Mechanism of spontaneous initiation of ventricular fibrillation in patients with implantable defibrillators

Abstract

Introduction To improve the mechanistic understanding of spontaneous initiation of ventricular fibrillation (VF), we characterized the patterns of premature ventricular complex (PVC) preceding spontaneous VF in primary and secondary implantable cardioverter‐defibrillator (ICD) recipients. Methods and Results A single‐center, cross‐sectional analysis of 1209 patients with primary and secondary prevention ICD identified 190 patients who received ICD therapy (firing or antitachycardia pacing) for VF or monomorphic ventricular tachycardia (MMVT). Initiation was quantified by the coupling interval (CI), the cycle length immediately preceding the CI (CL(−1)), the CI corrected by CL(−1) using Fridericia's formula (CIc), and the prematurity index (PI). In both VF (n = 44; 23%) and MMVT (n = 134; 71%), the most common pattern of initiation was late‐coupled PVC, followed by the short‐long‐short pattern. The parameters such as pre‐initiation median CL, CL(−1), CI, and PI were not significantly different between VF and MMVT for any patterns. At least some events (45% of VF and 63% of MMVT) had extremely long CIs beyond the QTc cut‐off estimated from the CL(−1), suggestive of initiation by a train of multiple PVCs or nonsustained VT instead of a single PVC. Conclusion Some spontaneous VF events in ICD recipients appear to be initiated by a train of multiple PVC or nonsustained VT rather than a single PVC. This finding indicates that patterns of a single PVC are not an important determinant of VF initiation and thus account for conflicting results in previous studies.

Mechanism of Ventricular Tachycardia Occurring in Chronic Myocardial Infarction Scar

“…However, even in the acute MI setting, reentry plays a prominent role secondary to heterogeneous conduction and repolarization of myocardial tissue in the border of infarct and noninfarcted/ischemic territory. 5,39,40 While case reports have detailed triggered activity as the mechanisms for VT in patients with a chronic MI, 41 as determined by reproducible initiation with atrial and ventricular stimulation with a long pause followed by a short coupling interval between subsequent beats, computational modeling and invasive electrophysiological studies in humans with chronic MI consistently support reentry as the primary mechanisms for the maintenance of VT. [42][43][44]…”

“…While case reports have detailed triggered activity as the mechanisms for VT in patients with a chronic MI, 41 as determined by reproducible initiation with atrial and ventricular stimulation with a long pause followed by a short coupling interval between subsequent beats, computational modeling and invasive electrophysiological studies in humans with chronic MI consistently support reentry as the primary mechanisms for the maintenance of VT. 42–44…”