32 research outputs found

    Noninvasive risk stratification of lethal ventricular arrhythmias and sudden cardiac death after myocardial infarction

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    Prediction of lethal ventricular arrhythmias leading to sudden cardiac death is one of the most important and challenging problems after myocardial infarction (MI). Identification of MI patients who are prone to ventricular tachyarrhythmias allows for an indication of implantable cardioverter-defibrillator placement. To date, noninvasive techniques such as microvolt T-wave alternans (MTWA), signal-averaged electrocardiography (SAECG), heart rate variability (HRV), and heart rate turbulence (HRT) have been developed for this purpose. MTWA is an indicator of repolarization abnormality and is currently the most promising risk-stratification tool for predicting malignant ventricular arrhythmias. Similarly, late potentials detected by SAECG are indices of depolarization abnormality and are useful in risk stratification. However, the role of SAECG is limited because of its low predictive accuracy. Abnormal HRV and HRT patterns reflect autonomic disturbances, which may increase the risk of lethal ventricular arrhythmias, but the existing evidence is insufficient. Further studies of noninvasive assessment may provide a new insight into risk stratification in post-MI patients

    The role of Purkinje fibers in the emergence of an incessant form of polymorphic ventricular tachycardia or ventricular fibrillation associated with ischemic heart disease

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    Background: The clinical and electrophysiological characteristic of ventricular premature contractions (VPCs) which trigger the incessant form of polymorphic ventricular tachycardia (VT), so-called “electrical storm” associated with ischemic heart disease, remains unclarified. The aim of this study was to evaluate those matters and the possible role of the Purkinje network in the emergence of an electrical storm. Methods and results: We experienced 5 patients (68 ± 5 years, mean LVEF: 29%) with electrical storms which occurred during the acute phase of an infarction in 3 patients and the remote phase in 2. The triggering VPCs were multifocal in 3 patients and monofocal in the remaining 2. Radiofrequency (RF) catheter ablation was performed for a goal of eliminating the triggering VPCs. A total of 9 different kinds of VPCs differentiated by their morphology were successfully eliminated by the RF deliveries targeting the VPCs’ foci. At the successful ablation sites, Purkinje potentials preceded the QRS onset of the VPC by 67 ± 23 ms, suggesting the VPCs originated in the surviving Purkinje fibers. Moreover, the extensive RF deliveries applied at the surviving Purkinje network rendered the polymorphic VT unable to be induced by programmed stimulation which reproducibly induced it before the ablation in 2 patients. Conclusion: A surviving Purkinje network might contribute not only to the initiation of the repetitive form of lethal ventricular arrhythmias, but also to the perpetuation of the arrhythmias in patients with ischemic heart disease
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