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Dynamics of Heart Rate Turbulence Axel Bauer, Raphael Schneider, Petra Barthel, Marek Malik and Georg Schmidt Deutsches Herzzentrum München & 1. Medizinische Klinik der Technischen Universität München, Germany Medical School, St. George’s Hospital, London, United Kingdom Compensatory Pause RR-interval [ms] 1000 -3 -2 -1 Turbulence Slope Turbulence Onset 800 Heart Rate Turbulence 600 Coupling Interval 0 5 10 Beat Number 15 Methods: This study was performed in 743 patients of the placebo arm of the EMIAT trial. Of these, 151 patients were excluded because of atrial fibrillation, no VPC during the Holter recording or missing Holter recording. During a median follow up of 21 months, 509 patients survived and 82 patients died. Holter recordings were obtained in the second or third week after index infarction. VPCs were included, if they featured ≥3 consecutive sinus intervals before and ≥15 consecutive sinus intervals after the ectopic beat, and if they were followed by a compensatory pause (defined as coupling interval + post-extrasystolic pause = 2 normal-to-normal intervals ±10%). Actual Heart Rate = 1 3 60.000 ⋅ (RRI (−3) + RRI (−2) + RRI (−1) ) The impact of the heart rate heart-rate turbulence was separately analyzed in surviving and non-surviving patients. The VPCs were sorted according to the actual heart rate. For each percentile of heart rate, an averaged tachogram was calculated. In each tachogram, the HRT-parameters TO and TS were derived according to the previously published technology. Results: In surviving patients, 75.391 VPCs met the inclusion criteria. In non-surviving patients, this figure was 24.816. In both, surviving and non-surviving patients, heart-rate turbulence decreased with increasing heart rates. The characteristics of the correlations were somewhat different for both parameters. Turbulence Onset was highest at low heart rates and gradually decreased at higher heart rates. At a heart rate of 80 bpm (non-survivors) and 100 bpm (survivors) TO almost abolished, whereas Turbulence Slope decreased over the whole range of heart rates. The slopes of the regression lines were generally higher in surviving patients than in non-surviving patients (Table). Conclusions: The impact of heart rate on HRT maybe twofold. At high heart rates, the duration of the postextrasystolic pause progressively shortens, so that the drop in diastolic arterial pressure diminishes and the hemodynamic trigger of heart-rate turbulence becomes weaker. Moreover, the sympatho-vagal balance is shifted in favor of a prevailing sympathetic tone, so that the baroreflex sensitivity may be attenuated. VPC of survivors VPC of non-survivors -2 -1 0 40 60 80 100 6 Turbulence Slope [ms/RRI] For each VPC, the actual heart rate was calculated from the last three normal intervals by the formula: Turbulence Onset [%] Introduction: Heart-Rate Turbulence (HRT) is the physiological short-term oscillation of the heart rate after a single ventricular premature complex (VPC)1. HRT probably reflects baroreflex activity triggered by the transient perturbation of arterial blood pressure after a VPC2,3. Therefore, the heart rate directly preceding the VPC should influence HRT. Aim of this study is to analyze the impact of the heart rate on HRT. 4 2 0 40 120 Survivors TO Actual Heart Rate 60 80 100 120 Heart Rate [bpm] Heart Rate [bpm] Non-Survivors TS r = 0.93 1) r = 0.85 2) TO TS r = 0.65 3) r = 0.85 4) 1) TO = 0.044 ⋅ HR − 4.535 3) TO = 0.02 ⋅ HR − 2.134 2) TS = −0.061 ⋅ HR + 8.281 4) TS = −0.044 ⋅ HR + 5.176 all correlations p < 0.0001 Literature: 1) Schmidt, G., et al., Heart-rate turbulence after ventricular premature beats as a predictor of mortality after acute myocardial infarction Lancet, 1999. 353(9162): p. 1390-6. 2) Malik, M., D. Wichterle, and G. Schmidt, Heart-Rate Turbulence. G Ital Cardiol, 1999. 29: p. 65-9. 3) Mrowka, R., et al., Blunted arterial baroreflexes causes "pathological" heart rate turbulence. Am J Physiol Regulatory Integrative Comp Physiol, 2000. 279: p. 1171-5.