From the Guidelines
Liver cirrhosis can cause heart failure through various mechanisms, including cirrhotic cardiomyopathy, hyperdynamic circulation, and hepatopulmonary syndrome. This occurs when the chronic liver disease leads to structural and functional abnormalities in the heart, resulting in a weakened and less efficient heart muscle that can eventually progress to heart failure 1. Additionally, advanced cirrhosis often leads to a hyperdynamic circulation state with increased cardiac output and decreased systemic vascular resistance, which can further strain the heart. Portal hypertension from cirrhosis can also contribute to pulmonary hypertension, affecting oxygen levels and heart function.
Key Mechanisms
- Cirrhotic cardiomyopathy: characterized by diastolic dysfunction, which can be diagnosed using the recent ASE guidelines, namely: Average E/e’>14; Tricuspid velocity >2.8 m/s and LAVI >34 ml/m2 1
- Hyperdynamic circulation: demonstrated by a low arterial blood pressure and increased cardiac output, which can be exacerbated by worsening inflammation in patients with acute-on-chronic liver failure 1
- Hepatopulmonary syndrome: characterized by abnormal dilation of lung blood vessels, affecting oxygen levels and heart function 1
Management
Patients with cirrhosis should undergo regular cardiac evaluation, including echocardiograms and electrocardiograms. Management typically involves treating the underlying liver disease while addressing cardiac symptoms with medications like beta-blockers, ACE inhibitors, or diuretics as needed 1. The connection between these two organs highlights the importance of a comprehensive approach to treating patients with liver cirrhosis. According to the most recent guidelines, early baseline assessment of volume status, perfusion, and cardiovascular function should be performed in all critically ill patients with cirrhosis, and bedside echocardiography can be useful to evaluate volume status and cardiac function in patients with cirrhosis and hypotension or shock 1.
From the Research
Liver Cirrhosis and Heart Failure
- Liver cirrhosis can lead to a condition known as cirrhotic cardiomyopathy (CCM), which is defined as cardiac dysfunction associated with cirrhosis in the absence of pre-existing heart disease 2, 3, 4.
- CCM can manifest as the enlargement of cardiac chambers, attenuated systolic and diastolic contractile responses to stress stimuli, and repolarization changes 2.
- The condition can significantly contribute to mortality and morbidity in patients who undergo liver transplantation and contributes to the pathogenesis of hepatorenal syndrome/acute kidney injury 2, 3.
Pathophysiology of Cirrhotic Cardiomyopathy
- The principal pathophysiological mechanisms of CCM include hyperdynamic circulation with increased cardiac output, heart rate, and reduced systemic vascular resistance 3.
- Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output, lead to fluid accumulation, venostasis, and cardiac dysfunction 4.
- Autocrine and endocrine proinflammatory cytokines, as well as systemic endotoxemia, contribute to myocardial remodeling and fibrosis, which further compromise the contractility and relaxation of the heart 4.
Clinical Implications and Treatment
- CCM can progress to heart failure during invasive procedures such as surgery, insertion of a transjugular intrahepatic portosystemic shunting (TIPS), and liver transplantation 3, 5.
- The treatment of CCM is largely similar to that of heart failure, with diuretics playing a central role 4, 6.
- Non-selective beta-blockers may be used to optimize the neurohumoral pathologic axis that perpetuates CCM, although their effect on prognosis is unclear 4, 6.
- Liver transplantation is considered the most effective treatment for CCM, with significant improvement in cardiac function and survival rates 6, 5.