New onset nonischemic cardiomyopathy post liver transplantation

Abstract

A new onset acute heart failure (HF) with a sudden drop in the left ventricular ejection fraction (LVEF) post orthotopic liver transplant (LT) is a rare but a potentially fatal complication. Because in most of the cases there is no evidence of coronary thrombosis, it can be classified as nonischemic cardiomyopathy. More specifically, clinical presentation of this syndrome shares many features with stress-induced or takotsubo cardiomyopathy. The known factors that predispose these patients to acute HF during or shortly after LT include cirrhotic cardiomyopathy, rapid hemodynamic changes during LT surgery, and the large concentrations of catecholamines, either administered or released endogenously during surgery. The hemodynamic changes during surgery, such as the drop in preload during the anhepatic phase (occasionally requiring massive transfusions and vasopressors) and subsequent increase in preload with acidic and hyperkalemic plasma in the reperfusion phase, lead to rapid electrolyte and hemodynamic shifts. In several cases, intraoperative onset of HF, with or without ventricular arrythmia, could be timed to the reperfusion phase (and occasionally in the anhepatic and pre-anhepatic phases). In other cases, the HF syndrome started hours to days post-surgery. Recovery of cardiac function occurred in the majority of patients during the same admission; however, these patients generally need significantly longer hospitalizations and aggressive supportive care (occasionally requiring mechanical ionotropic and ventilatory support). If recover, the patients have a similar 1-year mortality as those LT patients that did not have this complication. Because no reliable risk stratification currently exists, intraoperative transesophageal echocardiography might be the most dependable way of detecting and addressing this syndrome promptly. Given the mechanism of takotsubo cardiomyopathy, beta-blockade and a preferential use of non-catecholaminergic vasopressors may be a reasonable way to manage this syndrome.

The predictive value of revised diastolic dysfunction in outcomes of liver transplantation: A propensity score matching analysis

“…Upon encountering environmental stress, such as transplantation, impaired contractility fails to adapt to initial changes. Decreased vascular resistance and increased cardiac output increase cardiac preload, resulting in abnormal filling of the ventricle and blood redistribution (12,13). Histological examination of a heart with CCM revealed edema, cardiomyocyte hypertrophy, nuclear vacuolization, and fibrosis, which occurred in conjunction with enhanced accumulation of collagen.…”

Hepatic Ischemia/Reperfusion Injury After Liver Transplantation Is Not Associated with Early Impairment of Left Ventricular Ejection Fraction

“…In our study population, we observed that patients with severe hIRI required a significantly greater cumulative dose of intraoperative inotropic and vasopressor medications. Pressor use is an established risk factor for development of stress-induced cardiomyopathy, which is a known post-LT cardiac complication that has significant impact on recipient mortality [ 10 , 15 – 20 ]. It is also hypothesized that cirrhotic cardiomyopathy can be responsible for post-LT cardiac dysfunction [ 10 , 21 ].…”

Characteristics, Risk Factors, and Outcome of New-onset Systolic Heart Failure After Liver Transplantation: A Single-center Cohort

“…The etiology of nonischemic HF was stress-induced Takotsubo cardiomyopathy (11/24), sepsis (8/24), and other causes (5/24; see Supplementary File 1, SDC, http://links.lww.com/TXD/A538 for details). Compared to sepsis-induced cardiomyopathy, the median time for the onset of stress-induced HF was significantly shorter (31 [15-104] versus 4 [3][4][5][6] d, respectively; χ 2 = 11, P < 0.001). Complete, partial, and no recovery of heart function was recorded in 14-6-4 of 24 patients, respectively.…”

“…Regrettably, 2 decades of research into the diagnostic, therapeutic, and preventive strategies of post-LT myocardial dysfunction have provided scant data regarding its etiology, characteristics, and prognosis. 6,7 Thus, there remains a dire need to fill this knowledge gap so that the loss of both lives and grafts can be minimized.…”