Introduction: We hypothesized that autonomic activity preceding spontaneous sustained monomorphic ventricular tachycardia (VTsm) as assessed by heart rate (HR) and RR interval variability (RRV) differs between type 1 VTsm which is initiated by morphologically distinct, early cycle, possibly triggering premature ventricular complexes (PVCs) and type 2 VTsm in which the initial complex has a QRS waveform identical to subsequent complexes.
Methods and results: Baseline Holter tapes (1,646) from a clinical trial were scanned for VTsm. QRS complexes of VTsm were compared by two-lead cross-correlation to distinguish type 1 and type 2 VTsm. Frequency domain RRV index were estimated over 5 minutes, 15 minutes, and 24 hours. Type 1 and type 2 VTsm were present in 15 (group 1) and 33 (group 2) of 48 patients, respectively. HR did not change in group 1 (88.4+/-15.2 to 89.7+/-13.0 beats/min, P = 0.89), but increased before the onset of VTsm in group 2 (74.3+/-16.3 to 81.2+/-18.0 beats/min, P < 0.001). RRV index were severely depressed in both groups. No RRV index changed significantly before the onset of type 1 VTsm, whereas significant changes occurred before type 2 VTsm from 24-hour average to 30 minutes before VTsm in very low (very low-frequency power [VLFP]: 6.62+/-1.53 to 6.20+/-2.07 ln msec2, P = 0.036), low (low-frequency power [LFP]: 5.61+/-1.43 to 5.28+/-1.59 ln msec2, P = 0.004), normalized low (normalized low-frequency power [LFPn]: -0.48+/-0.58 to -0.55+/-0.64 normalized units [nu], P = 0.05) and the ratio of LFP to high-frequency power (HFP) (LFP/HFP: 4.20+/-3.47 to 3.45+/-2.53, P = 0.017). Declines in RRV index between 2 hours to the 30-minute period before VTsm occurred in group 2 but not group 1 in LFP (5.85 +/- 1.42 to 5.28 +/- 1.59 In msec, P = 0.043) and HFP (4.94 +/- 5.14 to 3.46 +/- 2.52 In msec2, P = 0.008), with a downward trend in LFP/HFP (4.94+/-5.14 to 3.45+/-2.53, P = 0.127) and LFPn (-0.38+/-0.36 to -0.55+/-0.64, P = 0.15), while HFPn tended to rise (-1.47+/-0.65 to -1.27+/-0.64, P = 0.15).
Conclusions: HR and RRV did not change before type 1 VTsm, suggesting that short-term changes in autonomic activity were not essential to initiation of apparent PVC-triggered VTsm. In contrast, RR interval dynamics before type 2 VTsm suggested that short-term changes in neurohormonal activity contributed to arrhythmia initiation. Heterogeneities in arrhythmia onset may reflect distinct triggers and substrate properties that could provide a basis for effective therapeutic targets.