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Purpose of Review: Cirrhotic cardiomyopathy (CCM) is a clinical entity that reflects the maladaptive responses of the heart to advanced chronic liver disease. With the recent developments in this field, this review details the most up to date knowledge about the pathogenesis of CCM, recent changes in its diagnostic criteria, and its clinical relevance. Recent Findings: Advances in echocardiographic techniques over the last several years and recent research have highlighted the high prevalence of CCM approaching 35% and demonstrated adverse impact of CCM on clinical outcomes following transjugular intrahepatic portosystemic shunting (TIPS) and liver transplantation (LT). Summary: The diagnostic criteria for cirrhotic cardiomyopathy have evolved with advancements in echocardiographic techniques allowing for precise and perhaps timely identification of those with subclinical cardiac impairment. CCM increases the risk for adverse outcomes in patients with cirrhosis and liver transplant recipients. Future studies are needed to identify subgroups of patients at highest risk for cirrhotic cardiomyopathy, the frequency and duration of monitoring for those with CCM, and potential therapeutics for patients with cirrhosis and liver transplant who have been diagnosed with cirrhotic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Background: Cirrhotic cardiomyopathy, an intricate and multifaceted complication of end-stage liver disease, manifests as systolic and diastolic dysfunction in patients without previously diagnosed cardiac disease. Our study aims to investigate the prevalence of systolic and diastolic function in patients with cirrhotic cardiomyopathy in our region. Methods: We conducted a cross-sectional study on 68 patients with established cirrhosis, and no overt cardiac manifestations, who consequently underwent 2D echocardiography to quantify systolic and diastolic dysfunction, as defined by the 2019 Cirrhotic Cardiomyopathy Consortium. The severity of cirrhosis was determined using various validated scoring systems. Results: A total of 19 out of 68 (28%) had systolic dysfunction, while 6/68 (9%) had evidence of diastolic dysfunction. Overall prevalence of cirrhotic cardiomyopathy was 23/68 (34%), and the presence of hepatitis C was strongly associated with systolic dysfunction with p-value of 0.007. However, it was not significantly associated with diastolic dysfunction, p-value = 0.59. Logistic regression analysis did not show any significant association between cardiac dysfunction and the severity of liver cirrhosis, as assessed by Child–Pugh, MELD, ALBI, PALBI, portal hypertension, and FIB-4 score (R2 = 3.66, F (13, 39) = 1.33, p = 0.234). Conclusion: Our study reveals a remarkable prevalence of cirrhotic cardiomyopathy, which despite being a frequently occurring phenomenon often goes unrecognized. Lack of correlation with the severity of liver cirrhosis, based on currently available scoring system, suggests either a still poorly understood pathological mechanism or requires the development of a new validated reliable scoring system through multi-center longitudinal studies. [ABSTRACT FROM AUTHOR]

The systemic sequelae of chronic liver disease (CLD) may be due to portal hypertension and shunting, malnutrition, and/or a low grade inflammatory state. This article will focus on the consequences of chronic liver disease affecting extrahepatic organs. Portal hypertension underlies many systemic complications of CLD. Aside from varices and ascites, portal hypertension may cause both hepatopulmonary syndrome and portopulmonary hypertension leading to respiratory compromise. Cardiomyopathy may also occur secondary to end stage liver disease. Hepatorenal syndrome is also well recognised and hepatic encephalopathy is a consequence of the effect of liver dysfunction on the brain. Compromise of the immune system is well described in end-stage liver disease leading to sepsis and its consequences. Bony disease including osteoporosis and hepatic arthropathy may both be seen in children with CLD. CLD may be asymptomatic initially but then complications may present as the disease progresses. Furthermore, systemic effects of end stage liver disease may complicate liver transplant. These complications often present insidiously or at the time of acute decompensation. Thus, it is important that healthcare providers are vigilant when caring for children with CLD. This article outlines the secondary complications of CLD with an overview of the definition and diagnosis, pathophysiology, management and prognosis of each. [ABSTRACT FROM AUTHOR]

Liver diseases affect the heart and the vascular system. Cardiovascular complications appear to be a leading cause of death in patients with non-alcoholic fatty liver disease (NAFLD) and cirrhosis. The predominant histological changes in the liver range from steatosis to fibrosis to cirrhosis, which can each affect the cardiovascular system differently. Patients with cirrhotic cardiomyopathy (CCM) and NAFLD are at increased risk of impaired systolic and diastolic dysfunction and for suffering major cardiovascular events. However, the pathophysiological mechanisms behind these risks differ depending on the nature of the liver disease. Accurate assessment of symptoms by contemporary diagnostic modalities is essential for identifying patients at risk, for evaluating candidates for treatment, and prior to any invasive procedures. This review explores current perspectives within this field. [ABSTRACT FROM AUTHOR]

Background: Without firm diagnostic criteria, the exact prevalence of cirrhotic cardiomyopathy still remains unknown. Its estimation is rather a difficult task as the disease is generally latent and shows itself only when the patient is subjected to overt stress such as body position changes, exercise, drugs, hemorrhage, and surgery. In this study, we aim to assess cardiac dysfunction in patients with end-stage liver disease, study the correlation between cardiac dysfunction and Child-Pugh classification of patients with liver cell failure, and study the prevalence and impact of cardiac dysfunction on the clinical outcome of patients with child B and child C liver disease. Results: Diastolic dysfunction was more prevalent among the patients' group (p < 0.001). It was absent in 28 (70%) of control group, with grade 1 diastolic dysfunction in 12 (30%). Only one patient (2.5%) had no diastolic dysfunction, 21 patients (52.5%) had grade 1 diastolic dysfunction, 12 (30%) patients had grade 2 diastolic dysfunction, and 6 patients (15%) had grade 3 diastolic dysfunction. QTc interval was significantly prolonged in the patients' group when compared to controls (p < 0.001). Echocardiographic parameters and QTc interval were comparable in child B and child C patients. All patients were followed up for a period of 3 months. Sixteen of 40 patients died in this period of time. Only child classification was found to significantly predict mortality, and patients with child C liver cirrhosis had worse survival when compared to patients with child B liver cirrhosis. Conclusion: Most of the patients had cardiac dysfunction, mainly diastolic dysfunction (87.5%). The study detected the prevalence of diastolic dysfunction among end-stage liver disease when measuring E/É using TDI which proved to be more accurate than E/A ratio. Diastolic dysfunction is proved to be the most sensitive parameter in the diagnosis of cirrhotic cardiomyopathy, being the most parameter affected early. No correlation was found between cardiac dysfunction and the severity of hepatic illness, but the severity of hepatic illness affects the outcome rather than cardiac dysfunction. [ABSTRACT FROM AUTHOR]

Cirrhotic cardiomyopathy (CCM) is a recognized complication of cirrhosis and is associated with poor outcomes, especially under challenges such as surgery/liver transplantation. However, the mechanism is not clear, and the treatment is not specific. The present study aimed to evaluate the role of anti-β1-adrenergic receptor antibodies (anti-β1-AR) in CCM. We enrolled 3 groups: healthy controls, cirrhotic patients without CCM, and patients with CCM. We found that the anti-β1-AR levels in the CCM group were significantly higher than that in the non-CCM group; anti-β1-AR was positively correlated to NT-proBNP, negatively correlated to left ventricular ejection fraction, fractional shortening ((r = − 0.466, P < 0.05), and the ratio of peak early (E wave) and atrial (A wave) flow velocities (E/A (r = − 0.475, P < 0.05) in CCM patients. Anti-β1-AR is a useful predictive biomarker for the presence of CCM and eventually may also have therapeutic implications. Clinical Trials Registration: Chinese Clinical Trials No. ChiCTR 2,000,037,730 [ABSTRACT FROM AUTHOR]

Cirrhotic cardiomyopathy is a condition where liver cirrhosis is associated with cardiac dysfunction. Triggers and blockers of cirrhotic cardiomyopathy are poorly understood, which might compromise the prognosis of chronic liver disease patients. We tested whether exercise training would reduce liver damage induced by thioacetamide and prevent liver cirrhosis-associated cardiomyopathy. Wistar rats were divided into three groups: control, thioacetamide (TAA), or TAA plus exercise. Thioacetamide increased liver weight and serum alanine aminotransferase and aspartate aminotransferase levels. Also, TAA treatment was involved with hepatic nodule formation, fibrotic septa, inflammatory infiltration, and hepatocyte necrosis. The exercise group presented with a reduction in liver injury status. We found that liver injury was associated with disordered cardiac hypertrophy as well as diastolic and systolic dysfunction. Exercise training attenuated cirrhosis-associated cardiac remodeling and diastolic dysfunction and prevented systolic impairment. These results provided insights that exercise training can mitigate cirrhotic cardiomyopathy phenotype. [ABSTRACT FROM AUTHOR]

Purpose of Review: The aim of this study is to review current echocardiographic modalities utilized in the assessment of the preoperative liver transplant candidate with an emphasis on newer techniques. We sought to assess if newer methods imparted additional diagnostic or prognostic accuracy compared to prior methods based on existing studies. Recent Findings: Standard dobutamine stress echocardiography offers important information regarding operative risk and post-operative survival in liver transplant candidates; however, technologies such as speckle-tracking echocardiography (STE) and evaluation of diastolic function have emerged as useful tools as well. Summary: 2D-STE and diastolic echocardiography offer additional parameters such as global longitudinal strain and measures of diastolic dysfunction that can better predict peri-operative and post-operative complications in liver transplant candidates. If able, practitioners should utilize these methods routinely in their assessment of liver transplant candidates. [ABSTRACT FROM AUTHOR]

Background: The accuracy of diagnosis and clinical implications of the hepatoadrenal syndrome, as currently diagnosed using total cortisol, remain to be validated.Aim: The aim of this study was to assess adrenal function using free cortisol in stable cirrhosis and study the potential implications of any abnormalities for renal and/or cardiac function.Methods: Sixty-one stable consecutively enrolled patients with cirrhosis underwent assessment of adrenal function using the low-dose short Synacthen test, renal function by 51Cr-EDTA glomerular filtration rate (GFR), and cardiac function by two-dimensional echocardiography.Results: Eleven patients (18%) had total peak cortisol (PC) < 500 nmol/L, but no patient had free PC < 33 nmol/L indicating that diagnosis of AI using total cortisol is not confirmed using free cortisol. Free cortisol did not correlate with GFR or parameters of cardiac function. Patients with higher Child-Pugh class had progressively lower free cortisol. Patients with low GFR < 60 mL/min (N = 22) had more frequently grade II-III diastolic dysfunction (66.7% vs. 17.6%; p = 0.005) and had higher Child-Pugh and MELD score compared to those with normal GFR.Conclusions: Diagnosis of AI using total cortisol is not confirmed using free cortisol and is thus considered unreliable in cirrhosis. Free cortisol is not associated with renal or cardiac dysfunction. Lower free cortisol in more advanced stages of liver disease might be secondary to decreased synthesis due to lower cholesterol levels. Irrespective of free cortisol, parameters of cardiac dysfunction are associated with renal impairment supporting the cardio-renal hypothesis. [ABSTRACT FROM AUTHOR]

Background: There are scanty data from India on the prevalence and clinical profile of cirrhotic cardiomyopathy (CCM). Aim: To identify the prevalence and clinical presentation of CCM in patients with liver cirrhosis. Methods: Five hundred and eighty-six patients with liver cirrhosis were recruited based on inclusion criteria and evaluated for cardiac parameters using electrocardiography, 2-dimensional echocardiography, dobutamine stress test and coronary angiography as needed. Baseline demographic data, liver biochemistry, endoscopic and radiological findings were recorded in all the patients. Appropriate statistical analyses were performed. Results: Four thousand eight hundred and seventy-seven patients with liver disease were registered during the study period. Five hundred and eighty-six cirrhotic patients had cardiac evaluation as per the study protocol. One hundred fifty-nine had coronary artery disease and were excluded. One hundred and ninety-eight of 427 remaining patients (46.4%) had CCM. The median age of patients with CCM was higher compared with those without CCM (52 years vs. 46 years; p-value < 0.00001). Likewise, cirrhosis-related complications ([isolated or in combination], lower pulse rate [< 60/min] and prolonged corrected QT interval [QTc]; p<0.00001) were more frequent in patients with CCM. After excluding known risk factors for CCM such as alcohol, diabetes, hypothyroidism, hypertension, the true prevalence of CCM was 8.2% (48 out of 586). Hepatotropic viral infections (p 0.03) and prolonged QTc (p 0.0004) were commoner in CCM. Conclusion: Prevalence of CCM in our setting is 33.8%. CCM is commoner in males and is independent of the etiology of cirrhosis, comorbidity and severity of liver disease. Diastolic dysfunction and prolonged QTc interval are common in CCM. [ABSTRACT FROM AUTHOR]

Keywords: Cirrhotic cardiomyopathy; Systolic dysfunction; Cirrhosis; Cardiac outcomes EN Cirrhotic cardiomyopathy Systolic dysfunction Cirrhosis Cardiac outcomes 5714 5715 2 11/15/22 20221201 NES 221201 To the Editor We read with interest the article titled "Impact of Cirrhotic Cardiomyopathy Diagnosed According to Different Criteria on Patients with Cirrhosis Awaiting Liver Transplantation: A Retrospective Cohort Study" by Singh et al. [[1]]. In the study by Singh et al. [[1]], the prevalence of systolic dysfunction, based on GLS, according to CCMC criteria is reported as 89% (213/238 patients) [[1]]. We agree with their observation that the prevalence of systolic dysfunction based on global longitudinal strain (GLS) using speckle tracking analysis was much higher in our patient population compared to the prior studies. [Extracted from the article]

Purpose of Review: Insertion of a transjugular intrahepatic portosystemic shunt (TIPS) has proven effective in alleviating complications to portal hypertension such as refractory ascites and variceal bleeding in patients with cirrhosis. Moreover, it increases survival in selected patient groups. However, TIPS also causes marked circulatory changes and a central concern has been whether this could negatively affect cardiac function. Therefore, this review aims to critically discuss our knowledge on cardiovascular effects of a TIPS in cirrhosis. Recent Findings: These suggest that TIPS does not worsen cardiac function. Careful cardiac evaluation prior to TIPS is, however, a prerequisite in order to prevent cardiac complications after TIPS insertion. Summary: The focus on cirrhotic cardiomyopathy has raised the awareness on specific procedures such as TIPS. Thus, previous studies have demonstrated that TIPS seemingly worsens cardiac function with a negative effect on ascites clearance and survival. However, recent studies have not been able to establish this deleterious interplay and the overall frequency of cardiac failure after TIPS still remains low. Hence, TIPS seems to be safe with regard to cardiac function in patients with cirrhosis. [ABSTRACT FROM AUTHOR]

Development of esophageal varices, ascites, and hepatic nephropathy is among the major complications of cirrhosis. The presence of cirrhotic cardiomyopathy, which includes a left ventricular diastolic dysfunction (DD), seems to deteriorate the course of the disease and the prognosis. Increased stiffness of the cirrhotic heart may decrease the compliance and result in DD. The prevalence of DD in cirrhotic patients averages about 50 %. It can be evaluated by transmitral Doppler echocardiography, tissue Doppler echocardiography, and cardiac magnetic resonance imaging. There seems to be a relation between DD and the severity of liver dysfunction and the presence of ascites. After liver transplantation, DD worsens the prognosis and increases the risk of graft rejection, but DD improves after few months. Insertion of a transjugular intrahepatic portosystemic shunt increases left ventricular diastolic volumes, and DD is a predictor of poorer survival in these patients. Future studies should aim at disclosing pathophysiological mechanisms behind the developing of DD in cirrhosis in relation to patient characteristics, development of complications, treatment, and risk associated with interventional procedures. [ABSTRACT FROM AUTHOR]

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Patients with cirrhosis and portal hypertension are at an increased risk of the development of circulatory dysfunction that may potentially result in multiple organ failure. Apart from the liver, this may involve the heart, lungs, kidneys, the immune system, the adrenal glands, and other organ systems. As the disease progresses, the circulation becomes hyperdynamic, and signs of cardiac, pulmonary, and renal dysfunction are observed, in addition to reduced survival. Infections and an altered cardiac function known as cirrhotic cardiomyopathy may be precipitators for the development of other complications such as hepatorenal syndrome. In patients with chronic organ dysfunction, various precipitating events may induce an acute-on-chronic renal failure and acute-on-chronic liver failure that negatively affect the prognosis. Future research on the pathophysiologic mechanisms of the complications and the precipitating factors is essential to understand the basics of the treatment of these challenging conditions. The aim of the present review is to focus on the development and precipitating factors of various organ failures in patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Cirrhotic cardiomyopathy is a cardiac condition observed in patients with cirrhotic regardless of the etiologies. It is characterized by the impaired systolic response to physical stress, diastolic dysfunction, and electrophysiological abnormalities, especially QT interval prolongation. Its pathophysiology and clinical significance has been a focus of various researchers for the past decades. The impairment of β-adrenergic receptor, the increase in endogenous cannabinoids, the presence of cardiosuppressants such as nitric oxide and inflammatory cytokines are the proposed mechanisms of systolic dysfunction. The activation of cardiac renin-angiotensin system and salt retention play the role in the development of cardiac hypertrophy and impaired diastolic function. QT interval prolongation, which is observed in 40-50 % of cirrhotic patients, occurs as a result of the derangement in membrane fluidity and ion channel defect. The increased recognition of this disease will prevent the complications of overt heart failure after procedures such as transjugular intrahepatic portosystemic shunt (TIPS) and liver transplantation. Better understandings of the pathogenesis and pathology of cirrhotic cardiomyopathy is crucial in developing more accurate diagnostic tools and specific treatments of this condition. [ABSTRACT FROM AUTHOR]

Subtle abnormalities of cardiac structure or function are often identified in patients with liver cirrhosis and have been termed cirrhotic cardiomyopathy. However, in the absence of a precise definition, its diagnosis remains a challenge. Cardiac dysfunction in patients with cirrhosis can often be attributed to concomitant diseases such as hypertension, ischaemic heart disease or excess alcohol consumption in many patients. Further research is required to identify the existence, origin and importance of abnormal cardiac function due specifically to liver disease. Cardiac dysfunction may be masked by treatments given to cirrhotic patients, such as mineral-corticoid receptor antagonists, or by co-existing conditions, such as anaemia. New imaging tests or plasma biomarkers might be able to detect abnormal cardiac function at an early stage of its development. [ABSTRACT FROM AUTHOR]

Marked hemodynamic changes occur in humans and experimental animals with cirrhotic liver disease. In the heart, basal contractility, responsiveness to β-adrenoceptor activation, and excitation–contraction coupling (ECC) are negatively affected in models of cirrhosis and portal hypertension with portosystemic shunting (PVS), and comprise what has been called cirrhotic cardiomyopathy. These effects are accompanied by elevated circulating levels of bile acids. We investigated whether elevated bile acids act as a myocardial toxicant by exposing cardiac muscle in vitro to bile acids and compared these results with two models of cirrhotic cardiomyopathy with elevated bile acids: CCl4-induced cirrhosis and PVS. Cholic acid, a lipophilic bile acid, produced a decrease in basal cardiac contractility and responsiveness to β-adrenoceptor activation, both of which appeared to result from altered ECC. β-Adrenoceptor density and signaling were unaffected. Acutely, ursodeoxycholic acid, a more hydrophilic bile acid, had no effect. Cirrhosis produced a decrease in basal force, depressed β-adrenoceptor responsiveness, and altered ECC similar to cholic acid. However, cirrhosis also altered β-adrenoceptor signaling including decreases in cyclic AMP formation, expression of the stimulatory G protein, GS, and β-adrenoceptor density. Displacement of lipophilic bile acids by chronic administration of ursodeoxycholic acid to rats during the development of cirrhotic cardiomyopathy produced by PVS produced attenuation of the effect on ECC. These results suggest a possible role for lipophilic bile acids in some, but not all of the myocardial consequences of chronic portal vein stenosis and CCl4-induced cirrhosis. [ABSTRACT FROM AUTHOR]

Purpose of Review: Cirrhotic cardiomyopathy is a syndrome of depressed cardiac function in patients with cirrhosis. We aimed to review the historical background, pathophysiology and pathogenesis, diagnostic definitions, clinical relevance, and management of this syndrome. Recent Findings: An inflammatory phenotype underlies the pathogenesis: gut bacterial translocation with endotoxemia stimulates cytokines and cardiodepressant factors, such as nitric oxide and endocannabinoids. Cardiomyocyte plasma membrane biochemical and biophysical changes also play a pathogenic role. These factors lead to impaired beta-adrenergic function. Proposed new echocardiographic criteria for the diagnosis of cirrhotic cardiomyopathy include systolic global longitudinal strain and indices of diastolic dysfunction. Cardiac dysfunction participates in the pathogenesis of hepatorenal syndrome and increased morbidity/mortality of cirrhotic patients to hemorrhage, infection, and surgery, including liver transplantation. There is no specific treatment, although β-adrenergic blockade and supportive management have been proposed, but it needs further study. Summary: Cirrhotic cardiomyopathy is a clinically relevant syndrome afflicting patients with established cirrhosis. Optimum management remains unclear, and further study is needed in this area. [ABSTRACT FROM AUTHOR]