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Aims: The involvement of arterial baroreflex function in the pathophysiology of vasovagal syncope (VVS) is controversial, and there are no published data supporting its clinical usefulness. The aim of this study was to evaluate the role of arterial baroreflex sensitivity (BRS) at baseline and during head-up tilt testing (HUT) in predicting the recurrence of VVS., Methods and Results: The study involved otherwise healthy patients with a history of unexplained syncope who underwent diagnostic HUT by being tilted to 70 degrees after 10 min supine rest; the test was potentiated by the administration of 300 microg of nitroglycerine (NTG) after 20 min. Beat-to-beat heart rate and systolic blood pressure were continuously recorded, and the sequence method was used to measure arterial baroreflex control of heart rate. The 190 enrolled patients were followed up for 18 +/- 6 months, during which 34 experienced a total of 90 episodes of syncope recurrence. In a stepwise multivariate analysis, female gender [hazard ratio (HR): 2.74; P = 0.008], the presence of >or=3 syncope events before HUT (HR: 3.36; P = 0.004), and BRS below median value after the start of HUT or after the administration of NTG (HR: 3.79; P = 0.006) were significantly and independently associated with the recurrence of syncope. Moreover, when a BRS value of less than the median was added to the other independent factors in a stepwise model, a significant increase in discrimination (C-index: 0.77) and model fitting (P = 0.001) was observed., Conclusion: Reduced BRS during HUT has independent and incremental value in predicting the recurrence of syncope, thus supporting its potential usefulness in the clinical management of patients.

Aims: The aim of this study was to evaluate arterial baroreflex control of heart rate immediately before head-up tilt test (HUT)-induced vasovagal syncope (VVS)., Methods and Results: We enrolled 97 otherwise healthy subjects with recurrent unexplained syncope. After 10 min of rest in supine position, they underwent a passive HUT potentiated with nitroglycerin administration after 20 min. Beat-to-beat heart rate and systolic blood pressure were continuously recorded. Sequence method was used to measure two complementary parameters reflecting arterial baroreflex control of heart rate: the baroreflex sensitivity (BRS) and the baroreflex effectiveness index (BEI). Twenty-one patients fainted before nitrate administration (HUT+) and 37 after nitrate administration (NTG+). Immediately before syncope, the NTG+ patients showed significantly lower BRS values than those observed at the end of the test in the patients without syncope (5.5 +/- 2.8 vs. 7.7 +/- 3.4 ms/mmHg; P = 0.004) and a significantly lower BEI (30 +/- 20% vs. 53 +/- 24%; P < 0.001). The HUT+ patients did not show any significant differences in BRS and BEI before syncope from the values observed during the corresponding tilt period in the other groups., Conclusion: A significant depression in BRS and BEI occurs immediately before syncope in patients who faint after nitrate administration, thus suggesting that arterial baroreflex dysfunction plays a role in mediating nitrate-induced VVS.

Background: We investigated the effects of subdiastolic variations of the pressure inside the thigh cuffs on cardiovascular oscillations and arterial baroreflex sensitivity in humans., Methods: During 10 min of controlled breathing at low (0.1 Hz) and high (0.25 Hz) frequencies, 30 healthy subjects underwent variations of the pressure inside the thigh cuffs (from 0 to 40 mmHg) at 0.25 and 0.1 Hz respectively; the periods of controlled breathing without cuff pressure modulation were used as a control. The frequency responses of cardiovascular signals were assessed using spectral analysis, and baroreflex sensitivity by the sequence method., Results: Cuff pressure modulation at 0.25 Hz did not affect the RR interval, arterial pressure, or baroreflex sensitivity; at 0.1 Hz it did not change the RR interval and arterial pressure, but engaged (0.76 +/- 0.2 of coherence) and increased the low frequency oscillations of the RR interval (from 5.6 +/- 1 to 6.1 +/- 0.9 ln ms2, p < 0.05) and improved baroreflex sensitivity by 25% (from 14.2 +/- 9 to 17.7 +/- 10 ms/mmHg, p < 0.01)., Conclusions: Subdiastolic thigh cuff pressure modulation at 0.1 Hz improved the low frequency oscillations of heart rate and baroreflex sensitivity. This approach represents a new and simple non-pharmacological strategy for acutely improving baroreflex sensitivity in humans.

The determinants of diastolic dysfunction in patients with systemic hypertension are not completely known. To evaluate the possible role of age, arterial blood pressure, and baroreflex heart rate response impairment in causing diastolic dysfunction, we studied 61 patients (42 male; mean+/-SD age, 43.9+/-12 years) with newly recognized and therefore previously untreated systemic hypertension. Diastolic dysfunction was evaluated by means of Doppler echocardiography (and diagnosed as such when the early to atrial peak velocity ratio corrected to heart rate was <1), arterial blood pressure by 24-hour ambulatory monitoring, and baroreflex heart rate response by means of the spectral technique (alpha index) during paced (0.27 Hz) and spontaneous breathing (in a supine position and during tilt). Nineteen patients had diastolic dysfunction, the most powerful predictor of which was age (r=-0.63, P<0.001). The patients with diastolic dysfunction had significantly lower values for spectral baroreflex gain in the high-frequency band than those without (5.2+/-3 versus 8.4+/-5 ms/mm Hg during paced breathing, P<0.05; 7. 4+/-4 versus 13.3+/-7 ms/mm Hg in a supine position, P<0.05; 4.3+/-4 versus 5+/-2 ms/mm Hg during tilt, P

Study Objective: The results of studies on the effect of beta-adrenergic blockade on respiratory sinus arrhythmia (RSA) are discordant. The aim of this study was to verify whether chronic beta-adrenergic blockade is capable of increasing RSA, and therefore vagal outflow, and to analyze whether the mechanism of action is central or peripheral., Participants and Design: Twenty normal subjects (28+/-2 years old) were randomized to receive a hydrophilic (nadolol) beta-blocker, a lipophilic (metoprolol) beta-blocker, and placebo., Measurements: After 1 week of therapy, a spectral analysis was made of the variability in heart rate and systolic BP during controlled breathing at 16 breaths/min. The high-frequency component was calculated for the RR interval (measure of RSA) and systolic pressure, and the squared coherence and phase functions were assessed between RR and systolic pressure fluctuations in the respiratory band; a negative phase means that RR changes follow systolic pressure changes. The gain in the relationship between the two signal fluctuations was also calculated., Results: Both beta-blockers increased the mean (+/-SD) RR interval (placebo=808+/-21, nadolol=1,054+/-30, metoprolol=1,031+/-27 ms; p<0.0001), RSA (placebo=542, nadolol=1,177, metoprolol=1,316 ms2; p=0.002), and the gain (placebo=13.6+/-1.5, nadolol=21.9+/-2.8, metoprolol=24.5+/-3.6 ms/mm Hg; p<0.002), and both modified the phase function (placebo=-21.1+/-5.3, nadolol=-1.8+/-4.9, metoprolol=-2.9+/-4.2 degree; p<0.0001). No difference was found between nadolol and metoprolol., Conclusions: Chronic beta-adrenergic blockade enhanced both RSA and baroreflex gain and reduced the phase between the RR interval and systolic pressure oscillations. Since no difference was found between the hydrophilic and the lipophilic beta-blockers, these changes seem to be due to a peripheral effect.

Background: Depressed baroreflex sensitivity obtained by means of a phenylephrine test plays a prognostic role in patients with a previous myocardial infarction. Our purpose was to evaluate the correlation and agreement between the baroreflex sensitivity obtained with phenylephrine and that obtained by two noninvasive methods: the alpha-index and sequence analysis., Methods and Results: The alpha-index was measured by means of the spectral analysis of RR and systolic blood pressure variabilities in both the high- and low-frequency bands; sequences were identified from simultaneously recorded time series in which the RR and systolic blood pressure concurrently increased or decreased. Noninvasive baroreflex sensitivity tests were performed during both spontaneous and controlled respiration. Fifty-two consecutive patients with recent myocardial infarction underwent the analyses. Although the correlations between phenylephrine and either of the noninvasive methods were always significant, those found during controlled respiration had the highest r values (r=.70). However, the limits of agreement calculated by means of the Bland and Altman method were wide for both noninvasive methods., Conclusions: The results obtained by means of noninvasive baroreflex sensitivity assessments should not be used in clinical practice as an alternative to those obtained by the phenylephrine method.

To evaluate the effect of a hydrophilic and a lipophilic beta-blocker on the autonomic nervous system, 20 normal subjects were studied under baseline conditions and 7 days after being randomly assigned to metoprolol (200 mg/day), nadolol (80 mg/day), and placebo. Under each condition, the time-domain parameters were analyzed by means of 24-hour ECG monitoring and the frequency-domain parameters by means of the autoregressive method using 10-minute ECGs during rest, controlled respiration, and after a head-up tilt test. The alpha index (the gain in the relationship between the RR period and systolic arterial pressure variability) was also calculated. Both nadolol and metoprolol significantly increased all of the time-domain parameters except the standard deviation of the RH intervals; they also modified the frequency-domain parameters. Both blunted the significant reduction in the high frequency (HF) component and alpha index during tilt. In normal subjects, hydrophilic and lipophilic beta-blockers similarly modify the time- and frequency-domain parameters that are particularly evident when high sympathetic tone is present (during daytime and tilt). The value of the alpha index was increased by both beta-blockers in the HF, but not in the low frequency band; this difference might be due to the fact that the former is a measure of the vagal component of the baroreflex control and the latter a measure of the sympathetic component. The effects of hydrophilic and lipophilic beta-blockers on the time- and frequency-domain parameters of heart rate variability are similar.