Peripheral vasodilatation exists universally in patients with cirrhosis and therefore, unless the heart is stressed, overt ventricular failure is usually absent. In effect, the vasodilatation “auto-treats” the latent heart failure and may mask its presence. Physicians need to be vigilant when patients with cirrhosis face challenges such as TIPS insertion, infection, or LT. If overt heart failure occurs, general supportive treatment should be applied which includes bed rest, administration of oxygen, salt and water restriction, diuretic therapy, and careful preload reduction by appropriate drugs.

One of the effective treatments for noncirrhotic heart failure is vasodilators. However, due to the peculiar hemodynamic disturbances of cirrhosis that includes marked vasodilatation, afterload reduction with vasodilators may not be useful in cirrhotic cardiomyopathy. Indeed, vasodilators may aggravate the arterial hypotension and further decrease the effective circulating volume. In terms of other, more specific treatments to improve heart failure in cirrhotic cardiomyopathy, there is a major paucity of clinical trials in an area of urgent need for such studies. The scant evidence of various drug treatments can be summarized as follows.

Sympathetic nervous activity is significantly increased in cirrhotic patients [53]; thus, β-blockers may protect the heart from damage resulting from the over-activated sympathetic system. It is well documented that β-blockers (propranolol/nadolol) and combined α- and β-blockers (carvedilol) are effective in decreasing portal venous hypertension and for prophylaxis of variceal bleeding in cirrhotic patients [54].

As mentioned previously, cardiovascular events occur in many patients after LT. Chopra et al. [55] demonstrated that during the perioperative period, a significant catecholamine surge occurs, producing elevations in heart rate and blood pressure. Safadi and colleagues tested the protective effects of β-blockers in the perioperative period of LT [56]. They found that these drugs attenuate both the sympathetic and neuroendocrine responses to stress; they balance myocardial oxygen supply/demand mismatch, and reduce inflammatory markers and free radicals. Therefore, β-blockers protected patients undergoing LT from adverse cardiac outcomes during the perioperative period. β-blockers significantly increased the probability of survival in the early postoperative period (30 days) in liver recipients [56].

Prolonged QT interval is associated with severe arrhythmias and sudden death in patients with noncirrhotic heart disease, but whether this applies to cirrhotic patients with prolonged QT interval remains unclear [53]. However, Zambruni and colleagues showed that in 30 patients with cirrhosis, chronic β-blocker dosing over 1–3 months significantly shortened the QTc interval, but only in the subgroup of those who had a baseline prolonged QTc interval [57]. Again, whether normalizing the prolonged QT interval exerts any long-term beneficial effect remains unknown, but most clinicians would agree that this certainly could not do any harm and may very well be beneficial.

There are some controversies over β-blocker usage in some specific subgroups of patients with cirrhosis. Krag and colleagues postulated that in HRS, treatment with β-blockers further decreases heart rate and CO and may therefore have deleterious effects on hemodynamics and renal function and thereby reduce survival [58].

For type 1 HRS, systemic vasoconstrictors combined with plasma expansion are currently the only available form of pharmacologic therapy. The combined administration of intravenous albumin and vasoconstrictors (e.g., terlipressin or alpha-1 agonists) normalizes circulatory function and serum creatinine in a significant number of patients with type 1 HRS. These effects, however, are rarely obtained when vasoconstrictors or intravenous albumin are given alone [51].

Splanchnic vasoconstrictors and albumin coadministration counteract the intense vasodilation in the splanchnic bed, thereby improving effective arterial blood volume. This improvement, in turn, suppresses the endogenous vasoconstrictors (e.g., renin-angiotensin-aldosterone system, RAAS;SNS) that are responsible for renal vasoconstriction. Albumin administration, by expanding the circulating blood volume, on one hand, increases cardiac preload and CO and on the other hand, improves glomerular filtration rate [59].

The RAAS is the most important system controlling blood pressure, cardiovascular, and renal function. Moreover, RAAS activation may be a prime regulator of fibrogenesis in several tissues including the heart. Several clinical trials suggest that RAAS blockade is the single most important cardioprotective strategy for cardiovascular diseases [60]. Since the RAAS is activated in cirrhotic patients [61], it is rational to speculate that RAAS blockade will exert cardioprotective effects on cirrhotic cardiomyopathy. Ponzi et al. conducted the only RAAS-related study on cirrhotic cardiomyopathy [62]. They administrated the aldosterone antagonist potassium canrenoate to Child class A post-viral preascitic cirrhotic patients. After 6 months of treatment, the authors found some improvement in left ventricular hypertrophy and wall thickness, and a trend towards improved diastolic function indices that did not reach statistical significance; however, they suggested that 6 months was an insufficient duration to see significant normalization of diastolic dysfunction ; a longer course of treatment was probably needed. These results suggest that aldosterone antagonists, probably through an anti-fibrogenic effect may improve the morphologic myocardial changes or at least retard or block the contractility deterioration in cirrhotic cardiomyopathy. These results also suggest that drugs blocking the fibrogenic effects of the aldosterone system are beneficial, and that cardiac remodeling might occur in cirrhosis. Much more research is necessary.

In summary, cirrhotic cardiomyopathy manifests as heart failure under challenges such as physical stress and surgery. The mechanisms are not clear—NO, carbon monoxide, endocanabinoinds, and apoptosis may all play a role. There is no specific treatment. β-adrenergic blocker may protect the heart from damage resulting from the over-activated sympathetic system, while long-term aldosterone antagonists administration may be helpful. Albumin may improve cardiac function. LT eventually normalizes heart function.