Cirrhotic Cardiomyopathy: Getting to the Heart of the Matter

Abstract

can lead to liver dysfunction and damage. How unexpected In cirrhosis, cardiac contractile function has been exand gratifying, therefore, to find a voice as eloquent as the tensively documented to be abnormal. At baseline, carlate Chilean Nobel laureate's to not only extoll the many diac output is increased, and this is one of the charactervirtues of the liver, but also remind us that sometimes the istics of hyperdynamic circulation. However, when liver takes precedence over the heart, i.e., that liver failure cirrhotic patients are challenged by pharmacological or can also lead to cardiac dysfunction. physiological stress, ventricular hyporesponsiveness is It has been known for more than four decades that hepatic revealed. Similar patterns have been noted in cirrhotic cirrhosis is associated with a host of cardiovascular abnoranimal models. This phenomenon has been termed ''cirmalities. The initial studies in the early 1950s documented rhotic cardiomyopathy.'' Although alcohol abuse may the existence of hyperdynamic circulation in cirrhosis, manicontribute to some cases of cirrhotic cardiomyopathy, it has been clearly documented to occur even in the ab-fested by increased cardiac output and reduced systemic vassence of alcohol ingestion. Diminished myocardial b-ad-cular resistance. This latter phenomenon, the peripheral varenergic receptor signal transduction function, possibly sodilatation, continues to fascinate investigators even up to caused by a persistent elevation in norepinephrine con-the present, and recent studies have examined the possible tent, has been shown to play an important role. Alter-role of nitric oxide and other endothelium-dependent factors ation in cardiac plasma membrane properties due to im-in mediating the vasodilatation. The heart itself was not expaired lipid metabolism is also crucial. Other possible amined until about three decades ago, and around that time pathogenic factors are reviewed, including accumula-studies of cardiac contractile function in patients with alcotion of cardiodepressant substances caused by hepato-holic-induced liver disease started consistently showing that cellular insufficiency, and ventricular overload sec-despite the increased baseline cardiac output, when ventricuondary to increased blood volume and hyperdynamic lar contractile responses were tested under conditions of circulation. Because the cardiac reserve function is bor-pharmacological or physiological stress, the heart behaved derline in patients with cirrhosis, cardiovascular status abnormally in a blunted manner. For many years, this was should be carefully monitored, especially when patients ascribed to the well-known direct toxic effects of alcohol on undergo stresses such as liver transplantation or porto-cardiac muscle, i.e., as a manifestation of latent or subclinical systemic shunting procedures. (HEPATOLOGY 1996;24: alcoholic cardiomyopathy, and relegated to the scientific 451-459.)backwaters as a clinically insignificant curiosity. However, recently several studies have emerged in both ...

Beneficial hemodynamic effects of bosentan, a mixed ETA and ETB receptor antagonist, in portal hypertensive rats

“…Some studies have demonstrated that bile salts affect heart contractility. 32 Because we have previously demonstrated a clear correlation between ET-1 plasma concentrations and bilirubin levels in cirrhotic patients by multiple regression analysis, 5 there may be more marked effect of an ET-1 antagonist in secondary biliary cirrhosis rats with high plasma bilirubin levels.…”

Post-liver transplantation myocardial dysfunction

“…This phenomenon has been termed cirrhotic cardiomyopathy and is believed to be caused by a combination of factors, including impairment of cardiac ␤-adrenergic receptors, changes in the properties of the cardiac cell membrane, abnormalities in circulating humoral factors, and ventricular overload induced by the hyperdynamic circulation. 10 It is also known that intraoperative manipulation of the liver during OLT releases cytokines and endotoxins that mediate an inflammatory response. 11,12 In animal studies, infusion of these cytokines has been shown to cause myocardial depression.…”

Efecto de la pentoxifilina en la supervivencia, la función cardiaca y en la hemodinámica portal y sistémica de la cirrosis alcohólica avanzada: a randomized double-blind placebo-controlled trial

“…Estas alteraciones hemodinámicas predicen una supervivencia menor en estos pacientes (6). Estos pacientes también presentan modificaciones cardiacas subclínicas como una disfunción diastólica y disminución de la contractilidad cardiaca con el esfuerzo físico o cuando son sometidos a una sobrecarga farmacológica, lo que puede contribuir al empeoramiento de las alteraciones hemodinámicas sistémicas (7,8). Ma y Lee fueron los primeros en describir esta miocardiopatía (8), que se asocia a la aparición de áreas de fibrosis ventricular, focos de edema e hipertrofia o dilatación (9,10).…”