BACKGROUND: The vasoconstrictor terlipressin is widely used in the treatment of the hepatorenal syndrome and variceal bleeding. However, terlipressin may compromise cardiac function and induce ischemia. AIM: Therefore, we aimed to assess the effects of terlipressin on cardiac function and perfusion. METHODS:Twenty-four patients with cirrhosis and ascites participated, including nine with refractory ascites. Gated myocardial perfusion imaging, mean arterial blood pressure (MAP), cardiac output (CO), ejection fraction (EF), end-diastolic volume (EDV), perfusion, and motion of the myocardium were determined before and after a bolus injection of 2 mg terlipressin. RESULTS: MAP increased after terlipressin (P value of less than 0.001). EF and CO fell by -16 and -17%, respectively in the terlipressin group versus 1 and -2%, respectively in the placebo group (P value of less than 0.001 and P value of less than 0.01). In the terlipressin group, EDV increased by 18 versus -4% in the placebo group (P value of less than 0.01). Wall motion in the anterior and posterior walls fell by -18 and -22%, respectively after terlipressin treatment versus 0 and 0% in the placebo group (P value of less than 0.01). In contrast, myocardial perfusion and stroke volume were unaltered in both the groups. The change in EF during terlipressin treatment correlated significantly with the change in MAP (r=-0.60, P value <0.002). Patients with refractory ascites had a higher EF and lower EDV and ESV than the patients with nonrefractory ascites, both at baseline and after terlipressin treatment. The decrease in the left ventricular wall thickening and wall motion correlated with the Child--Pugh score, r=-0.59, P=0.005 and r=-0.48, P=0.03. CONCLUSION: In advanced cirrhosis, the increase in afterload and EDV after terlipressin treatment result in a decrease in left ventricular wall motion, resulting in reduced CO and EF, but myocardial perfusion is preserved. Alteration in cardiac function at baseline and after terlipressin treatment relates to the stage of decompensation.
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BACKGROUND: The vasoconstrictor terlipressin is widely used in the treatment of the hepatorenal syndrome and variceal bleeding. However, terlipressin may compromise cardiac function and induce ischemia. AIM: Therefore, we aimed to assess the effects of terlipressin on cardiac function and perfusion. METHODS: Twenty-four patients with cirrhosis and ascites participated, including nine with refractory ascites. Gated myocardial perfusion imaging, mean arterial blood pressure (MAP), cardiac output (CO), ejection fraction (EF), end-diastolic volume (EDV), perfusion, and motion of the myocardium were determined before and after a bolus injection of 2 mg terlipressin. RESULTS: MAP increased after terlipressin (P value of less than 0.001). EF and CO fell by -16 and -17%, respectively in the terlipressin group versus 1 and -2%, respectively in the placebo group (P value of less than 0.001 and P value of less than 0.01). In the terlipressin group, EDV increased by 18 versus -4% in the placebo group (P value of less than 0.01). Wall motion in the anterior and posterior walls fell by -18 and -22%, respectively after terlipressin treatment versus 0 and 0% in the placebo group (P value of less than 0.01). In contrast, myocardial perfusion and stroke volume were unaltered in both the groups. The change in EF during terlipressin treatment correlated significantly with the change in MAP (r=-0.60, P value <0.002). Patients with refractory ascites had a higher EF and lower EDV and ESV than the patients with nonrefractory ascites, both at baseline and after terlipressin treatment. The decrease in the left ventricular wall thickening and wall motion correlated with the Child--Pugh score, r=-0.59, P=0.005 and r=-0.48, P=0.03. CONCLUSION: In advanced cirrhosis, the increase in afterload and EDV after terlipressin treatment result in a decrease in left ventricular wall motion, resulting in reduced CO and EF, but myocardial perfusion is preserved. Alteration in cardiac function at baseline and after terlipressin treatment relates to the stage of decompensation.
Authors: Francisco Sampaio; Pablo Lamata; Nuno Bettencourt; Sophie Charlotte Alt; Nuno Ferreira; Johannes Tammo Kowallick; Joana Pimenta; Shelby Kutty; José Fraga; Michael Steinmetz; Paulo Bettencourt; Vasco Gama; Andreas Schuster Journal: J Cardiovasc Magn Reson Date: 2015-07-18 Impact factor: 5.364
Authors: Banu Demet Ozel Coskun; Ahmet Karaman; Hasan Gorkem; Irfan Buğday; Orhan Kursad Poyrazoğlu; Fatma Senel Journal: Am J Case Rep Date: 2014-10-31