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Notes: RR Dynamics Before VT. 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 In msec2, P = 0.036), low (low-frequency power [LFP]: 5.61 ± 1.43 to 5.28 ± 1.59 in 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) (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 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.

Notes: Introduction: Estrogen is an important modulator of cardiovascular risk, but its mechanism of action is not fully understood. We investigated the effect of ovariectomy and its timing on the cardiac electrophysiology in mice. Methods: Thirty female mice (age 18.8 ± 3.1 weeks) underwent in vivo electrophysiologic testing before and after autonomic blockade. Fifteen mice were ovariectomized prepuberty (PRE) and ten postpuberty (POST), 2 weeks prior to electrophysiologic testing. Five age-matched sham-operated female mice (Control) served as controls. A subset of 13 mice (5 PRE, 3 POST, and 5 Controls) underwent 24-hour ambulatory monitoring. Results: With ambulatory monitoring, the average (668 ± 28 vs 769 ± 52 b/min, P = 0.008) and minimum (485 ± 47 vs 587 ± 53 b/min, P = 0.02) heart rates were significantly slower in the ovariectomized mice (PRE and POST groups) compared to the Control group. At baseline electrophysiologic testing, there were no significant differences among the ovariectomized and intact mice in any of the measured parameters. With autonomic blockade, the Control group had a significantly larger change (▵) in the atrioventricular (AV) nodal Wenckebach (AVW) periodicity (▵AVW = 11.3 ± 2.9 vs 2.1 ± 7.3 ms, P = 0.05) and functional refractory period (▵FRP = 11.3 ± 2.1 vs 1.25 ± 6.8 ms, P = 0.02) compared to the ovariectomized mice. These results were not altered by the time of ovariectomy (PRE vs POST groups). Conclusion: Our results suggest that estrogen modulates the autonomic inputs into the murine sinus and AV nodes. These findings, if replicated in humans, might underlie the observed clustering of certain arrhythmias around menstruation and explain the higher incidence of arrhythmias in men and postmenopausal women.

Notes: Background:The implantable cardioverter defibrillator (ICD) has underscored the limitations of our methods of risk assessment. ICDs should be available to patients at high risk for arrhythmic death, but because of the potential for adverse effects and high cost it should be scrupulously avoided in patients whose lives will not be prolonged. Unfortunately, discrimination between these two groups of patients remains a challenge. Recent clinical trial results have not only shown that electrophysiological studies (EPS) in combination with other risk stratifiers identify patients with ischemic heart disease at high risk for arrhythmic death, but they have linked the efficacy of ICD therapy to the results of EPS. However, to perform EPS in all potential candidates for ICD therapy would be a time-consuming and costly burden to medical services and would expose many patients to the risks and discomfort of an invasive procedure. Noninvasive identification of appropriate candidates is therefore essential to successful application of EPS. Methods:Nonsustained ventricular tachycardia (NSVT) and a reduced left ventricular ejection fraction (EF) was used to select patients for EPS in two important trials, but it is not certain that these are the optimal tests or that the optimal thresholds 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:1082720X:ANEC434:ges" location="ges.gif"/〉 1 episode of NSVT 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:1082720X:ANEC434:ges" location="ges.gif"/〉 3 beats; EF 〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:1082720X:ANEC434:les" location="les.gif"/〉 0.35 or EF 〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:1082720X:ANEC434:les" location="les.gif"/〉 0.40) were used. A number of studies have addressed the accuracy of clinical factors for predicting the results of EPS and a number of noninvasive tests have been proposed including the signal-averaged electrocardiogram, heart rate variability, T-wave alternans, and high spatial resolution (multilead) electrocardiography. In some contexts, combinations of factors provide significant improvements in accuracy. However, the populations studied were often highly selected, which makes comparisons between techniques or prediction of responses in the populations that would require screening difficult. Results from recently completed and ongoing clinical trials should provide important new information. A greater problem is that EPS has not been shown to consistently provide accurate discrimination of patients with nonischemic cardiac disorders. Conclusions:Effective widespread application of ICD therapy will require greater precision of patient selection. Noninvasive tests under investigation demonstrate considerable promise in selecting appropriate candidates for EPS. However, because the most precise methods of risk assessment are likely to be those most closely linked to the mechanisms of fatal arrhythmias, it is important that further development of noninvasive techniques incorporates advances in basic cardiac electrophysiology. A.N.E. 1999;4(4):434–442

Notes: Introduction: Psychological stress can precipitate ventricular arrhythmias in patients with ICDs, as well as sudden death. However, the physiologic pathways remain unknown. We sought to determine whether psychological stress induced in the laboratory setting alters indices of repolarization associated with arrhythmogenesis. Methods and Results: Patients with ICDs and a history of ventricular arrhythmia underwent ambulatory ECG monitoring during a laboratory mental stress protocol (anger recall and mental arithmetic). Continuous changes in repolarization indices which have correlated with temporal and spatial myocardial heterogeneity of repolarization, including T-wave alternans (TWA), T-wave amplitude (Tamp), and T-wave area (Tarea) were analyzed in the time domain. In the 33 patients (85% male, 88% with coronary artery disease, mean ejection fraction 30%), norepinephrine, epinephrine, BP, and HR increased during mental stress. TWA increased from 22 (interquartile range 16–27) at baseline to 29 (21–38) uV during mental stress (P 〈 0.001). Changes in TWA correlated with changes in HR, systolic BP, and catecholamines. Tamp and Tarea also increased with mental stress (P 〈 0.01) but did not correlate with changes in other variables. Conclusion: Psychological stress increased TWA, Tamp, and Tarea. Autonomically mediated repolarization changes may be a pathophysiologic link between emotion and arrhythmia in susceptible patients.

Notes: Abstract High-resolution measurement of skin temperature in 11 normal subjects revealed low-amplitude temperature oscillations (40 × 10−3°C). The temperature signal measured on two hands during baseline, stress, and recovery periods, was filtered to separate the low-amplitude oscillations from the temperature signal. Spectral analysis of the filtered signal showed that most of the energy of the signal is in a range of 0.01 to 0.03 Hz. Frequency shifts and amplitude changes of the largest component were observed in response to mental stress. In subjects with high baseline values of either of these two variables, a decrease was observed in response to stress. An opposite response was observed in subjects with significantly lower baseline levels. Stress-related changes in peak frequency ranged from −25% to +18.2%; changes in peak amplitude ranged from −74.6% to +280%. Changes in the mean temperature were limited to 2.4%. Thus, the oscillatory component showed higher sensitivity to psychological stress than mean temperature. The spectrum of this component was compared to the spectrum of the blood pressure waves measured noninvasively. Both exhibited similar dynamics of energy, peak amplitude, and peak frequency in response to psychological stress. This similarity suggests that the oscillatory temperature component reflects stress-related changes of peripheral vasomotor activity.