Premium
Distinctive RR Dynamics Preceding Two Modes of Onset of Spontaneous Sustained Ventricular Tachycardia
Author(s) -
ANDERSON KELLEY P.,
SHUSTERMAN VLADIMIR,
AYSIN BENHUR,
WEISS RAUL,
BRODE SUSAN,
GOTTIPATY VENKATESHWAR
Publication year - 1999
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1999.tb01260.x
Subject(s) - medicine , cardiology , ventricular tachycardia , qrs complex , heart rate , heart rate variability , tachycardia , blood pressure
RR Dynamics Before VT.Introduction: We hypothesized that autonomic activity preceding spontaneous sustained monomorphic ventricular tachycardia (VT sm ) as assessed by heart rate (HR) and RR interval variability (RRV) differs between type 1 VT sm which is initiated by morphologically distinct, early cycle, possibly triggering premature ventricular complexes (PVCs) and type 2 VT sm 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 VT sm . QRS complexes of VT sm , were compared by two‐lead cross‐correlation to distinguish type 1 and type 2 VT sm , Frequency domain RRV index were estimated over 5 minutes, 15 minutes, and 24 hours. Type 1 and type 2 VT sm , 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 VT sm 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 VT sm , whereas significant changes occurred before type 2 VT sm from 24‐hour average to 30 minutes before VT sm in very low (very low‐frequency power [VLFP]: 6.62 ± 1.53 to 6.20 ± 2.07 In msec 2 , P = 0.036), low (low‐frequency power [LFP]: 5.61 ± 1.43 to 5.28 ± 1.59 in msec 2 , P = 0.004), normalized low (normalized low‐frequency power [LFP n ]: ‐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) (LPP/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 VT sm , 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 msec 2 P = 0.008), with a downward trend in LFP/HFP (4.94 ± 5.14 to 3.45 ± 2.53, P = 0.127) and LFP n (‐0.38 ± 0.36 to ‐0.55 ± 0.64, P = 0.15), while HFP n 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 VT sm , suggesting that short‐term changes in autonomic activity were not essential to initiation of apparent PVC‐triggered VT sm . In contrast, RR interval dynamics before type 2 VT sm 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.