Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations

Abstract

Cardiac hepatopathy, hepatic injury caused by cardiac dysfunction, is a common entity but has been characterized incompletely, particularly the relationship between hemodynamics and histology. We aimed to describe the clinical, biochemical, hemodynamic, and histologic characteristics of this disorder. Eighty-three patients from 2 tertiary referral centers were studied. Patients were divided into 3 groups based on the duration of cardiac dysfunction: (1) acute (n ‫؍‬ 12); (2) chronic (n ‫؍‬ 53); and (3) acute on chronic (n ‫؍‬ 18). Results showed that serum aminotransferase levels were increased typically, particularly in the acute group (median aspartate aminotransferase level was 30. . The hepatic venous pressure gradient was normal in most (81%), correlated moderately with the aminotransferase levels (aspartate aminotransferase level: r ‫؍‬ .59; P < .0001), and associated with the presence of centrilobular necrosis and inflammation, periportal necrosis, and stainable hepatic iron (P < .05 for all comparisons), but not fibrosis. Sinusoidal dilatation was associated with higher right atrial (P ‫؍‬ .047) and free hepatic venous pressures (P ‫؍‬ .06). Although cirrhosis was rare (n ‫؍‬ 1), centrilobular fibrosis was common (74%) and not associated with any hemodynamic measurement. In conclusion, cardiac hepatopathy has diverse clinical, hemodynamic, and histologic manifestations that vary with the temporal course of cardiac dysfunction. Hepatic fibrosis is common, but does not correlate with systemic or hepatic hemodynamics. (HEPATOLOGY 2003;37:393-400.)

Congestive hepatic fibrosis score: a novel histologic assessment of clinical severity

“…Sinusoidal dilatation was also associated with higher right atrial and free hepatic venous pressures. 5 It is noteworthy that the aforementioned studies included a heterogeneous patient cohort with various cardiac diseases and shock. In a large autopsy series of 1000 subjects with cardiac dysfunction, Arcidi et al 3 reported that hepatic centrilobular necrosis often occurred in the setting of shock, whereas elevated central venous pressure often manifested as centrilobular congestion.…”

“…[2][3][4] The progression to advanced-stage disease (cardiac cirrhosis), however, remains rare, despite the common manifestation of centrilobular fibrosis. 2,5 In one pertinent autopsy series, centrilobular congestion was closely associated with clinical conditions that present as elevated central venous pressure, whereas centrilobular necrosis often occurred in the setting of shock. 3 Although hemodynamic derangement induces cardiac hepatopathy, very few studies have correlated hemodynamic parameters with histological findings.…”

“…3 Although hemodynamic derangement induces cardiac hepatopathy, very few studies have correlated hemodynamic parameters with histological findings. In one such analysis, Myers et al 5 reported that elevated right atrial pressure and hepatic venous pressure were associated with the presence of centrilobular necrosis, inflammation, and sinusoidal dilatation, but surprisingly, not with hepatic fibrosis. Because the latter observations raise concerns about the reproducibility of histopathologic observations in cardiac hepatopathy, we believe that ongoing investigations of this condition, including metaanalyses of existing studies, would be aided by a robust histologic scoring system.…”

How to interpret liver function tests in heart failure patients?

“…Although there is no consensus on terminology, "cardiac hepatopathy" has generally been used to describe any liver damage caused by cardiac disorders in the absence of other possible causes of liver damage (13)(14)(15)(16). In cardiac hepatopathy, the primary pathophysiology is either passive venous congestion that results in "congestive hepatopathy (CH)" or low cardiac output and arterial hypoperfusion that results in "acute cardiogenic liver injury (ACLI)" (14,15,17,18).…”

“…The main histological finding in a congestive liver is hemorrhage and necrosis of zone 3 of the Rappaport acinus with normal or mildly steatotic areas in zones 1 and 2 (9,11,13,21). Because obesity, hyperlipidemia, and diabetes are common risk factors for both HF and hepatosteatosis, non-alcoholic hepatosteatosis is frequently observed in CH patients (9,14,22).…”