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Increased sympathetic activity and endothelial dysfunction are the proposed mechanisms underlying exaggerated blood pressure response to exercise (EBPR). However, data regarding heart rate behavior in patients with EBPR are lacking. We hypothesized that heart rate recovery (HRR) could be impaired in patients with EBPR. A total of 75 normotensive subjects who were referred for exercise treadmill test examination and experienced EBPR were included to this cross-sectional case-control study. The control group consisted of 75 age- and gender-matched normotensive subjects without EBPR. EBPR was defined as a peak exercise systolic blood pressure (BP) ≥210 mmHg in men and ≥190 mmHg in women. HRR was defined as the difference in HR from peak exercise to 1 min in recovery; abnormal HRR was defined as ≤12 beats/min. These parameters were compared with respect to occurrence of EBPR. Mean values of systolic and diastolic BP at baseline, peak exercise, and the first minute of the recovery were significantly higher in the subjects with EBPR. Mean HRR values were significantly lower (P < 0.001) in subjects with EBPR when compared with those without. Pearson's correlation analysis revealed a significant positive correlation between the decrease in systolic BP during the recovery and degree of HRR in individuals without EBPR (r = 0.42, P < 0.001). Such a correlation was not observed in subjects with EBPR (r = 0.11, P = 0.34). The percentage of abnormal HRR indicating impaired parasympathetic reactivation was higher in subjects with EBPR (29 % vs 13 %, P = 0.02). In logistic regression analyses, HRR and resting systolic BP were the only determinants associated with the occurrence of EBPR (P = 0.001 and P < 0.001, respectively). Decreased HRR was observed in normotensive individuals with EBPR. In subjects with normal BP response to exercise, a linear correlation existed between the degree of HRR and decrease in systolic BP during the recovery period. However, such a correlation was not found in subjects with EBPR. Our data suggest that mechanisms underlying the blunting of the HRR might be associated with the genesis of EBPR. The association between the extent of HRR and adverse cardiovascular outcomes in patients with EBPR needs to be investigated in detail in future research.

Objective: The goal of the study described here was to evaluate interictal heart rate variability (HRV) in young patients with epilepsy, a patient population in whom sudden unexpected death in epilepsy (SUDEP) is known to be more common., Methods: Twenty-four-hour ambulatory ECG Holter recordings of 37 patients (15-40 years old) and 32 healthy controls were compared., Results: All of the time domain indices (SDNN, SDANN, RMSSD, and HRV triangular index) were significantly suppressed (P<0.001), and there was a marked reduction in parasympathetic tone (reduced HF(nu,)P<0.001) and an increase in sympathetic tone (increased LF(nu) and LF/HF ratio, P<0.001) in the patient group. Stepwise linear regression analysis revealed that polytherapy and epilepsy duration >10 years were independent variables associated with a reduction in SDNN., Conclusion: Our data suggest that the major determinants of suppressed SDNN are polytherapy and epilepsy duration >10 years. Analysis of spectral measures of frequency domain indices suggests that an increased sympathetic tone in association with a decreased parasympathetic tone may constitute the mechanism underlying SUDEP in young people with epilepsy., (Copyright © 2010 Elsevier Inc. All rights reserved.)