Cirrhotic cardiomyopathy: Implications for the perioperative management of liver transplant patients

Abstract

Cirrhotic cardiomyopathy is a disease that has only recently been recognised as a definitive clinical entity. In the setting of liver cirrhosis, it is characterized by a blunted inotropic and chronotropic response to stress, impaired diastolic relaxation of the myocardium and prolongation of the QT interval in the absence of other known cardiac disease. A key pathological feature is the persistent over-activation of the sympathetic nervous system in cirrhosis, which leads to down-regulation and dysfunction of the β-adrenergic receptor. Diagnosis can be made using a combination of echocardiography (resting and stress), tissue Doppler imaging, cardiac magnetic resonance imaging, 12-lead electrocardiogram and measurement of biomarkers. There are significant implications of cirrhotic cardiomyopathy in a number of clinical situations in which there is an increased physiological demand, which can lead to acute cardiac decompensation and heart failure. Prior to transplantation there is an increased risk of hepatorenal syndrome, cardiac failure following transjugular intrahepatic portosystemic shunt insertion and increased risk of arrhythmias during acute gastrointestinal bleeding. Liver transplantation presents the greatest physiological challenge with a further risk of acute cardiac decompensation. Peri-operative management should involve appropriate choice of graft and minimization of large fluctuations in preload and afterload. The avoidance of cardiac failure during this period has important prognostic implications, as there is evidence to suggest a long-term resolution of the abnormalities in cirrhotic cardiomyopathy.

Keywords: Cirrhotic cardiomyopathy; Diastolic dysfunction; Electrophysiological abnormalities; Liver transplantation; Perioperative care.

Figure 1

Left ventricular diastolic function in normal subjects (A); cirrhosis (B); cirrhosis with tense ascites (C); cirrhosis with ascites after paracentesis (D). ^aP < 0.05, E/A ratio: (early peak: late peak filling velocities). Ratio declines with worsening LVDD. Pozzi et al[24].

Figure 2

Differences in survival of patients according to the presence of left ventricular diastolic dysfunction. LVDD: Left ventricular diastolic dysfunction. Karagiannakis et al[22].

Figure 3

Individual values of QTc interval in patients with cirrhosis (divided according to Child-Pugh classes) and controls. Bernardi et al[26].

Figure 4

Estimated 1 year probability of dying as a function of: (A) MELD score alone; (B) MELD score and hs-TnT of 4-8 ng/L; and (C) MELD score and hs-TnT of > 8 ng/L. Taken from Wiese et al[64].

Figure 5

Probability of patients still having ascites after transjugular intrahepatic portosystemic shunts insertion in the group with diastolic dysfunction (E/A ≤ 1) and the group without (E/A > 1). Rabie et al[45].

Figure 6

Probability of survival in patients with (E/A ≤ 1) or without (E/A > 1) diastolic dysfunction. Rabie et al[45].

Figure 7

Probability of developing hepatorenal syndrome during follow-up in patients with baseline cardiac output higher and lower than 6 L/min. Ruiz-del-Arbol et al[71].

Figure 8

Time to acute rejection for various grades of left ventricular diastolic dysfunction. Mittal et al[74].

Figure 9

Survival analysis for patients with left ventricular diastolic dysfunction vs patients without. Mittal et al[74].

Figure 10

Graft (A) and overall (B) survival in patients with highly possible (continuous line) and those with unlikely (dashed line) peri-transplant heart failure. Josefsson et al[25].