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Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations
Robert P Myers1, Raimondo Cerini, Raymond Sayegh
1Liver Unit, University of Calgary, Alberta, Canada.
Insights
Cardiac hepatopathy, liver injury from heart dysfunction, shows varied clinical and histological signs based on duration. Elevated liver enzymes and fibrosis are common, but don't always link to heart pressures.
Area of Science:
- Cardiology
- Hepatology
- Pathology
Background:
- Cardiac hepatopathy, liver injury due to cardiac dysfunction, is prevalent but incompletely understood.
- The interplay between hemodynamic status and histological liver changes requires further elucidation.
Purpose of the Study:
- To comprehensively describe the clinical, biochemical, hemodynamic, and histological features of cardiac hepatopathy.
- To investigate the relationship between cardiac dysfunction duration, hemodynamics, and liver histology.
Main Methods:
- Retrospective analysis of 83 patients with cardiac dysfunction from two tertiary centers.
- Categorization into acute, chronic, and acute-on-chronic cardiac dysfunction groups.
- Assessment of clinical, biochemical (serum aminotransferases), hemodynamic (pressures), and histological (liver biopsy) data.
Main Results:
- Elevated aminotransferase levels were prominent, especially in acute cardiac dysfunction.
- Key hemodynamic findings included elevated right atrial and hepatic venous pressures.
- Histology revealed centrilobular necrosis, inflammation, and hepatic iron, with common centrilobular fibrosis (74%) unrelated to hemodynamics.
Conclusions:
- Cardiac hepatopathy presents diverse manifestations influenced by the temporal course of cardiac dysfunction.
- While hepatic fibrosis is frequent, it does not correlate with systemic or hepatic hemodynamic parameters.
- Understanding these varied presentations is crucial for managing patients with heart failure and liver injury.
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 30.2 times the upper limit of normal [range, 1-100]; P <.0001 vs. the chronic group). The most salient hemodynamic features were elevated right atrial (14 mm Hg [range, 1-29]), and hepatic venous pressures (wedged: 18 mm Hg [range, 5-35]; free: 15 mm Hg [range, 2-30]). 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.