Impact of metformin on the incidence of human cholangiocarcinoma in diabetic patients: a systematic review and meta-analysis.

Cholangiocarcinoma (CCA) is the second most common liver cancer. Diabetes is a well-known risk factor; however, treatment with metformin has been reported to be protective for several cancers, but data on CCA are still sparse and heterogeneous. We performed this meta-analysis to investigate the role of metformin as a potential protective factor for CCA. In this systematic review and meta-analysis, we searched PubMed/MEDLINE and EMBASE databases, from the date of inception to November 2022, for studies analyzing CCA rate in patients taking metformin. Twenty-nine articles were initially identified, of which four were eligible and included in our systematic review and meta-analysis, from which we estimated the relative risk (RR). The rate of CCA was lower for diabetic patients taking metformin than diabetic patients without metformin intake when comparing two highest quality studies [RR, 0.38; 95% confidence interval (CI), 0.290-0.508; P < 0.001], and three studies with similar inclusion criteria (RR, 0.34; 95% CI, 0.51-0.35; P < 0.001) without significant statistical heterogeneity among them (I2 = 29.83%, P = 0,2326 and I2 = 35.08%; P = 0.2143, respectively). Our study demonstrated a significant impact of metformin in reducing the risk of CCA by nearly 62-66% in diabetic patients taking metformin.

Clinical challenge for gastroenterologists-Gastrointestinal manifestations of systemic mastocytosis: A comprehensive review.

Mastocytosis is a rare and heterogeneous disease characterized by various clinical and biological features that affect different prognoses and treatments. The disease is usually divided into 2 principal categories: cutaneous and systemic disease (SM). Clinical features can be related to mast cell (MC) mediator release or pathological MC infiltration. SM is a disease often hard to identify, and the diagnosis is based on clinical, biological, histological, and molecular criteria with different specialists involved in the patient's clinical work-up. Among all manifestations of the disease, gastrointestinal (GI) symptoms are common, being present in 14%-85% of patients, and can significantly impair the quality of life. Here we review the data regarding GI involvement in SM, in terms of clinical presentations, histological and endoscopic features, the pathogenesis of GI symptoms, and their treatment.

Fibrosis is associated with adiponectin resistance in chronic hepatitis C virus infection.

BACKGROUND: Chronic hepatitis C virus (HCV) infection is frequently associated with insulin resistance which has been suggested to promote fibrotic progression. Adiponectin, an adipocyte-derived insulin-sensitizing hormone, might play a protective role against hepatic fibrosis. MATERIALS AND METHODS: This observational case-control study investigated the adiponectin status in insulin resistant, nondiabetic, chronic HCV-infected patients (n=54; 13 women, 41 men) compared with age-, sex- and BMI-matched healthy controls. Liver biopsies from patients with chronic HCV hepatitis were analysed for the adiponectin and adiponectin receptors (ADIPOR) 1 and 2 mRNA and protein expressions. RESULTS: Serum adiponectin levels were higher in patients with chronic HCV hepatitis than in healthy controls (12·1±4·7 vs. 9·5±4·4 mg L(-1) in men, P = 0·01; 18·2±4·4 vs. 13·6±5·3mgL(-1) in women, P=0·02). BMI, HDL cholesterol and triglycerides levels correlated with adiponectin levels both in patients and in controls, while no correlation with glucose, insulin and HOMA-IR values could be detected. Nonetheless, insulin resistance was predictive of steatosis and fibrosis in chronic HCV-infected patients. Interestingly, patients with none or mild fibrosis showed serum adiponectin levels similar to those in healthy controls, while hyperadiponectinemia was associated with moderate to severe stages of fibrosis. Hyperadiponectinemia was unlikely sustained by liver production as hepatocytes did not express the protein. ADIPOR1 mRNA, but not ADIPOR2 levels, was reduced in chronic HCV hepatitis. The reduced ADIPOR1 expression was confirmed by immunohistochemistry. CONCLUSIONS: In patients with chronic HCV hepatitis, fibrosis was associated with hyperadiponectinemia. Chronic HCV-infected hepatocytes showed reduced ADIPOR1 expression, suggesting a pattern of adiponectin resistance.

Acute mesenteric ischemia and small bowel imaging findings in COVID-19: A comprehensive review of the literature.

BACKGROUND: Coronavirus disease 2019 (COVID-19), an infectious condition caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide since its first description in Wuhan in December 2019. Even though respiratory manifestations are the most prevalent and responsible for disease morbidity and mortality, extrapulmonary involvement has progressively gained relevance. In particular, gastrointestinal (GI) signs and symptoms, reported in up to two-thirds of patients with COVID-19, might represent the first and, in some cases, the only disease presentation. Their presence has been associated in some studies with an increased risk of a severe disease course. Proposed pathogenic mechanisms explaining GI tract involvement are either direct viral access to intestinal cells via angiotensin-converting enzyme 2 or indirect damage of the intestinal wall through mesenteric ischemia induced by the hypercoagulable state associated with COVID-19 infection. Although not typical of SARS-CoV-2 infection, several small bowel manifestations have been described in infected patients who underwent any form of abdominal imaging. The radiological findings were mainly reported in patients with abdominal symptoms, among which abdominal pain was the most common. AIM: To discuss small bowel radiological manifestations of SARS-CoV-2 infection in abdominal imaging studies. METHODS: Bibliographical searches were performed in PubMed, using the following keywords: "COVID-19" AND "imaging" AND "gastrointestinal" OR "abdominal" OR "small bowel". RESULTS: Of 62 patients with described radiologic small bowel alterations, mesenteric ischemia was diagnosed in 31 cases (50%), small bowel wall thickening in 10 cases (16%), pneumatosis in nine cases (15%), intussusception in eight cases (13%), pneumoperitoneum in two cases (3%) and paralytic ileus in two cases (3%). We also reported mesenteric adipose tissue hypertrophy and lymph nodes enlargement in a young woman. CONCLUSION: So far it is difficult to establish whether these manifestations are the direct consequence of SARS-CoV-2 infection or collateral findings in infected patients, but their recognition would be pivotal to set a closer follow-up and to reduce missed diagnoses.

Baroreceptor sensitivity and baroreceptor effectiveness index in cirrhosis: the relevance of hepatic venous pressure gradient.

BACKGROUND: Autonomic dysfunction has been reported as one of the complications of cirrhosis. AIMS: The aim of this study was to test autonomic dysfunction in cirrhotic patients by analysing the baroreflex sensitivity and the baroreceptor effectiveness index (BEI), in order to determine its correlation with the severity and the aetiology of liver disease. Moreover, we explored the relationship between baroreceptor function and mortality in our cohort of patients. METHODS: Clinical and laboratory evaluation, hepatic venous pressure gradient (HVPG) and haemodynamic setting and baroreceptor function were assessed in 45 cirrhotic patients (median age 55, range 38-72 years) divided in groups according to the severity of their disease (26 patients Child A, 13 patients Child B and six patients Child C). RESULTS: Baroreceptor sensitivity and BEI were impaired in more advanced cirrhotic patients compared with subjects with milder disease (P<0.001). HVPG was significantly, independently and inversely correlated with baroreceptor sensitivity (P=0.003). More severe impairment of baroreceptor function was associated with a higher mortality (P=0.04) and subjects with alcohol-related cirrhosis presented worse baroreceptor function (P=0.032) and poorer survival (P=0.003) compared with subjects with post-viral liver disease. CONCLUSIONS: These data support the hypothesis that liver disease severity and particularly portal hypertension have an important role in the derangement of baroreceptor function. The aetiology of cirrhosis seems to be related to baroreceptor impairment as well. Mortality rate is higher in subjects with a more damaged autonomic system, strengthening the idea of a worse prognosis in cirrhotic patients with autonomic neuropathy.

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium.

A prolongation of QT interval has been shown in patients with cirrhosis and it is considered as part of the definition of the so-called 'cirrhotic cardiomyopathy'. The aim of the present study was to assess the determinants of QT interval prolongation in cirrhotic patients. Forty-eight male patients with different stages of liver disease were divided into three subgroups according to the Child-Pugh classification. All patients underwent a 24-h ECG Holter recording. The 24-h mean of QT intervals corrected for heart rate (termed QTc) and the slope of the regression line QT/RR were calculated. HRV (heart rate variability), plasma calcium and potassium concentration and HVPG (hepatic venous pressure gradient) were measured. QTc was progressively prolonged from Child A to Child C patients (P=0.001). A significant correlation between QTc and HVPG was found (P=0.003). Patients with alcohol-related cirrhosis presented QTc prolongation more frequently than patients with post-viral cirrhosis (P<0.001). The QT/RR slope was steeper in subjects with alcoholic aetiology as compared with viral aetiology (P=0.02), suggesting that these patients have a further QTc prolongation when heart rate decreases. The plasma calcium concentration was inversely correlated with QTc (P<0.001). The presence of severe portal hypertension was associated with decreased HRV (P<0.001). Cirrhotic patients with a more severe disease, especially of alcoholic aetiology, who have greater HVPG and lower calcium plasma levels, have an altered ventricular repolarization and a reduced vagal activity to the heart, which may predispose to life-threatening arrhythmias.

Portal pressure reduction after entecavir treatment in compensated HBV cirrhosis.

A Caucasian male aged 54 year was referred to our liver centre for the management of HBV-related cirrhosis. Prior treatment with recombinant alpha-interferon followed by lymphoblastoid interferon was only temporarily effective and the patient refused antiviral treatment with lamivudine. When admitted to our unit, the patient had a Child-Pugh score of A6, high HBV DNA load (4 x 10(6) IU/ml) and evidence of cirrhotic cardiomyopathy. Hepatic venous pressure gradient (HVPG) was 29mm Hg, indicative of clinically severe portal hypertension. Following 3 months of treatment with entecavir, tests for HBV DNA were negative, and 9 months after therapy started, HVPG was measured as 24mm Hg, a reduction from baseline of 17%. These findings indicate that sustained suppression of HBV DNA replication by entecavir in compensated cirrhosis with severe portal hypertension leads to a portal pressure reduction, without the need for vaso-active drugs, as measured using the transjugular HVPG approach described here.

Hepatocellular carcinoma in cirrhotic liver disease: functional computed tomography with perfusion imaging in the assessment of tumor vascularization.

RATIONALE AND OBJECTIVES: Our goal was to prospectively determine the value of perfusion computed tomography (CT) in the quantitative assessment of tumor-related angiogenesis in cirrhotic patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: Forty-seven patients met all the following inclusion criteria: 1) Child-Pugh class A or B liver cirrhosis; 2) presence of a single lesion suspected as HCC at screening ultrasound examination; and 3) lesion diameter between 1 and 3 cm. All patients underwent contrast-enhanced ultrasound, pre- and post-contrast triple-phase CT, and perfusion computed tomographic study using multidetector 16-slice CT. Six parameters related to the blood microcirculation and tissue perfusion were measured for the focal liver lesion and cirrhotic parenchyma: perfusion (P), tissue blood volume (BV), hepatic perfusion index (HPI), arterial perfusion (AP), portal perfusion (PP), and time to peak (TTP). Perfusion parameters were described with quartile values of their distribution; univariate paired and unpaired Wilcoxon signed rank tests were used for statistical analysis. RESULTS: HCC was diagnosed in 21 of the 47 patients; in the remaining 26, HCC was not found at contrast-enhanced ultrasound and multidetector 16-slice computed tomographic study. The values of perfusion parameters measured within tumor tissue were: P (ml/s/100 g): median = 47.0 (first quartile = 36.0, third quartile = 61.4); BV (ml/100 mg): median = 24.0 (first quartile = 18.7, third quartile = 29.3); HPI (%): median = 78.4 (first quartile = 62.9, third quartile = 100); AP (ml/min): median = 45.9 (first quartile = 39.0, third quartile = 60.1); PP (ml/min): median = 9.0 (first quartile = 0.0, third quartile = 24.5); and TTP (seconds): median = 18.7 (first quartile = 16.3, third quartile = 26.5). The corresponding values calculated in cirrhotic surrounding parenchyma were P (ml/s/100 g): median = 11.5 (first quartile = 9.4, third quartile = 13.9); BV (ml/100 mg): median = 10.7 (first quartile = 7.1, third quartile = 14.2); HPI (%): median = 10.6 (first quartile = 8.7, third quartile = 11.9); AP (ml/min): median = 13.2 (first quartile = 10.1, third quartile = 15.5); PP (ml/min) median = 55.2 (first quartile = 40.1, third quartile = 79.5); and TTP (seconds): median = 41.7 (first quartile = 38.9, third quartile = 44.6). P, BV, HPI, and AP values were higher (P < .001), whereas PP and TTP were lower (P < .001) in HCC relative to the surrounding liver. Values of perfusion parameters in the cirrhotic liver of patients with and without HCC were not significantly different (P > .001). CONCLUSION: In cirrhotic patients with HCC, perfusion computed tomographic technique can provide quantitative information about tumor-related angiogenesis.

Perfusion computed tomographic assessment of early hepatocellular carcinoma in cirrhotic liver disease: initial observations.

OBJECTIVE: To prospectively assess perfusion computed tomography (CT) for evaluation of tumor vascularity of early hepatocellular carcinoma (HCC) in patients with cirrhosis. METHODS: The study cohort included 30 patients who had Child-Pugh class A or B liver cirrhosis and a single histopathologically confirmed HCC not exceeding 3 cm in diameter. All patients underwent perfusion CT study using a multidetector 16-slice CT. Four perfusion parameters were measured for the HCCs and cirrhotic liver parenchyma: hepatic perfusion (HP), blood volume (BV), arterial perfusion (AP), and time to peak (TTP). Perfusion parameters were described with quartile (qt) values of their distribution; univariate paired Wilcoxon signed rank test was used for statistical analysis. RESULTS: The values of perfusion parameters measured within tumor tissue were the following: HP (milliliters per 100 g per minute): median = 45.7 (first qt = 35.3; third qt = 61.3); BV (milliliters per 100 mg): median = 20.6 (first qt = 13.0; third qt = 27.6); AP (milliliters per minute): median = 44.2 (first qt = 36.7; third qt = 57.0); TTP (seconds): median = 18.7 (first q = 15.9; third qt = 24.0). Our data showed that HP, BV, and AP values were higher (P < 0.001), whereas TTP was lower (P < 0.001), in HCCs relative to the cirrhotic liver parenchyma. For all the CT perfusion parameters calculated, there was a significant difference between HCC and background cirrhotic liver. CONCLUSIONS: Preliminary results suggest that in patients with cirrhosis and early HCC, perfusion CT is a feasible technique for noninvasive assessment of tumor vascularity.

Perfusion CT in cirrhotic patients with early stage hepatocellular carcinoma: assessment of tumor-related vascularization.

PURPOSE: To assess the value of CT-perfusion in determining the quantitative vascularization features of early hepatocellular carcinoma (HCC) in cirrhotic patients. MATERIALS AND METHODS: A total of 35 cirrhotic patients with single histologically proven HCC not exceeding 3cm in diameter underwent conventional triple-phase multidetector computed tomography (MDCT) examination. All patients were also examined with CT-perfusion (CTp) technique after i.v. injection of 50mL of iodinated contrast. Data were analyzed using a dedicated software which generated a quantitative map of liver parenchyma perfusion. The following parameters were assessed: hepatic perfusion (HP); blood volume (BV); arterial perfusion (AP); time to peak (TTP) and hepatic perfusion index (HPI). Univariate Wilcoxon signed rank test was used for statistical analysis. RESULTS: In the 35 HCCs evaluated, the following quantitative data were obtained: HP (mL/s/100g): median=47.0 (1(st)qt=35.5; 3(st)qt=61.2); BV (mL/100mg): median=22.5 (1(st)qt=18.4; 3(st)qt=27.7); AP (mL/min): median=42.9 (1(st)qt=35.8; 3(st)qt=55.6); HPI(%): median=75.3 (1(st)qt=63.1; 3(st)qt=100); TTP(s): median=18.7 (1(st)qt=16.8; 3(st)qt=24.5). Perfusion values calculated in cirrhotic liver parenchyma were HP: median=10.3 (1(st)qt=9.1; 3(st)qt=13.2); BV: median=11.7 (1(st)qt=9.6; 3(st)qt=15.5); AP: median=10.4 (1(st)qt=8.6; 3(st)qt=11.3); HPI: median=17.5 (1(st)qt=14.3; 3(st)qt=19.7); TTP: median=44.6 (1(st)qt=40.3; 3(st)qt=50.1). HP, BV, HPI and AP were found to be significantly higher in HCC lesion than in liver parenchyma (p<0.001), while TTP was significantly lower (p<0.001). CONCLUSION: CT-perfusion technique allows obtaining quantitative information about tumor-related vascularization of early HCC, in patients with liver cirrhosis.

Hepatocellular carcinoma treated with transarterial chemoembolization: dynamic perfusion-CT in the assessment of residual tumor.

AIM: To asses the value of computed tomography (CT)-perfusion in the detection of residual hepatocellular carcinoma (HCC) vascularization after transarterial chemoembolization (TACE). METHODS: Thirty-two consecutive patients were prospectively included in this study. All patients had liver cirrhosis and a confirmed HCC lesion which was treated with TACE. One month after treatment, perfusion measurements of treated lesions were carried out. The CT-perfusion (CT-p) protocol was performed with 16 slice multidetector computed tomography which included the following parameters: 8 dynamic slices/scan per 40 scans after iv injection of 50 mL of iodinated contrast (350 mg/mL) at a flow rate of 6 mL/s. Treated lesions were evaluated using dedicated perfusion software, which generated a quantitative colour map of perfusion. The following parameters were considered: hepatic perfusion (HP), arterial perfusion (AP), blood volume (BV), hepatic perfusion index (HPI), and time to peak (TTP). Perfusion parameters were described with quartile values of their distribution and statistically analyzed. RESULTS: Perfusion parameters of the treated lesions could be quantitatively assessed using CT-p analysis. The presence of residual tumor tissue was observed in 13 of the 32 patients. The values of the perfusion parameters measured within the relapse tissue were: HP (mL/100 g per minute): median = 44.4 (1(st)qt = 31.3, 3(rd)qt = 55.8); BV (mL/100 g): median = 18.7 (1(st)qt = 11.5, 3(rd)qt = 22.5); AP (mL/min): median = 39.0 (1(st)qt = 36.5, 3(rd)qt = 61.3); HPI (%): median = 34.0 (1(st)qt = 30.4, 3(rd)qt = 38.9); TTP (s): median = 17.3 (1(st)qt = 15.8, 3(rd)qt = 26.5). With the use of the univariate paired Wilcoxon signed rank test, HP, AP and HPI were shown to be significantly higher (P < 0.001) in the relapse site than in the primary lesion. The BV and TTP parameters showed a tendency to be greater and lower, respectively, in the relapse site than in the primary lesion. CONCLUSION: In patients with HCC treated with TACE, CT-p provides measurement of flow parameters related to residual arterial structures in viable tumor, thus helping in the assessment of therapeutic response.

Potential therapeutic targets in cirrhotic cardiomyopathy.

Cirrhotic cardiomyopathy is a recently identified pathological condition defined as "a chronic cardiac dysfunction in patients with cirrhosis characterized by blunted contractile responsiveness to stress and/or altered diastolic relaxation with electrophysiological abnormalities, in the absence of known cardiac disease". Overall there seems to be a link between the progression of liver function impairment, the development of portal hypertension and the degree of hyperdynamic circulation, the hallmark of the deranged cardiovascular function in advanced liver diseases. Although mechanical factors contribute to much of the increased resistance within the liver in portal hypertension, there is clearly a vasculogenic component to the development, perpetuation and progression of this syndrome as well. The vascular component of portal hypertension includes an increase in splanchnic blood flow, as well as an increase in intrahepatic vascular resistance. Dysregulation of the nitric oxide system appears to play a key role in both these processes with a paradoxical reduction of intrahepatic availability despite increased disposal in the splanchnic and other vascular districts with adverse effects on cardiac function and structure. Nevertheless, other putative mediators of cardiac damage in cirrhosis have been proposed and their role in the pathogenesis of cirrhotic cardiomyopathy investigated. This review involves a discussion of data achieved on pathogenesis and clinical features of cirrhotic cardiomyopathy but mainly focuses on considerations on potential therapeutic targets, in the light of the evidence that this mainly subclinical condition merges to clinical relevance when challenged with those therapeutic interventions and procedures currently employed to treat the major complications of cirrhosis that might produce a negative impact on the cardiovascular system.

Cardiac, neuroadrenergic, and portal hemodynamic effects of prolonged aldosterone blockade in postviral child A cirrhosis.

OBJECTIVES: The present study was designed to determine the effects of long-term antialdosterone treatment on cardiac structural and functional alterations, portal and systemic hemodynamic as well as adrenergic dysfunction characterizing Child A cirrhotic patients with F1 esophageal varices. METHODS: Twenty-two Child A postviral preascitic cirrhotic patients were randomly allocated to 200 mg/day K-Canrenoate (13 patients, age 59.6 +/- 2.2 yr, mean + SEM) or no-drug treatment (9 patients, age 61.8 +/- 2.3) for a 6-month-period. Measurements, which included hepatic venous pressure gradient (HVPG), left ventricular wall thickness, left ventricular end-diastolic volume and diastolic function (LVWT, LVEDV, and E/A ratio, echocardiography), and muscle sympathetic nerve activity (MSNA, microneurography, peroneal nerve), were obtained at baseline and following 6 months of drug or no-drug treatment. Ten healthy age-matched subjects served as controls. RESULTS: Cirrhotic patients were characterized by increased HVPG, LVWT, and MSNA values and by a depressed E/A ratio. K-Canrenoate treatment significantly reduced HVPG (from 15.3 +/- 1.0 to 13.8 +/- 0.8 mmHg, p < 0.05), LVWT (from 21.8 +/- 0.5 to 20.7 +/- 0.6 mm, p < 0.02), and LVEDV (from 99.2 +/- 7 to 86.4 +/- 6 ml, p < 0.01), leaving E/A ratio and MSNA almost unaltered. No significant change was observed in the untreated group of cirrhotic patients followed for 6 months without intervention. CONCLUSIONS: These data provide evidence that aldosterone blockade by long-term K-Canrenoate administration improves hepatic hemodynamics by lowering HVPG and ameliorates cardiac structure and function by favoring a reduction in LVWT and LVEDV as well. They also show, however, that this therapeutic intervention neither improves left ventricular diastolic dysfunction nor exerts sympathoinhibitory effects.

El impacto de las complicaciones y los tratamientos sobre los cambios cardiovasculares en la cirrosis: [revisión] / The cirrhotic heart: cirrhotic cardiomyopathy and circulatory derangement: [review]

En tiempos recientes, la miocardiopatía cirrótica ha pasado a ser considerada una nueva entidad clínica. El reconocimiento de cambios leves en la estructura cardíaca que pueden ser detectados incluso en las etapas iniciales de la cirrosis preascítica ha contribuido a una mejor comprensión de los trastornos cardiovasculares que se observan a medida que progresa la enfermedad. Se han categorizado cambios cardíacos estructurales y se diagnóstica, con frecuencia, la disfunción diastólica. La cirrosis descompensada se caracteriza por una disminución de la presión sanguínea y de la resistencia vascular periférica, y un aumento del gasto cardíaco y de la frecuencia cardíaca, los cuales se producen en un escenario de circulación hiperdinámica favorecida por la expansión del volumen total sanguíneo, la sobrecarga circulatoria y la hiperactividad de los sistemas endógenos vasoactivos. La vasodilatación periférica evita la insuficiencia cardíaca. Recientemente se ha reconocido la existencia de una menor respuesta cardíaca en situaciones de estrés como son los cambios en las condiciones de la carga cardíaca en presencia de un mayor deterioro de la función hepática, tales como la ascitis refractaria, el síndrome hepatorrenal, la peritonitis bacteriana espontánea y la hemorragia de várices esofágicas. Ante la disponibilidad de intervenciones terapéuticas (paracentesis, comunicación portosistémica intrahepática transyugular, comunicación venosa peritoneal, trasplante hepático) utilizadas actualmente para manejar las complicaciones potencialmente mortalesen las formas más avanzadas de cirrosis, el conocimiento del impacto que tienen en la función cardiovascular es de suma importancia. Se encuentran en progreso las intervenciones terapéuticas dirigidas a prevenir y manejar el deterioro cardiovascular.

El impacto de las complicaciones y los tratamientos sobre los cambios cardiovasculares en la cirrosis: [revisión] / The cirrhotic heart: cirrhotic cardiomyopathy and circulatory derangement: [review]

En tiempos recientes, la miocardiopatía cirrótica ha pasado a ser considerada una nueva entidad clínica. El reconocimiento de cambios leves en la estructura cardíaca que pueden ser detectados incluso en las etapas iniciales de la cirrosis preascítica ha contribuido a una mejor comprensión de los trastornos cardiovasculares que se observan a medida que progresa la enfermedad. Se han categorizado cambios cardíacos estructurales y se diagnóstica, con frecuencia, la disfunción diastólica. La cirrosis descompensada se caracteriza por una disminución de la presión sanguínea y de la resistencia vascular periférica, y un aumento del gasto cardíaco y de la frecuencia cardíaca, los cuales se producen en un escenario de circulación hiperdinámica favorecida por la expansión del volumen total sanguíneo, la sobrecarga circulatoria y la hiperactividad de los sistemas endógenos vasoactivos. La vasodilatación periférica evita la insuficiencia cardíaca. Recientemente se ha reconocido la existencia de una menor respuesta cardíaca en situaciones de estrés como son los cambios en las condiciones de la carga cardíaca en presencia de un mayor deterioro de la función hepática, tales como la ascitis refractaria, el síndrome hepatorrenal, la peritonitis bacteriana espontánea y la hemorragia de várices esofágicas. Ante la disponibilidad de intervenciones terapéuticas (paracentesis, comunicación portosistémica intrahepática transyugular, comunicación venosa peritoneal, trasplante hepático) utilizadas actualmente para manejar las complicaciones potencialmente mortalesen las formas más avanzadas de cirrosis, el conocimiento del impacto que tienen en la función cardiovascular es de suma importancia. Se encuentran en progreso las intervenciones terapéuticas dirigidas a prevenir y manejar el deterioro cardiovascular.(AU)