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Fifty one patients (pts) with various heart diseases and 6 normal subjects (N) were studied. Four of the 51 pts showed unusually high GOT values (greater than 3000 IU) without preceding evidence of acute heart failure, myocardial infarction, or hepatitis. Of these 4 pts, either ventricular tachyarrhythmias, marked bradycardia, or rapid ventricular response with atrial fibrillation (af) were evident a few days prior to the GOT elevation. GOT values returned to below 100 IU within a few days, but hypotension and frequent arrhythmias were sustained in 3 of the 4 pts and these 3 pts died about one month later. The symptoms of the remaining one improved but he too died 9 months later of ventricular fibrillation. A postmortem histological examination revealed centrilobular necrosis of the liver cells. Thus, abnormal GOT elevation may result from hepatic cell necrosis, which is probably due to tissue hypoperfusion caused by severe arrhythmias. Hepatic venous flow velocity (HFV) was measured in the remaining 47 pts and 6N using a pulsed doppler echocardiogram. The HFV curve was biphasic, with the first curve corresponding to the forward flow velocity during ventricular systole (s-HFV) and the second corresponding to ventricular diastole (d-HFV). The ratio of the area under s-HFV curve to the sum of areas under s-HFV and d-HFV curves was defined as the VI ratio. In N, the VI ratio was 0.7 +/- 0.06 whereas the VI ratio in pts in sinus rhythm tended to be above 0.7. This indicated that s-HFV is greater than d-HFV in N while s-HFV is less than d-HFV in pts in sinus rhythm. There was a good negative correlation (n = 15: r = -0.70) between VI ratio and cardiac index (CI) in these pts, suggesting that the contribution of s-HFV to the venous return becomes greater as the cardiac function becomes more impaired. In pts with af, the VI ratio was below 0.5 and there was a good positive correlation (n = 14: r = 0.82) between the VI ratio and CI. This suggested that the s-HFV may be reduced due to a lack of atrial contribution in af so that contribution of d-HFV to venous return becomes greater as the cardiac function becomes more impaired. Thus, the HFV pattern may reflect the abnormality of the cardiac pump function in human beings.

Liver function in congestive heart failure: Abnormal elevation of serum hepatic enzyme and hepatic venous flow velocity.