Liver disease in tricuspid regurgitation: from congestion to cirrhosis

Tricuspid regurgitation (TR) and right-sided heart failure are firmly established as markers of adverse prognosis.1,2 Over the past decade, the expansion of surgical and transcatheter tricuspid interventions has reinforced the concept that TR is not an isolated valvular lesion but a systemic disorder with multisystem consequences.3,4 Hepatic involvement represents one of the most characteristic yet incompletely defined manifestations. Greater TR severity, longer disease duration, and elevated right-sided filling pressures are associated with increased liver stiffness, consistent with progressive congestive hepatopathy.5,6 Hemodynamically, sustained elevation of right atrial pressure leads to transmission of venous hypertension to the hepatic circulation, exposing the liver to chronic backward failure. Over time, persistent congestion results in sinusoidal dilatation and centrilobular injury, which may progress to centrilobular and central–central bridging fibrosis. In advanced stages, regenerative nodules can develop, a pattern histologically referred to as cardiac cirrhosis.7 This pattern differs from cirrhosis due to primary liver diseases, which is characterized by predominantly portal-based fibrosis. Whether chronic venous congestion alone is sufficient to cause true cirrhosis with clinically relevant complications, including hepatocellular carcinoma (HCC), remains a matter of ongoing debate.8