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The liver is a crucial metabolic organ that has a key role in maintaining immune and endocrine homeostasis. Accumulating evidence suggests that chronic liver disease might promote the development of various cardiac disorders (such as arrhythmias and cardiomyopathy) and circulatory complications (including systemic, splanchnic and pulmonary complications), which can eventually culminate in clinical conditions ranging from portal and pulmonary hypertension to pulmonary, cardiac and renal failure, ascites and encephalopathy. Liver diseases can affect cardiovascular function during the early stages of disease progression. The development of cardiovascular diseases in patients with chronic liver failure is associated with increased morbidity and mortality, and cardiovascular complications can in turn affect liver function and liver disease progression. Furthermore, numerous infectious, inflammatory, metabolic and genetic diseases, as well as alcohol abuse can also influence both hepatic and cardiovascular outcomes. In this Review, we highlight how chronic liver diseases and associated cardiovascular effects can influence different organ pathologies. Furthermore, we explore the potential roles of inflammation, oxidative stress, vasoactive mediator imbalance, dysregulated endocannabinoid and autonomic nervous systems and endothelial dysfunction in mediating the complex interplay between the liver and the systemic vasculature that results in the development of the extrahepatic complications of chronic liver disease. The roles of ageing, sex, the gut microbiome and organ transplantation in this complex interplay are also discussed.

Interplay of cardiovascular mediators, oxidative stress and inflammation in liver disease and its complications.

Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Ce signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models.

Peripheral systems: neuropathy.

Reduced heart rate variability and baroreflex sensitivity in primary biliary cirrhosis

In patients affected by hepatic cirrhosis, autonomic dysfunction is a common finding; usually it is asymptomatic but it may correlate with increased mortality and morbidity before, during and after liver transplant, due to hemodynamic instability in the course of stressful events like sepsis, gastrointestinal bleeding and reperfusion after transplantation surgery. Hyperdynamic circulation and hepatic dysfunction seem to play a role in the pathogenesis of autonomic dysfunction, even if pathophysiological mechanisms are not completely known. We present a revision of previous literature about prevalence, pathophysiological mechanisms, clinical features, and mortality and morbidity of autonomic dysfunction secondary to hepatic cirrhosis.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/liv.13126

The role of autonomic dysfunction in cirrhotic patients before and after liver transplantation. Review of the literature

Patients with liver cirrhosis have autonomic dysfunction and complex cardiovascular changes. Increases risk for sudden cardiac death (SCD) was recently recognized in liver cirrhosis. This study analyzed risk predictors for SCD related to autonomic dysfunction in patients with alcoholic liver cirrhosis (ALC). Twenty five patients with ALC were examined and compared with healthy control group. Cardiovascular autonomic reflex tests, comprehensive ECG with QTc interval, late potentials, short-term heart rate variability (HRV) analysis (time domain, spectral and nonlinear-Poincare plot analysis) and 24-h Holter ECG with long-term HRV analysis were done. According to autonomic reflex tests patients with ALC had high incidence (56%) of severe autonomic dysfunction, manifested as pronounced damage of vagal function. Patients had significantly depressed HRV (SDNN, SDANN, triangular index, LF and HF) and more frequently had serious arrhythmias, prolonged QTc and Poincare plot in a shape of dot (p < 0.001). In patient group QTc significantly inversely correlated with spectral components from short-term HRV analysis (ln(LF): r = -0.53, ln(HF): r = -0.47; p < 0.05), and Lown class significantly correlated with total autonomic function score (r = 0.64, p = 0.04). This study indicates that in ALC autonomic neuropathy with vagal impairment and sympathetic predominance is related to SCD risk predictors and onset of serious ventricular arrhythmias.

/pdf/autonomic-dysfunction-in-alcoholic-cirrhosis-and-its-3bld7k4li8.pdf

Danijela Trifunovic

Papers

Autonomic dysfunction in alcoholic cirrhosis and its relation to sudden cardiac death risk predictors.