Hence, it is easily accessible as 12-lead ECGs are noninvasive, simple, inexpensive and routinely done in hospitalized and ambulatory patients to detect a long QT syndrome (LQTS). The QTc interval can easily be obtained from a 12-lead electrocardiogram (ECG). Proposed mechanisms such as bile salt accumulation, altered autonomic tone, shifts in gonadal hormone balance and cirrhotic cardiomyopathy have been suggested. Despite these efforts, the underlying pathophysiology of QT prolongation in cirrhosis is poorly understood. 5 Since then hundreds of studies of repolarization in cirrhosis have appeared. 5 performed a detailed study of QT prolongation in cirrhosis and found a significant correlation between the rate-corrected QT (QTc) interval and the Child-Pugh score, and that QTc prolongation may be associated with poor outcomes including mortality. This phenomenon then remained ignored until 1998, when Bernardi et al. Unfortunately, it was merely an incidental finding that was not further discussed, as the main point of the paper was the demonstration of hyperdynamic circulation in cirrhosis. 2, 3 In fact, the seminal paper by Kowalski and Abelmann 4 that launched the modern era of cardio-hepatology in 1953 already reported a prolonged QT interval in eight of the 22 subjects. The prevalence of electrocardiographic QT interval prolongation in patients with cirrhosis ranges between 30% and 70%. Keywords: Acquired long QT syndrome, Torsade de pointes, Cirrhosis, Drug interaction, Ventricular repolarization In cirrhotic patients with prolonged QTc interval, a joint effort by cardiologists and hepatologists may be useful and significantly improve the clinical course and outcome. While some risk factors are unavoidable, overall risk can be mitigated by electrocardiogram monitoring and avoiding drug interactions and electrolyte and acidbase disturbances. In patients with cirrhosis, multiple hits and cardiac-hepatic interactions are often required to sufficiently erode the repolarization reserve before long QT syndrome and TdP can occur. Additional external risk factors for QTc prolongation include medication (I Kr blockade and altered cytochrome P450 activity), bradycardia, electrolyte abnormalities, underlying cardiomyopathy and acute illness. The pathophysiological mechanism remains incompletely understood, but may include metabolic, autonomic or hormonal imbalances, cirrhotic heart failure and/or genetic predisposition. A QTc interval >450 ms in males and >470 ms in females is considered prolonged. To compare the QT interval in time it should be corrected for heart rate (QTc), preferably by the Fridericia method. The QT interval is mainly determined by ventricular repolarization. We present a stepwise overview of the pathophysiology and management of acquired long QT syndrome in cirrhosis. In cirrhotic patients, there is likely a significant association between the corrected QT (QTc) interval and the severity of liver disease, and possibly with increased mortality. In patients without cirrhosis, QT prolongation is associated with an increased risk of ventricular arrhythmias, such as torsade de pointes (TdP). The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.Īpproximately 30% to 70% of patients with cirrhosis have QT interval prolongation. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The final responsibility for the decision to accept or reject lies with the editors. We reserve the right to return manuscripts in which no reviewers are suggested. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer in the end, everyone will benefit.
It would be very helpful if you could suggest a selection of reviewers and include their contact details. The remaining articles are usually sent to two reviewers. A decision about these papers will usually be made within two or three weeks.
All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal.
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