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Background: Increased spatial and temporal dispersion of repolarization contributes to ventricular arrhythmogenesis. Beat-to-beat fluctuations in T-wave timing are thought to represent such dispersion and may predict clinical events.Objective: The purpose of this study was to assess whether a novel noninvasive measure of beat-to-beat instability in T-wave timing would provide additive prognostic information in post-myocardial infarction patients.Methods: We studied 678 patients from 12 hospitals with 32-lead 5-minute electrocardiogram recordings 6-8 weeks after myocardial infarction. Custom software identified R wave-to-T wave intervals (RTIs) and diastolic intervals (DIs). Repolarization scatter (RTI:DI(StdErr)) was then calculated as the standard error about the RTI:DI regression line. In addition, left ventricular ejection fraction (LVEF), short-term heart rate variability (HRV) parameters, and QT variability index were measured. Patients were followed for the composite endpoint of death or life-threatening ventricular arrhythmia.Results: After a mean follow-up of 63 months, 134 patients met the composite endpoint. An RTI:DI(StdErr) >5.50 ms was associated with a 210% increase in arrhythmias or deaths (P <.001). After adjusting for LVEF, RTI:DI(StdErr) remained an independent predictor (P <.001). RTI:DI(StdErr) was also independent of short-term HRV parameters and the QT variability index.Conclusions: Increased repolarization scatter, a measure of high-frequency, cycle-length-dependent repolarization instability, predicts poor outcomes in patients after myocardial infarction. [ABSTRACT FROM AUTHOR]

Competing Interests: Disclosures Drs Hamdan, Brignole, Michelet, Deharo, and Guieu have an approved (EU) and pending (US) patent application entitled Sublingual Formulation for Hypotension and Syncope.

Background: Obesity is associated with significantly increased cardiovascular mortality that has been attributed, in part, to sympathetic activation. Gastric bypass surgery (GBS) appears to increase long-term survival in the severely obese, but the mechanisms responsible for this increase are still being sought. Heart rate (HR) recovery after exercise reflects the balance of cardiac autonomic input from the sympathetic and parasympathetic systems. Blunted HR recovery is a very powerful predictor of increased mortality, whereas enhanced HR recovery portends a good prognosis., Objective: The purpose of this study was to evaluate the effect of marked weight loss achieved via GBS on HR recovery., Methods: Severely obese patients underwent submaximal exercise testing (80% predicted maximum HR) at baseline and 2 years after GBS (n = 153) or nonsurgical treatment (n = 188)., Results: Patients in the GBS group lost an average of 100 ± 37 lb compared to 3 ± 22 lb in the nonsurgical group (P <.001, GBS vs nonsurgical). Resting HR decreased from 73 bpm to 60 bpm in the GBS group and from 74 bpm to 68 bpm in nonsurgical patients (P <.001). HR recovery improved by 13 bpm in the GBS group but did not change in the nonsurgical group (P <.001 GBS vs nonsurgical). In multivariable analysis, the independent correlates of HR recovery at the 2-year time point were resting HR, treadmill time, age, body mass index, and HOMA-IR (an index of insulin resistance)., Conclusion: Marked weight loss 2 years after GBS resulted in a significant decrease in resting HR and an enhancement in HR recovery after exercise. These changes likely are attributable to improvement in insulin sensitivity and cardiac autonomic balance. Whether and to what extent this contributes to a reduction in cardiovascular mortality with GBS remains to be determined., (Published by Elsevier Inc.)

Background: Sudden cardiac death is usually caused by ventricular arrhythmias and in many cases, is preceded by frequent ventricular ectopy. It is known that ectopic beats cause transient increases in sympathetic nerve activity (SNA)., Objective: Because high SNA is known to be arrhythmogenic, we hypothesized that high rates of ectopy increase SNA, thereby creating a milieu that favors development of ventricular tachycardia and/or fibrillation., Methods: This study measured muscle SNA, coronary sinus catecholamine, and arterial pressure during graded rates of ventricular ectopy (from 4:1 to 1:1, sinus to ectopic beat ratio) in a total of 21 patients referred for electrophysiologic testing., Results: Both muscle SNA and coronary sinus norepinephrine increased significantly with increased ectopy frequency (P < .05). Moreover, the change in muscle SNA correlated significantly with the change in coronary sinus norepinephrine levels (r = .72, P < .001)., Conclusion: These data demonstrate that sympathoexcitation evoked by high rates of ventricular ectopy can contribute to a state of elevated SNA both in peripheral tissues and within the heart. This altered autonomic state may contribute to an increased susceptibility to life-threatening tachyarrhythmias in patients with high rates of ectopy., (Copyright 2010 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Heart rate turbulence (HRT) has been shown to be vagally mediated with a strong correlation to baroreflex indices. However, the relationship between HRT and peripheral sympathetic nerve activity (SNA) after a premature ventricular contraction (PVC) remains unclear., Objective: We sought to evaluate the relationship between HRT and the changes in peripheral SNA after PVCs., Methods: We recorded postganglionic muscle SNA during electrocardiogram monitoring in eight patients with spontaneous PVCs. Fifty-two PVCs were observed and analyzed for turbulence onset (TO) and slope (TS). SNA was quantified during (1) the dominant burst after the PVC (dominant burst area) and (2) the 10 seconds after the dominant burst (postburst SNA)., Results: The mean TO was 0.1% +/- 4.6%, and the mean TS was 6.1 +/- 6.6. The dominant burst area negatively correlated with TO (r = -0.50, P = .0002). The postburst SNA showed a significant positive correlation with TO (r = 0.44, P = .001) and a negative correlation with TS (r = -0.42, P = .002). These correlations remained significant after controlling for either the PVC coupling interval or the left ventricular ejection fraction., Conclusions: Our findings highlight the relationship between perturbations in HRT and pathology in the sympathetic limb of the autonomic nervous system. Future studies are needed to evaluate the prognostic role of baroreflex control of sympathetic activity in patients with structural heart disease.

Background: We have recently shown that atrial fibrillation is associated with an increase in sympathetic nerve activity (SNA) compared with sinus rhythm. It remains unclear, however, whether these findings are true at various rates and whether the magnitude of sympathoexcitation is related to the degree of irregularity., Objective: To determine the role of irregularity in mediating the SNA changes at various pacing rates. Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001) but that MAP and DBP did not change significantly., Methods: Using custom-made software, atrioventricular sequential pacing with predetermined rates (100, 120, and 140 bpm) and irregularities (standard deviation = 0%, 5%, 15%, and 25% of mean cycle length) was performed in 23 patients referred for electrophysiologic evaluation. Pacing at each rate/irregularity was performed for 2 minutes, with 2 minutes of recovery in between. Systolic, diastolic, and mean arterial blood pressure (SBP, DBP, and MAP), central venous pressure (CVP), and SNA were measured at baseline and during pacing., Results: Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001 but that MAP and DBP did not change significantly. A significant correlation was found between the pacing irregularity and SNA, with greater sympathoexcitation noted at greater degrees of irregularity (r = 0.2, P = .04). A five-variable linear model using DBP, MAP, CVP, and degree of pacing irregularity to predict SNA was highly statistically significant (r = 0.46, P < .001). After controlling for hemodynamic changes, for every 1% increase in irregularity, there was a 6.1% increase in SNA., Conclusion: We have shown that greater degrees of irregularity cause greater sympathoexcitation and that the effects of irregular pacing on SNA are independent of the hemodynamic changes.

Objectives: The aim of the present study was to evaluate in a prospective randomized fashion the electrophysiologic effects of acute biventricular (BV) pacing. We hypothesized that (1) the local coupling interval in the left ventricle in response to right-sided ventricular premature beats is prolonged when BV pacing is applied during the drive train compared with right ventricular (RV) pacing, and (2) BV programmed electrical stimulation (PES) decreases the induction of ventricular arrhythmias compared with standard RV-PES, regardless of the presence of intraventricular conduction delay., Background: Previous studies have suggested that BV pacing might decrease the frequency of ventricular arrhythmias; however, the mechanism of arrhythmia suppression remains unclear., Methods: Eighteen patients with coronary artery disease were randomized to RV-PES or BV-PES with a repeat study using the other pacing mode. The RV effective refractory periods were measured during RV-PES and BV-PES. In addition, the local LV S(1)-S(2) coupling interval was measured at 600/450 ms and 400/350 ms during RV-PES and BV-PES., Results: BV-PES had no effect on RV effective refractory periods. On the other hand, the local LV S(1)-S(2) coupling intervals increased significantly during BV-PES compared with RV-PES (P < .0001). Ventricular tachycardia was induced in six patients using RV-PES but in only one patient with BV-PES (RR = 83%, P = .01). No difference was observed in the induction of ventricular fibrillation., Conclusions: BV-PES significantly reduced the induction of ventricular tachycardia compared to RV-PES, with no significant effect on ventricular fibrillation induction. Our findings may help explain the reduced incidence of ventricular arrhythmias noted with chronic BV pacing.