Value of Programmed Ventricular Stimulation in Patients with Congenital Heart Disease

Me, Alexander; Ep, Walsh; Jp, Saul; Mr, Epstein; Jk, Triedman

doi:10.1111/j.1540-8167.1999.tb00274.x

Cited by 107 publications

(47 citation statements)

References 28 publications

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“…Although not assessed in the present study, inducible nonsustained VT has also been associated with decreased survival in a mixed cohort of congenital heart patients. 10 Although the value of inducible VT as a risk factor after tetralogy of Fallot repair has been demonstrated, questions about patient selection for screening and the timing and frequency of testing remain to be elucidated. Test sensitivity, specificity, and likelihood ratios, increasingly considered the best available indexes to evaluate diagnostic tests, are independent of prevalence assumptions.…”

Section: Discussionmentioning

confidence: 99%

Value of Programmed Ventricular Stimulation After Tetralogy of Fallot Repair

et al. 2004

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Section: Discussionmentioning

confidence: 99%

Value of Programmed Ventricular Stimulation After Tetralogy of Fallot Repair

et al. 2004

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“…The investigators found that patients with low-grade ectopy (isolated beats or couplets) were less likely to have inducible VT than patients with high-grade ectopy (sustained or nonsustained VT). Furthermore, patients with inducible VT had a higher risk of sudden cardiac death, although there were many false negatives (12). Khairy et al (13) reported a multicentre study that examined the prognostic role of VSTIM in repaired tetralogy of Fallot patients in which inducible sustained VT predicted an increased risk of clinical VT or sudden cardiac death.…”

Section: Cardiac Tumours and Icdsmentioning

confidence: 99%

“…The role of programmed ventricular stimulation (VSTIM) to assess risk of mortality in this group of patients is also unclear. Alexander et al (12) used VSTIM in selected patients with palliated or repaired congenital heart disease, including tetralogy of Fallot, aortic stenosis and dextro-transposition of the great arteries. The investigators found that patients with low-grade ectopy (isolated beats or couplets) were less likely to have inducible VT than patients with high-grade ectopy (sustained or nonsustained VT).…”

Section: Cardiac Tumours and Icdsmentioning

confidence: 99%

Benign cardiac tumours, malignant arrhythmias

Myers

Wong

Tipple

et al. 2010

Canadian Journal of Cardiology

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“…However, the distinction between what is normal and abnormal in terms of VT inducibility has not yet been clearly substantiated (1,12,13). The susceptibility to inducible VT may be influenced by a variety of factors in addition to genotype, including age, sex, strain, and autonomic and catecholaminergic state.…”

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Implications of ventricular arrhythmia vulnerability during murine electrophysiology studies

Maguire

Wakimoto

Patel

et al. 2003

Physiological Genomics

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Programmed ventricular stimulation is being performed for the provocation of ventricular arrhythmias in genetically engineered mice. Despite the high level of interest in this area of translational research, little attention has been given to differentiating between selectivity and specificity of induced ventricular tachycardia (VT) in phenotypically normal mice. We aimed to assess factors that may enhance inducibility of VT in wild-type (WT) mice. In vivo intracardiac electrophysiological studies (EPS) were performed in 230 WT mice of 4 strains. An octapolar electrode catheter was inserted into a jugular vein and advanced to the right atrium and ventricle. Baseline ventricular conduction, refractoriness, and arrhythmia inducibility were assessed using programmed electrical stimulation (PES) and burst pacing. We found that nonsustained VT (Ն4 beats) was inducible in 68/230 (30%) mice. Duration of VT was 1.6 Ϯ 2.4 s, and the longest episode lasted 24 s. VT inducibility differed by strain and age. Ventricular effective refractory period (VERP) was shorter in mice with inducible VT (44 Ϯ 12 ms) compared with noninducible mice (61 Ϯ 16 ms, P Ͻ 0.001). VERP increased with age (P Ͻ 0.001), albeit with strain-related variability. We conclude that nonsustained VT in WT mice is reproducibly inducible and common. Genetic background variability may predispose certain strains to a higher incidence of arrhythmia induction. EPS methods impact prevalence and specificity of inducible VT. Increased VT inducibility was seen with shorter coupling intervals and application of tightly coupled extrastimuli techniques. These factors should be carefully considered when analyzing PES and burst pacing data in murine models to minimize false positives and optimize accuracy. mice; ventricular tachycardia; programmed stimulation; genetics MURINE MODELS FOR THE STUDY of cardiac arrhythmias have made steady gains in usage and basic research applicability. These models enable mechanistic studies that expose phenotypes including electrophysiological abnormalities and arrhythmias. In vivo mouse electrophysiology studies (EPS) are being performed to evaluate arrhythmia vulnerability and electrophysiological phenotypes of genetically manipulated mice (5,8,18). Standardized pacing and programmed electrical stimulation (PES) protocols are routinely used for EPS in mice to gauge the relative inducibility of ventricular arrhythmias. Genetics and molecular biological laboratories have a need for determination of which genotypes have an inherently greater susceptibility to arrhythmias such as ventricular tachycardia (VT). Several specific disease models have exhibited disproportionately higher rates of inducible VT compared with wild-type mice during EPS testing (6,9,28,31). Until recently, induction of VT in wild-type mice had been considered to be a relatively rare event. To evaluate pacing-induced ventricular arrhythmia vulnerability in mouse models of human diseases, it will be necessary to accurately interpret the EPS findings and determine the sen...

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Value of Programmed Ventricular Stimulation in Patients with Congenital Heart Disease

Cited by 107 publications

References 28 publications

Value of Programmed Ventricular Stimulation After Tetralogy of Fallot Repair

Value of Programmed Ventricular Stimulation After Tetralogy of Fallot Repair

Benign cardiac tumours, malignant arrhythmias

Implications of ventricular arrhythmia vulnerability during murine electrophysiology studies

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