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+/-1.2 mm; P < 0.05) and ejection fraction (73+/-6 vs. 65+/-4%, P < 0.001) than controls. Basal diastolic function was similar. During stress, cirrhotics 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+/-24 W; P < 0.001). Ascitic patients exhibited more diastolic dysfunction at rest and during stress compared to non-ascitic patients. Liver transplantation caused regression of ventricular wall thickness (10.2+/-1.3 vs. 9.5+/-1.2 mm; 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.
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+/-1.2 mm; P < 0.05) and ejection fraction (73+/-6 vs. 65+/-4%, P < 0.001) than controls. Basal diastolic function was similar. During stress, cirrhotics 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+/-24 W; P < 0.001). Asciticpatients exhibited more diastolic dysfunction at rest and during stress compared to non-asciticpatients. Liver transplantation caused regression of ventricular wall thickness (10.2+/-1.3 vs. 9.5+/-1.2 mm; 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.
Authors: Pierpaolo Pellicori; Concetta Torromeo; Angela Calicchia; Alessandra Ruffa; Martina Di Iorio; John G F Cleland; Manuela Merli Journal: Clin Res Cardiol Date: 2013-09-01 Impact factor: 5.460
Authors: Sachin Batra; Victor I Machicao; John S Bynon; Shivang Mehta; Rajasekhar Tanikella; Michael J Krowka; Steven Zacks; James Trotter; Kari E Roberts; Robert S Brown; Steven M Kawut; Michael B Fallon Journal: Liver Transpl Date: 2014-06 Impact factor: 5.799