A) ECG lead II shows a ventricular premature complex, prolonged QT interval leading to ventricular fibrillation. (B) ECG lead II shows torsades de pointes. 

A) ECG lead II shows a ventricular premature complex, prolonged QT interval leading to ventricular fibrillation. (B) ECG lead II shows torsades de pointes. 

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Article
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Severe QT interval prolongation >500 ms occurs in one quarter of cardiac surgical patients in the perioperative period while moderate prolongation occurs in most of them. Prolonged QT interval may be associated with torsades de pointes and lead to sudden cardiac death. Because of the high incidence of prolonged QT in cardiac surgery patients and it...

Citations

... The QT interval has been demonstrated to be lengthened by faulty electrical impulse propagation [40]. If left untreated, a long QT can cause torsades de pointes and eventually ventricular fibrillation, which can lead to abrupt cardiac death [41]. The QT interval duration is determined by ventricular depolarization and repolarization. ...
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Connexin 43 (Cx43) is the most important protein in the gap junction channel between cardiomyocytes. Abnormalities of Cx43 change the conduction velocity and direction of cardiomyocytes, leading to reentry and conduction block of the myocardium, thereby causing arrhythmia. It has been shown that IL-1β reduces the expression of Cx43 in astrocytes and cardiomyocytes in vitro. However, whether caspase-1 and IL-1β affect connexin 43 after myocardial infarction (MI) is uncertain. In this study we investigated the effects of VX765, a caspase-1 inhibitor, on the expression of Cx43 and cell-to-cell communication after MI. Rats were treated with VX765 (16 mg/kg, i.v.) 1 h before the left anterior descending artery (LAD) ligation, and then once daily for 7 days. The ischemic heart was collected for histochemical analysis and Western blot analysis. We showed that VX765 treatment significantly decreased the infarct area, and alleviated cardiac dysfunction and remodeling by suppressing the NLRP3 inflammasome/caspase-1/IL-1β expression in the heart after MI. In addition, VX765 treatment markedly raised Cx43 levels in the heart after MI. In vitro experiments were conducted in rat cardiac myocytes (RCMs) stimulated with the supernatant from LPS/ATP-treated rat cardiac fibroblasts (RCFs). Pretreatment of the RCFs with VX765 (25 μM) reversed the downregulation of Cx43 expression in RCMs and significantly improved intercellular communication detected using a scrape-loading/dye transfer assay. We revealed that VX765 suppressed the activation of p38 MAPK signaling in the heart tissue after MI as well as in RCMs stimulated with the supernatant from LPS/ATP-treated RCFs. Taken together, these data show that the caspase-1 inhibitor VX765 upregulates Cx43 expression and improves cell-to-cell communication in rat heart after MI via suppressing the IL-1β/p38 MAPK pathway.
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Background: Ventricular tachyarrhythmia is a potentially fatal outcome of cardiac surgery. Abrupt changes in the hemodynamics after surgical correction of valvular heart disease (VHD) can lead to alterations in ventricular repolarization. We compared the difference between temporal changes in repolarization parameters after correction of left-sided VHD. Methods: We retrospectively analyzed the electrograms of patients who underwent surgical correction of isolated VHD between 2006 and 2015 at Asan Medical Center, including mitral stenosis (MS), mitral regurgitation (MR), aortic stenosis (AS), and aortic regurgitation (AR). Ventricular repolarization parameters were measured at pre-specified time intervals after index surgery using a custom-made ECG analysis program. We compared repolarization parameters, including QT and corrected QT intervals, T peak-to-end interval, and corrected T peak-to-end interval. Results: Analysis of 8265 ECGs from 2110 patients (266 MS, 1059 MR, 421 AS, and 364 AR) was performed. Patients with AS were characterized by older age and more comorbidities than other VHDs. The corrected QT interval showed a peak value immediately after surgery and decreased thereafter in the AS groups. However, a gradual increase over 1 month after surgery in AR, MS, and MR groups was observed. The corrected T peak-to-end interval increased in the MS and MR groups and was unchanged in the AS and AR groups. Conclusions: The repolarization parameters of surgery changed dynamically after left-sided valvular surgery. Understanding differential temporal change of repolarization parameters according to the type of VHD would help clinicians avoid fatal arrhythmias related to the repolarization changes.
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Acquired long QT syndrome (aLQTS) can occur in up to one third of patients undergoing cardiac surgery and is often undisclosed. We present a case of a 55-year-old male patient admitted to our center for mitral valve replacement surgery, and, during the postoperative period, a long QT greater than 600 ms was confirmed and in the Holter monitoring Torsade de Pointes (TdP) was evidenced. The patient received appropriate medical treatment and was discharge in stable clinical conditions.