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Liver transplantation (LT) is the only life-saving treatment option in patients with advanced liver disease. Deceased-donor LT is not frequent but is increasing in Asian countries. Because current liver allocation policies follow the severity principle wherein patients at highest risk for mortality receive top priority, anesthesiologists may face severely ill patients more frequently with deceased-donor LT than with living-donor LT. In this regard, with the outstanding surgical success of recent LT, cardiovascular complications have emerged as the leading cause of death after LT, particularly among those with advanced liver cirrhosis
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Cardiovascular complications have emerged as the leading cause of death after liver transplantation, particularly among those with advanced liver cirrhosis. Therefore, a thorough and accurate cardiovascular evaluation with clear comprehension of cirrhotic cardiomyopathy is recommended for optimal anesthetic management. However, cirrhotic patients manifest cardiac dysfunction concomitant with pronounced systemic hemodynamic changes, characterized by hyperdynamic circulation such as increased cardiac output, high heart rate, and decreased systemic vascular resistance. These unique features mask significant manifestations of cardiac dysfunction at rest, which makes it difficult to accurately evaluate cardiovascular status As cardiovascular complications are leading causes of nongraft related mortality after LT [2], the importance of identifying masked intrinsic cardiac dysfunction or decreased capacity of cardiac contractility due to external stress has been emphasized. However, detecting ventricular dysfunction in a resting state is difficult, as marked vasodilation and increased arterial compliance lead to latent or mild cardiac manifestations [4]. Different stress tests, using drugs or exercise, have been applied to unmask cardiac dysfunction; however, achieving a target HR and blood pressure is difficult given the poor functional conditions of patients with LC [5].
Dobutamine stress echocardiography (DSE) is recommended to discriminate high-risk patients with ischemic heart disease; however, the accuracy of DSE varies widely among studies as a result of various selection criteria [3] and the inability to achieve the predicted target HR to provoke wall motion abnormalities. This inadequacy is based on the failure of beta receptors to respond to sympathetic stimulation in patients with LC or the use of beta blockers to prevent variceal bleeding. Therefore, the accuracy of DSE is questionable, and its sensitivity is reported as low as 13-14% [6-7]. Nicolau-Raducu et al. [8] demonstrated that DSE has 9% sensitivity, 33% positive predictive value, and 89% negative predictive value for predicting early cardiac events after LT.
The autonomic nervous system is an important regulator of cardiovascular homeostasis, and an HR analysis is considered a surrogate of vagal and sympathetic disturbances. Therefore, HR measurements have been recognized as a prognostic factor in many clinical investigations [9-12]. Studies showing reduced HR variability, which correlates with disease severity, central hypovolemia, and the degree of portal hypertension have also been reported [13-14]. Kim et al. [15] found that sympathetic withdrawal is associated with hypotension after graft reperfusion during LT.
Patients with LC have an increased resting HR due to hyperdynamic circulation, increased circulating catecholamines, and cirrhotic cardiomyopathy [16-17]. Kwon et al. [18] demonstrated that resting HR is associated with all-cause mortality in LT recipients and showed that patients with HR >80 beats/min are significantly associated with a higher risk for all-cause mortality (hazard ratio 1.83) compared to patients with HR ≤65 beats/min.
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