Sudden cardiac death and polymorphous ventricular tachycardia in pationts with normal QT intervals and normal systolic cardiac function

Eisenberg, Susan J.; Scheinman, Melvin M.; Duller, Navneet K.; Finkbeiner, Walter E.; Griffin, Jerry C.; Eldar, Michael; Franz, Michael R.; González, Rolando; Kadish, Alan H.; Lesh, Michael D.

doi:10.1016/s0002-9149(99)80654-7

Cited by 86 publications

(51 citation statements)

References 18 publications

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“…Torsade de pointes z krótkim sprzężeniem cechuje się niezwykle krótkim sprzężeniem (< 300 ms) pierwszego przedwczesnego pobudzenia komorowego, które inicjuje częstoskurcz. Arytmia ta występuje głównie u młodych pacjentów, u których często stwierdza się niewyjaśnione omdlenia oraz obciążające wywiady rodzinne w kierunku SCD [589][590][591]. W większości przypadków TdP przechodzi w VF.…”

Section: Torsade De Pointes Z Krótkimunclassified

“…Mimo że mechanizmy tej arytmii nie zostały dotychczas dobrze poznane, to może się ona wiązać z nierównowagą czynności autonomicznego układu nerwowego [592]. Wydaje się, że jedynym lekiem, który może wygaszać tę arytmię, jest werapamil podawany dożylnie, ale nie obniża on ryzyka SCD [590,591]. W rezultacie zdecydowanie zaleca się wszczepienie ICD [589].…”

Section: Torsade De Pointes Z Krótkimunclassified

See 1 more Smart Citation

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Priori

Blomström‐Lundqvist²,

Mazzanti³

et al. 2015

Kardiol Pol

233

337

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Section: Torsade De Pointes Z Krótkimunclassified

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Priori

Blomström‐Lundqvist²,

Mazzanti³

et al. 2015

Kardiol Pol

233

337

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“…[1][2][3][4][5][6][7][8][9][10][11] Mutations in the ryanodine 2 receptor (RyR2) gene [12][13][14][15] and calsequestrin 2 (CASQ2) gene 14,[16][17][18] have been identified in patients with CPVT, and triggered activity because of delayed afterdepolarization is thought to be the underlying cellular mechanism of the arrhythmias. 19 Although the clinical characteristics of patients with CPVT are well defined, atrial arrhythmias and sinus node (SN) function have not been evaluated in previously published studies.…”

mentioning

confidence: 99%

Association of Atrial Arrhythmia and Sinus Node Dysfunction in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia

Sumitomo

Sakurada

Taniguchi

et al. 2007

Circ J

122

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Statistical AnalysisAll numeric data are presented as the means ± SD. Because of differences in the variables and limited sample numbers, statistic analysis was performed using Wilcoxon nonparametric analysis or chi-square analysis when necessary. A p-value less than 0.05 was considered significant. Circ J 2007; 71: 1606 -1609 (Received May 8, 2007 revised manuscript received June 14, 2007; accepted June 22, 2007 Background This study was performed to investigate the frequency and importance of supraventricular arrhythmia and sinus node (SN) dysfunction in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT). Methods and ResultsEight patients with CPVT (mean age: 16.8±8.1 years) underwent an electrophysiological study. SN recovery time (1,389±394 ms) was slightly prolonged, and 4 of 8 patients had abnormal values. Atrial flutter (AF) was induced by low-rate atrial pacing in 2 patients and by isoproterenol infusion in 1 patient. Atrial fibrillation (Af) was induced by isoproterenol infusion in 2 patients. One patient presented with Af during the follow-up period, and 2 of 4 patients with AF/Af presented with increased SN recovery time.Conclusions Patients with CPVT frequently have associated with SN dysfunction, and inducible atrial tachyarrhythmias, which indicate that the pathogenesis of CPVT is limited not only to the ventricular myocardium, but also to broad regions of the heart, including the SN and atrial muscle. (Circ J 2007; 71: 1606 -1609)

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“…[124][125][126][127] CPVT is not associated with organic heart diseases, and there is no sex difference in incidence. In patients with CPVT, exercise and intravenous isoproterenol induce a gradual increase in PVC, which further lead to polymorphic or bidirectional VT, very fast polymorphic VT (350 to 400/min), and finally to VF.…”

Section: Catecholamine-induced Polymorphic Ventricular Tachycardiamentioning

confidence: 98%

Guidelines for Risks and Prevention of Sudden Cardiac Death (JCS 2010) - Digest Version -

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2012

Circ J

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Sudden cardiac death and polymorphous ventricular tachycardia in pationts with normal QT intervals and normal systolic cardiac function

Cited by 86 publications

References 18 publications

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Association of Atrial Arrhythmia and Sinus Node Dysfunction in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia

Guidelines for Risks and Prevention of Sudden Cardiac Death (JCS 2010) - Digest Version -

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