QT variability paradox after premature ventricular contraction in patients with structural heart disease and ventricular arrhythmias
Increased repolarization lability is known to be associated with the risk of ventricular tachycardia (VT)/ventricular fibrillation (VF). Premature ventricular contractions (PVCs) are excluded from the analysis of QT variability. However, QT dynamics after PVCs is poorly understood.We analyzed data of 33 patients with structural heart disease (mean age 60.5 ± 12.1; 24 (73%) men; 26 (79%) whites; 22 (67%) ischemic cardiomyopathy) and single-chamber ICD implanted for primary (28 patients, 85%) or secondary prevention of SCD. Arrhythmia group comprised 16 patients with VT/VF/death outcomes. Alive patients (n = 17) without VT/VF served as controls. The baseline far-field (FF) ICD electrogram (EGM) was recorded at rest. RR and QT intervals of 15 sinus beats before and after PVC in 33 patients were analyzed. The prematurity index, C(i)Mean(RR), where C(i) is coupling interval, was used to select the most premature PVC. QT variability index (QTVI) was calculated. Difference in QTVI was calculated as QTVI(diff) = QTVI(after)-QTVI(before.)In paired analysis QTVI significantly increased after PVC in controls (0.64 ± 1.02 vs. 0.26 ± 1.15; P = 0.046), but decreased in patients in the arrhythmia group (0.16 ± 0.85 vs. 0.43 ± 0.84; P = 0.190). QTVI(diff) was significantly lower in patients with VT/VF, as compared to controls (-0.197 ± 0.650 vs. 0.207 ± 0.723; P=0.030). In multivariate logistic regression after adjustment for the type of cardiomyopathy and NYHA class the decrease in QTVI after PVC was associated with increased risk of VT/VF (OR 9.24; 95% CI 1.11-76.82; P=0.040).Elevated at baseline QTVI is decreased during first 15 beats after PVC in patients at risk for VT/VF.