Frequency and significance of acute heart failure following liver transplantation.

Reversible cardiomyopathy has been reported in patients after liver transplantation. However, there are few data on the incidence, risk factors, and prognosis of this condition. Liver transplantation recipients who underwent preoperative right- and left-sided cardiac catheterization as well as preoperative transthoracic echocardiography from 2001 to 2005 were identified. Eighty-six patients met the outlined criteria and were included in the study. The incidence of severe heart failure (HF) after transplantation in this population was 6 of 86 (approximately 7%). Patients who developed HF were slightly older (mean age 61.2 +/- 8.9 vs 55.4 +/- 9.2 years, p = 0.08) but had similar preoperative ejection fractions (60 +/- 5% vs 57 +/- 8%, p = 0.22) and comparable systemic arterial blood pressure (116 +/- 22/62 +/- 11 vs 127 +/- 9/66 +/- 9, p >0.1). In addition, the severity of liver disease as measured by the model for end-stage liver disease score was not different between the 2 groups (23.9 +/- 9.7 vs 26 +/- 10.7, p = 0.5). There was also no significant difference in the preoperative cardiac index (3.8 +/- 1 vs 3.6 +/- 1.5 L/min/m2, p = 0.9) or pulmonary artery wedge pressure (13.6 +/- 5.8 vs 15.3 +/- 2.8 mm Hg, p = 0.42). The incidence of alcohol use as the presumed cause of liver failure was equivalent in the 2 groups (33% vs 25%, p = 0.65). The patients who developed HF did have significantly higher preoperative mean pulmonary arterial systolic pressures (43 +/- 10 vs 30 +/- 9 mm Hg, p = 0.02) and right ventricular systolic pressures (44 +/- 13 vs 34 +/- 8 mm Hg, p = 0.05). In conclusion, severe systolic HF may occur after liver transplantation in patients without traditional risk factors for HF. This study suggests that those patients with preoperative elevated right-sided cardiac pressures, as well as older patients, may be at excess risk for developing HF after transplantation.

Reappraisal of beta-blocker therapy in the acute and chronic post-myocardial infarction period.

In patients presenting with acute myocardial infarction (MI), the early use of intravenous beta-blockade followed by short-term oral administration in the absence of reperfusion therapy has shown a modest reduction in mortality. In contrast, major reductions in mortality and reinfarction have been shown when beta-blockers have been used soon after an acute MI and continued long-term. These benefits were observed in trials conducted in the 1970s and 1980s, prior to the widespread use of reperfusion therapies, antiplatelet agents, and angiotensin-converting enzyme inhibitors; those trials excluded patients with postischemic heart failure. Recently, the CAPRICORN trial has shown a significant reduction in all-cause mortality and reinfarction in post-MI patients with systolic dysfunction, in response to carvedilol. In spite of compelling evidence supporting the use of beta-blockers in the post-MI setting, data published by the National Cooperative Cardiovascular Project have shown that fewer than half of all post-MI patients receive beta-blockers as long-term therapy. It appears that post-MI patients with perceived contraindications, such as advanced age, diabetes, heart failure, peripheral vascular disease, and/or chronic pulmonary obstructive disease, may derive a substantial benefit from the use of beta-blockers. Given the considerable evidence from randomized clinical trials, the use of beta-blockers is recommended in all post-MI patients without a contraindication, particularly in those with left ventricular systolic dysfunction.