Appraising cardiac dysfunction in liver transplantation: an ongoing challenge

Zaky, Ahmed; Bendjelid, Karim

doi:10.1111/liv.12582

Cited by 37 publications

(46 citation statements)

References 140 publications

(152 reference statements)

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“…Since, cardiac dysfunction in cirrhosis seems not to be associated with the severity of liver disease [27], both an accurate patient selection for liver transplant [28,29] and a precise investigation for cirrhotic cardiomyopathy are mandatory. Indeed, cirrhotic cardiomyopathy may influence the outcome after liver transplantation [30][31][32]; moreover, liver transplantation may be responsible for additional intra-and postoperative short-and long-term cardiac morbidity [33].…”

Section: Pre-transplant Investigative Methodsmentioning

confidence: 99%

Cirrhotic cardiomyopathy in the pre- and post-liver transplantation phase

Zardi

Chin

et al. 2016

Journal of Cardiology

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Patients with advanced liver cirrhosis may develop a clinical syndrome characterized by a blunted contractile responsiveness to stress and/or altered diastolic relaxation, called "cirrhotic cardiomyopathy." This syndrome, which is initially asymptomatic, is often misdiagnosed due to the presence of symptoms that characterize other disorders present in patients with advanced liver cirrhosis, such as exercise intolerance, fatigue, and dyspnea. Stress and other conditions such as liver transplantation and transjugular intrahepatic portosystemic shunt (TIPS) may unmask this syndrome. Liver transplantation in this group of patients results in a clinical improvement and can be a cure for the cardiomyopathy. However, post-transplant prognosis depends on the identification of cirrhotics with cardiomyopathy in the pre-transplant phase; an early diagnosis of cirrhotic cardiomyopathy in the pre-transplant phase may avoid an acute onset or worsening of cardiac failure after liver transplantation. Since a preserved left ventricular ejection fraction may mask the presence of cirrhotic cardiomyopathy, the use of newer noninvasive diagnostic techniques (i.e. tissue Doppler, myocardial strain) is necessary to identify cirrhotics with this syndrome, in the pre-transplant phase. A pre-transplant treatment of heart failure in cirrhotics with cardiomyopathy improves the quality of life in this phase and reduces the complications during and immediately after liver transplantation. Since specific therapies for cirrhotic cardiomyopathy are lacking, due to the absence of a clear understanding of the pathophysiology of the cardiomyopathy, further research in this field is required.

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Section: Pre-transplant Investigative Methodsmentioning

confidence: 99%

Cirrhotic cardiomyopathy in the pre- and post-liver transplantation phase

Zardi

Chin

et al. 2016

Journal of Cardiology

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“…(33,34) LT may be a major stress factor that can unmask preexisting CCMP. (8,9) Because of advances in surgical and anesthetic techniques, the main causes of death after LT at present are associated with early cardiovascular mortality. (7,13) Therefore, it is crucial to identify patients at higher risk of perioperative cardiovascular complications.…”

Section: Figmentioning

confidence: 99%

“…Consequently, the optimal LVEF thresholds predictive, if any, of early and late mortality are incompletely defined in patients with decompensated liver disease. (9)(10)(11) In liver transplantation (LT), the pretransplant assessment of cardiac risk remains uncertain and clinically challenging; however, recognizing LT patient with cardiac dysfunction is essential because it is associated with serious cardiovascular events, eventually increasing mortality (12,13) and risk of graft failure. (14)(15)(16) In the current study, considering that left ventricle (LV) systolic function is enhanced and vascular tone is reduced in patients with LC, we hypothesized that a higher LVEF cutoff may be predictive of mortality and graft failure in LT patients with decompensated liver disease than in those with compensated liver disease.…”

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confidence: 99%

Appraisal of Cardiac Ejection Fraction With Liver Disease Severity: Implication in Post–Liver Transplantation Mortality

et al. 2020

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Background and Aims Enhanced sympathetic nervous activation and peripheral vasodilation in end‐stage liver disease (ESLD) may limit the importance of left ventricular ejection fraction (LVEF) as an influential prognosticator. We sought to understand the LVEF and cardiac dimensions in ESLD patients in order to define the LVEF threshold to predict all‐cause mortality after liver transplantation (LT). Approach and Results Data were collected prospectively from the Asan LT Registry between 2008 and 2016, and outcomes were retrospectively reviewed. LVEF, end‐diastolic volume index (EDVI), and end‐diastolic elastance (Eed) were measured by preoperative echocardiography. Of 2,799 patients, 452 (16.2%) had LVEF ≤ 60%, with 29 (1.0%) having LVEF < 55% and 269 (9.6%) had LVEF ≥ 70%. Over a median of 5.4‐year follow‐up, 329 (11.8%) patients died: 104 (3.7%) died within 90 days. LVEF (range, 30%‐81%) was directly proportionate to Model for End‐stage Liver Disease (MELD) scores, an index of liver disease severity, in survivors but showed a fixed flat‐line pattern in nonsurvivors (interaction P = 0.004 between groups), with lower EDVI (P = 0.013) and higher Eed (P = 0.001) in the MELD ≥ 20 group. Patients with LVEF ≤ 60% had higher 90‐day (13% vs. 7.4%; log rank, P = 0.03) and median 5.4‐year (26.7% vs. 16.2%; log rank, P = 0.003) mortality rates in the MELD ≥ 20 group, respectively, compared to those with LVEF > 60%. Specifically, in the MELD > 35 group, median 5.4‐year mortality rate was 53.3% in patients with LVEF ≤ 60% versus 24% in those with LVEF > 60% (log rank P < 0.001). By contrast, mortality rates of LVEF ≤ 60% and > 60% were similar in the MELD < 20 group (log rank P = 0.817). Conclusions LVEF ≤ 60% is strongly associated with higher post‐LT mortality rates in the MELD ≥ 20 group, indicating the need to appraise both LVEF and liver disease severity simultaneously. Enhanced diastolic elastance with low EDVI provides insights into pathogenesis of low LVEF in nonsurvivors with MELD ≥ 20.

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“…But while HPS is a known risk factor for decreased survival in cirrhosis (12)(13)(14), comparatively less data regarding the relevance of cirrhotic cardiomyopathy are available (15)(16)(17). The proven major implication of CCM is its influence on post-procedural evolution in the setting of transjugular intrahepatic portosystemic shunt or liver transplantation (18)(19)(20)(21).…”

mentioning

confidence: 99%