Rimbas RC et al. direct toxic effects of alcohol around the heart. However, in 1953, Kowalski and Abelmann AZD1152-HQPA (Barasertib) (1) showed the presence of a circulatory dysfunction specific to liver cirrhosis. Since then, several studies have consistently reproduced those findings (2 C5). Successive publications of experimental and clinical studies have established the idea that cirrhotic cardiomyopathy AZD1152-HQPA (Barasertib) (CCM) is usually a clinical entity different from that seen in alcoholic heart muscle disease. Interference of liver disease with the cardiac and circulatory performance would be expected, considering that the liver receives 25% of the cardiac output. The term CCM was introduced more than three decades ago to describe a spectrum of chronic cardiac dysfunction in cirrhotic patients in the absence of known heart disease, regardless of the etiology of cirrhosis (4,6). Hepatic cirrhosis leads to a hyperdynamic circulatory state, which induces cardiac dysfunctions that characterize the CCM syndrome. This syndrome includes, in addition to the hyperdynamic circulation, a combination of systolic (7) and diastolic dysfunctions (8C11), prolonged ventricular repolarization (12), and inability of the sinus node to increase heart rate (HR) during exercise (13). Epidemiology and natural Rabbit Polyclonal to NAB2 history CCM is usually a condition easily tolerated, remaining asymptomatic for months to years because of the near-normal cardiac function at rest, manifesting only under conditions of physical or pharmacological stress. Therefore, the diagnosis of CCM is usually difficult and the exact prevalence of this condition remains unknown (7). However, it has been estimated that 40C50% of patients who underwent liver transplantation have some indicators of cardiac dysfunction, which means that these patients underwent surgery under a condition of CCM (7,11,14). Furthermore, since diagnosis of CCM is frequently missed or delayed, its natural history is usually unclear in terms of response to treatment and prognosis (7). As CCM is usually a relatively recent entity, the purpose of this review is usually to provide an explanation about its definition. Its pathophysiological mechanisms, criteria, and supplemental exams for its diagnosis are also included to show CCM relevance. Although the treatment of this condition is mainly supportive, the actions that should be taken to approach CCM are also commented. Material and Methods Structured medical subject headings (MeSH) were used to search original articles and reviews about CCM in MEDLINE by means of the PubMed database. The term “cirrhotic cardiomyopathy” was used. A total of 275 complete AZD1152-HQPA (Barasertib) articles, published until March 2018, were identified. All articles selected in the search were in English, and abstracts for oral presentations and letters to the editor were ignored. We also searched for further relevant articles in the reference lists of articles. First, titles and abstracts were read to know whether they fit the purpose of reviewing the issue. If their eligibility remained unclear, the full-text reports were then considered. Ninety studies were selected and organized to provide the authors of the present study with the means to write a narrative review including history, definition, epidemiologic data, clinical findings, diagnosis, and treatment. Definition of CCM A consensus diagnostic criterion for CCM (Table 1) was established at the World Congress of Gastroenterology held in Montreal in 2005 (10). Thus, CCM is usually defined as a cardiac dysfunction in patients with cirrhosis, which is usually characterized by impaired contractile responsiveness to stress and/or altered diastolic relaxation, with electrophysiological abnormalities, in the absence of other known cardiac disorder (9,10). Table 1 Proposal of diagnostic criteria for cirrhotic cardiomyopathy agreed upon at the 2005 World Congress of Gastroenterology in Montreal (10). There are suggestions (not included in this table) to improve these criteria considering dysfunction of right ventricle (15), biventricular diastolic dysfunction at rest, large left and right atria, higher systolic pulmonary arterial pressure and left ventricular mass (16) and evaluate systolic function assessment using tissue strain imaging (17). Systolic dysfunctionResting ejection fraction 55% br / Blunted increase in cardiac output with exercise or pharmacological stimuliDiastolic dysfunctionEarly diastolic atrial filling ratio (E/A ratio) 1.0 (age corrected) br / Deceleration time (DT) 200 ms br / Prolonged isovolumetric relaxation time 80 msSupportive criteriaElectrophysiological abnormalities (prolongation of QT) br / Abnormal chronotropic response br / Electromechanical uncoupling br / Enlarged left atrium br / Increased myocardial mass br / Increased brain natriuretic peptide and pro-peptide br / Increased troponin I Open in a separate window Recommendations 10. Wiese et.