunction Increases the Risk of Primary Graft Dysfunction after Lung Transplant

“…Chronically elevated RV afterload, RV dysfunction, and lung hyperinflation result in relative underfilling of the left ventricle in advanced lung disease. Animal models and human case series have demonstrated that, in response to a chronically reduced LV preload, there is a decrease in the LV myocyte cross-sectional area, a prolongation of LV action potential, and a decrease in the calcium-ATPase pump involved in myocyte relaxation, resulting in impaired LV relaxation and diminished compliance (16,19,(21)(22)(23)(24)45). In addition, the left ventricle's ability to relax may be further impaired perioperatively by the release of proinflammatory cytokines in PGD, including IL-6, which leads to a reduction in sarcoplasmic reticulum Ca 21 -ATPase (46)(47)(48).…”

“…In addition, the left ventricle's ability to relax may be further impaired perioperatively by the release of proinflammatory cytokines in PGD, including IL-6, which leads to a reduction in sarcoplasmic reticulum Ca 21 -ATPase (46)(47)(48). The left ventricle appears to undergo reverse remodeling following restoration of preload over time; however, this adaptation is not immediate, and abnormal filling may persist up to 1 year after transplant (16,23,(49)(50)(51)(52)(53)(54). Therefore, it is possible that acute and chronic impairment in LV diastolic function may contribute to pulmonary edema and PGD.…”

“…Furthermore, many of the advanced lung diseases treated with lung transplant are associated with a high prevalence of diastolic dysfunction, ranging from 20% to 70% (13)(14)(15)(16)(17)(18)(19). Multiple mechanisms may mediate the development of abnormal diastolic function in chronic lung diseases (16,(19)(20)(21)(22)(23)(24)(25)(26)(27). Chronically increased right ventricular (RV) afterload, RV dysfunction, and lung hyperinflation decrease LV preload, which can lead to LV atrophy and abnormal myocyte relaxation (16,19,(21)(22)(23)(24)(25)(26)(27).…”

“…Multiple mechanisms may mediate the development of abnormal diastolic function in chronic lung diseases (16,(19)(20)(21)(22)(23)(24)(25)(26)(27). Chronically increased right ventricular (RV) afterload, RV dysfunction, and lung hyperinflation decrease LV preload, which can lead to LV atrophy and abnormal myocyte relaxation (16,19,(21)(22)(23)(24)(25)(26)(27). Given the high prevalence of abnormal diastolic function in this population, as well as the association between higher LV filling pressures and other forms of acute lung injury, it is possible that higher LV end-diastolic pressure and pulmonary venous pressure after lung reperfusion could contribute to capillary leak and PGD.…”

Excitation propagation in three-dimensional engineered hearts using decellularized extracellular matrix

“…Synchronicity is an important factor for the construction of a transplantable artificial organ, since asynchronous regions impair the contractility, as well as potentially increase the risk of lethal cardiac arrhythmias. The calculated CV in our engineered heart tissues was markedly decreased (approximately 5 cm/s) as compared to that reported previously in an adult rat heart [22,23] or in an in vitro cultured neonatal rat cardiomyocyte (NRCM), whereas it was similar to that of NRCM with Cx43 mutation [24]. Slow conduction and electrical instability were more apparent in the whole heart.…”