Prediction of Ventricular Tachyarrhythmias by Intracardiac Repolarization Variability Analysis

Abstract

Background-Arrhythmic sudden cardiac death (SCD) is generally mediated by ventricular fibrillation (VF) or fast ventricular tachycardia (FVT). We studied the predictive value of temporal QT variability detected from various sources of cardiac electric signal: surface ECG, far-field (FF), and near-field (NF) intracardiac electrograms (EGMs) in patients with implantable cardioverter-defibrillators (ICDs

Beat-to-Beat Variability in Preload Unmasks Latent Risk of Torsade de Pointes in Anesthetized Chronic Atrioventricular Block Dogs

“…Pressure-volume (PV) loops were recorded in order to quantify the pacing-induced preload variability, with and without mechanical ventilation, simultaneously with LV MAP, in an additional set of 9 CAVB dogs (median 9 [7][8][9][10][11][12][13][14] weeks after AV-block). In the same experiment, the effect of SAC block by streptomycin on baseline BVR and arrhythmic response to dofetilide was tested; during pacing with alternating PQ, streptomycin was infused (40 mg/kg in 5 min i.v.…”

“…These results confirm the association between STVMAPD and proarrhythmia, and suggest involvement of the SAC in BVR in the CAVB dog. infusion: 27 vs. 4 [2][3][4][5][6][7][8][9][10][11][12][13] (P=0.07, Figure 6). However, this could not prevent an increase of STVMAPD, from 0.6±0.2 ms to 4.0±3.3 ms (P=0.006), and is similar to the value obtained in the group that received only dofetilide.…”

“…In these dogs, dofetilide infusion (0.025 mg · kg -1 · 5 min -1 ) was followed by streptomycin (40 mg · kg -1 · 5 min -1 , n=7), while in controls (n=10), only dofetilide was administered. Arrhythmia score, determined during the 15-25 min interval after the start of dofetilide administration, was significantly lower in the streptomycin-treated animals (2 [1][2][3] vs. 4 [2][3][4][5][6][7][8][9][10][11], P=0.049). Literature provides a possible role for ISAC in triggering of the ectopic beats that initiate the TdP arrhythmias; formation of early afterdepolarizations (EADs) in vivo may be a stochastic Figure 6.…”

How can we stabilize QT variability?

“…The magnitude of alternate and non-alternate T wave oscillations increased immediately before the onset of ventricular tachyarrhythimia 9 and the QTVI is a useful method to identify unstable repolarization variability that MTWA fails to detect. Previous studies showed patients with ischemic or non-ischemic dilated cardiomyopathy had increased QTVI compared to control subjects 8,10,11 . The value of QTVI depended on severity of New York Heart Association (NYHA) functional class and was a predictor of total mortality, sudden cardiac death, and occurrence of ventricular tachyarrhythmias.…”

Ventricular Tachyarrhythmia Prediction based on Heart Rate Variability and Genetic Algorithm

“…SCD accounts for one out of every two deaths from cardiovascular diseases [2]. Therefore, development of the reliable predictor of VTA onset, namely the ventricular tachycardia (VT) and ventricular fibrillation (VF), is clinical important because the prediction provides opportunity to timely prevention of the negative consequences brought by VTA through early termination by implantable cardioverter defibrillator (ICD) [3].…”