What happens to cirrhotic cardiomyopathy after liver transplantation?

BACKGROUND/AIMS: Liver cirrhosis induces cardiac alterations. We aimed to define these alterations and assess their reversibility after transplantation. METHODS: Cirrhotic patients (n 40) and controls (n 15) underwent echocardiography and stress ventriculography. Fifteen cirrhotics were reevaluated 6-12 months after transplantation. RESULTS: Cirrhotics had higher left ventricular wall thickness (9.6 1.2 vs. 8.8 1.2mm; p< 0.05) and ejection fraction (73 6 vs. 65 4%, p < 0.001) than controls. Basal diastolic function was similar. During stress, patients with cirrhosis presented lower increases of heart rate, left ventricular ejection fraction, stroke volume and cardiac index (p < 0.05 for all), and diastolic dysfunction with lower ventricular peak filling rate (p 0.001). Exercise capacity was reduced (48 21 vs. 76 24W; p < 0.001). Ascitic patients exhibited more diastolic dysfunction at rest and during stress compared with non-ascitic patients. Liver transplantation caused regression of ventricular wall thickness (10.2 1.3 vs. 9.5 1.2mm; p < 0.05), improvement of diastolic function, and normalization of systolic response and exercise capacity during stress (significant increases in heart rate, ventricular ejection fraction, stroke volume, and cardiac index; p < 0.05 for all). CONCLUSIONS: Cardiac alterations in cirrhosis present with mild increases in ventricular wall thickness, diastolic dysfunction that worsens with ascites and physical stress, and abnormal systolic response to stress limiting exercise capacity. Liver transplantation reverses these alterations. “A chance to cut is a chance to cure. ” — surgical proverb In patients with cirrhosis, myocardial contractile responsiveness is impaired under stressful stimuli such as exercise or pharmacological challenge, a condition termed cirrhotic cardiomyopathy.1 This syndrome has remained an academic curiosity until very recently, initially because it was misdiagnosed as alcoholic cardiomyopathy, then later because it appeared to have little clinical relevance. Because overt severe heart failure is rare in patients with cirrhosis, some even doubt the existence of cirrhotic cardiomyopathy. Skeptics contend that all changes of this syndrome can be explained by a cardiac adaptation to the hyperdynamic circulation, or ventricular hypertrophy due to chronic volume overload. However, the past decade has been edifying to those of us who believe in the syndrome. Recent research strongly suggests that cardiodepression in the face of sepsis contributes to the pathogenesis of hepatorenal syndrome.2,3 In addition, the advent of significant cardiac stresses such as TIPS insertion, or major surgery has precipitated cardiac dysfunction, even overt left ventricular failure in some patients.4-7 Of course, the most intense cardiovascular stress is induced by the acme of all surgeries, orthotopic liver transplantation. This operation has underscored the clinical significance of ventricular dysfunction in several ways. Before the idea of cirrhotic cardiomyopathy was raised, transplant specialists were puzzled by the apparently inexplicable appearance of sometimes severe cardiac dysfunction in the postoperative period, often in patients with no previous history or risk factors for heart disease. The myriad cardiac complications of liver transplantation have recently been reviewed in detail.8,9 However, a few points bear mention. Cardiac complications including hypotension due to postreperfusion syndrome, myocardial infarction, significant arrhythmias, heart failure, and sudden cardiac death afflict a significant percentage of patients in the immediate and delayed postoperative period. Moreover, the degree of cardiac reserve function may directly affect the survival chances of the transplanted patient. Those with higher cardiac output both preoperatively and after transplantation show better survival rates compared with those with lower cardiac output.10 Cardiac contractile function appears to undergo a biphasic or even triphasic response after transplantation. The immediate-early stresses of the transplantation surgery impose a significantly increased workload on the heart. Predominant among these is the rapid increase in arterial pressure and systemic vascular resistance, which abruptly increases the ventricular afterload. In conjunction with the typical volume challenges attendant with the surgery, these factors can precipitate acute left ventricular failure, manifesting as pulmonary edema. Clinical or radiographic evidence of pulmonary edema is surprisingly frequent, observed in 12% to 56% of patients during their hospitalization, usually in the first postoperative week.8,9 These episodes almost always resolve with appropriate treatment. Although most episodes are mild, a minority present with overt or severe dilated cardiomyopathy. A severe but reversible cardiomyopathy was observed in 7 of