Mechanism of ST Elevation and Ventricular Arrhythmias in an Experimental Brugada Syndrome Model
| العنوان: | Mechanism of ST Elevation and Ventricular Arrhythmias in an Experimental Brugada Syndrome Model |
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| المؤلفون: | Takumi Higuma, Shingen Owada, Shigeru Motomura, Takao Kobayashi, Shingo Sasaki, Ken Okumura, Masaomi Kimura, Atsushi Iwasa, Keiichi Ashikaga |
| المصدر: | Circulation. 109:125-131 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2004. |
| سنة النشر: | 2004 |
| مصطلحات موضوعية: | Male, Tachycardia, medicine.medical_specialty, Potassium Channels, Pilsicainide, In Vitro Techniques, Ventricular tachycardia, Electrocardiography, Dogs, Sodium channel blocker, Physiology (medical), Internal medicine, medicine, Animals, cardiovascular diseases, Endocardium, Brugada syndrome, medicine.diagnostic_test, business.industry, Pinacidil, ST elevation, Lidocaine, Syndrome, medicine.disease, Disease Models, Animal, Anesthesia, Tachycardia, Ventricular, cardiovascular system, Cardiology, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Sodium Channel Blockers, medicine.drug |
| الوصف: | Background— Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited. Methods and Results— We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35×30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a K ATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other. Conclusions— Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT. |
| تدمد: | 1524-4539 0009-7322 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2416dde5c56867ebfb5eb72114a9b8c7Test https://doi.org/10.1161/01.cir.0000105762.94855.46Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....2416dde5c56867ebfb5eb72114a9b8c7 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244539 00097322 |
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