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"Byung Su Yoo"

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"Byung Su Yoo"

Original Article
Dobutamine stress echocardiography for evaluating cirrhotic cardiomyopathy in liver cirrhosis
Moon Young Kim, Soon Koo Baik, Chan Sik Won, Hong Jun Park, Hyo Keun Jeon, Hyun Il Hong, Jae Woo Kim, Hyun Soo Kim, Sang Ok Kwon, Jang Young Kim, Byung Su Yoo, Seung Hwan Lee
Korean J Hepatol 2010;16(4):376-382.
Published online December 31, 2010
DOI: https://doi.org/10.3350/kjhep.2010.16.4.376
Background/Aims

The blunted ventricular systolic and diastolic contractile responses to physical and pharmacological stress in cirrhosis are termed cirrhotic cardiomyopathy (CCM). CCM has been known to involve multiple defects in the β-adrenergic signaling pathway. The aim of this study was to determine whether cirrhotic patients have blunted cardiac responses to catecholamine stimulation through dobutamine stress echocardiography (DSE).

Methods

Seventy-one cirrhotic patients with normal left ventricular (LV) chamber size and ejection fraction were enrolled. The LV systolic and diastolic functions were evaluated by two-dimensional and Doppler echocardiography at rest and during peak dobutamine infusion (40 µg/kg/min). An abnormal response was defined as a decrease of less than 10% in LV end-diastolic volume, a decrease of less than 20% in end-systolic volume, and an increase of less than 10% in LV ejection fraction (EF) at peak dobutamine infusion, based on previously used criteria. The early/late diastolic flow (E/A) ratio and diastolic parameters were also measured.

Results

A blunted LV response to dobutamine was observed in 18 of 71 cirrhotic patients (25.4%). The baseline EF was significantly higher in 18 patients with a blunted DSE response than that of those with a normal DSE response (P<0.05). The baseline and peak E/A ratios, which are common diastolic dysfunction markers, were higher in the cirrhosis group than in the control group (P<0.001). No adverse events associated with DSE were observed.

Conclusions

Blunted cardiac responses to dobutamine stimulation, which are implicated in defects in the β-adrenergic signaling pathway, might contribute to the pathogenesis of CCM in patients with cirrhosis.

Citations

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