Effects of a single terlipressin administration on cardiac function and perfusion in cirrhosis
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Effects of a single terlipressin administration on cardiac function and perfusion in cirrhosis. / Krag, Aleksander; Bendtsen, Flemming; Mortensen, Christian; Henriksen, Jens H; Møller, Søren.
I: European Journal of Gastroenterology and Hepathology, Bind 22, Nr. 9, 09.2010, s. 1085-92.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Effects of a single terlipressin administration on cardiac function and perfusion in cirrhosis
AU - Krag, Aleksander
AU - Bendtsen, Flemming
AU - Mortensen, Christian
AU - Henriksen, Jens H
AU - Møller, Søren
PY - 2010/9
Y1 - 2010/9
N2 - 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.
AB - 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.
KW - Aged
KW - Ascites
KW - Blood Pressure
KW - Cardiac Output
KW - Electrocardiography
KW - Female
KW - Heart Function Tests
KW - Humans
KW - Liver Cirrhosis
KW - Lypressin
KW - Male
KW - Middle Aged
KW - Stroke Volume
KW - Tomography, Emission-Computed, Single-Photon
KW - Vasoconstrictor Agents
KW - Ventricular Function, Left
U2 - 10.1097/MEG.0b013e32833a4822
DO - 10.1097/MEG.0b013e32833a4822
M3 - Journal article
C2 - 20453655
VL - 22
SP - 1085
EP - 1092
JO - European Journal of Gastroenterology and Hepatology, Supplement
JF - European Journal of Gastroenterology and Hepatology, Supplement
SN - 0954-691X
IS - 9
ER -
ID: 32478559