Etiology and Pathophysiology of ACS in LC
Several important considerations make the etiology and pathophysiology of ACS unique in patients with LC when compared to the general population.
The liver is a site of synthesis of most pro-coagulant and anticoagulant factors, which are collectively involved in the process of fibrinolysis. At the same time, it acts as a port in clearance of hemostatic and fibrinolytic proteins. Therefore, LC predisposes to a labile equilibrium of thrombosis and bleeding, the so called "rebalanced" hemostatic system (Figure 2). So, even those LC patients with low platelet counts or prolonged coagulation parameters have an increased tendency to present with arterial or venous thrombosis. From a clinical perspective, the common misperception that patients with LC are "auto-anticoagulated" and thereby protected from thrombotic disease frequently leads to inadequate dosing of antithrombotic agents. NAFLD patients have a similar metabolic as well as inflammatory milieu as observed in CAD. It is possible that this "double-hit" of cardiometabolic syndrome and hepatic dysfunction contribute to worse outcomes in this group. The presence of hypernatremia is associated with poor short- and long-term prognoses in LC patients presenting with ACS.
Schematic description of abnormalities of hemostatic mechanisms in LC patients. ADAMTS13 a disintegrin and metalloproteinase with a thrombospondin type 1 motif-member 13, AT III antithrombin III, LC liver cirrhosis, NO nitric oxide, PAI-1 plasminogen activator inhibitor-1, PC protein C, PS protein S, TAFI thrombin activatable fibrinolysis inhibitor, tPA tissue plasminogen activator, vWF von Willebrand factor
LC is a dynamic disease that adversely and mutually aggravates other organs such as the heart. The Child–Pugh classification has been used to assess the degree of severity as well as the subsequent risk of performing interventions in LC patients (Table 1).
Am J Cardiovasc Drugs. 2022;22(1):55-67. © 2022 Adis Springer International Publishing AG