Cirrhotic cardiomyopathy (CCM), cardiac dysfunction in end-stage liver disease in the absence of prior heart disease, is an important clinical entity that contributes significantly to morbidity and mortality. The original definition for CCM, established in 2005 at the World Congress of Gastroenterology (WCG), was based upon known echocardiographic parameters to identify subclinical cardiac dysfunction in the absence of overt structural abnormalities. Subsequent advances in cardiovascular imaging and in particular myocardial deformation imaging have rendered the WCG criteria outdated. A number of investigations have explored other factors relevant to CCM, including serum markers, electrocardiography, and magnetic resonance imaging. CCM characteristics include a hyperdynamic circulatory state, impaired contractility, altered diastolic relaxation, and electrophysiological abnormalities, particularly QT interval prolongation. It is now known that cardiac dysfunction worsens with the progression of cirrhosis. Treatment for CCM has traditionally been limited to supportive efforts, but new pharmacological studies appear promising. Left ventricular diastolic dysfunction in CCM can be improved by targeted heart rate reduction. Ivabradine combined with carvedilol improves left ventricular diastolic dysfunction through targeted heart rate reduction, and this regimen can improve survival in patients with cirrhosis. Orthotopic liver transplantation also appears to improve CCM.
1. Introduction
Cirrhosis is associated with multiple cardiovascular changes including the development of a hyperdynamic circulation and cardiac dysfunction. Cirrhotic cardiomyopathy, a form of cardiac failure associated with cirrhosis of any cause, is the end result of complex circulatory and humoral changes. Cirrhotic cardiomyopathy may have a prevalence of up to 60% [
1]. It is present in both adult and paediatric patients with cirrhosis and a major cause for morbidity and mortality [
2]. The Gastroenterology World Congress 2005 defined a triad () of clinical features associated with cirrhotic cardiomyopathy, such as systolic dysfunction, seen as a blunting of the usual cardiac response to stress; diastolic dysfunction; and electrical dysfunction [
3,
4]. The technical definition [
5] () has not kept pace with recent advances in cardiac imaging and the diagnosis of systolic and diastolic dysfunction. Izzy et al. have proposed new technical definitions [
6] () based on recent advances in cardiac imaging. In this review, we will comprehensively outline up to date research on the pathophysiology of CCM and address the latest advances in diagnostic imaging and management.
Table 1. Diagnostic criteria for cirrhotic cardiomyopathy, proposed by the Gastroenterology World Congress.
Systolic Dysfunction |
Diastolic Dysfunction |
Supportive Criteria |
Blunted increase in cardiac output on exercise, volume challenge or pharmacological stimuli |
E/A ratio <1.0 (age-corrected) |
Prolonged Q-Tc interval |
Resting ejection fraction <55% |
Prolonged deceleration time (<200 ms) |
Enlarged left atrium |
|
Prolonged isovolumetric relaxation time (<80 ms) |
Increased myocardial mass |
|
Electrophysiological abnormalities |
Increased BNP and pro-BNP |
|
Abnormal chronotropic response |
Increased troponin I |
|
Electromechanical uncoupling/dys-synchrony |
|
Table 2. Proposed updated criteria for cirrhotic cardiomyopathy.
Systolic Dysfunction |
Advanced Diastolic Dysfunction |
Areas for Future Research Which Require Further Validation |
Any of the following LV ejection fraction ≤50 % |
≥3 of the following |
Abnormal chronotropic or inotropic response |
Absolute GLS <18% or >22% |
Septal é velocity <7 cm/s |
Electrocardiographic changes |
|
E/é ratio ≥15 |
Electromechanical uncoupling |
|
LAVI >34 mL/m2 |
Myocardial mass change |
|
TR velocity >2.8 m/s |
Serum biomarkers |
|
|
Chamber enlargement |
|
|
CMRI |
This entry is adapted from the peer-reviewed paper 10.3390/gastroent12010008