Baroreflex sensitivity (BRS) and heart rate variability (HRV) are potential therapeutic targets. The present study was conducted to assess changes in BRS and HRV after monotherapy with losartan versus that of atenolol in uncomplicated essential hypertension. Thirty subjects with uncomplicated essential hypertension were randomized to receive atenolol 50 mg to 100 mg (n = 15) or losartan 50 mg to 100 mg (N = 15) daily for 6 months. Instantaneous systolic blood pressure (SBP) and heart rate were assessed using servo-controlled infrared finger plethysmography before treatment and at the end of 3 months and 6 months after treatment. The fluctuation in SBP and interpulse interval (IPI) was divided into three specific frequency ranges by fast Fourier transform as high frequency (HF; 0.15 Hz-0.4 Hz), low frequency (LF; 0.04 Hz-0.15 Hz), and very low frequency (VLF; 0.004 Hz-0.04 Hz). The BRS was expressed as (1) SBP-IPI transfer function with its magnitude in the HF and LF ranges and (2) BRS index alpha. The HRV was expressed as total power and power in the LF and HF ranges of interpulse interval. Blood pressure was reduced to a similar extent in both groups. Compared with the baseline, BRS did not improve in both groups at month 3. However, BRS was significantly improved in the losartan group (P < 0.05) but not in the atenolol group at month 6. In addition, BRS was significantly higher in the losartan group than the atenolol group at month 3 and month 6 (P < 0.05). Moreover, heart rate variability was significantly reduced in the atenolol group at month 6 (P < 0.05), but not in the losartan group. The HRV in the losartan group was significantly higher than that in the atenolol group at month 6 (P < 0.05). These findings suggest superior effects of losartan on BRS and HRV than atenolol in uncomplicated essential hypertension, which may be beyond blood pressure reduction/resetting.

Successful treatment of cough syncope depends on the correction of various pathogenetic mechanisms among different patients. The valsalva maneuver (VM), which elicits hemodynamic responses mimicking coughs, has potential for investigating the individual pathogenesis of cough syncope. Eighteen consecutive patients suffering from cough-induced syncope were examined. All patients were asked to cough and to perform VM several times under continuous cerebral blood-flow velocity and blood pressure (BP) monitoring by transcranial Doppler and finger plethysmography. Eight patients demonstrated abnormal VM characterized by the absent BP overshoot following the relief of straining. Patients demonstrating abnormal VM had delayed BP recovery after cough (median, 16.4; range, 8.7-25.6 seconds) compared to those demonstrating normal VM (2.6, 1.3-3.8 seconds, p < 0.001). Seven of the 10 patients exhibiting normal BP overshoot during VM had stenotic arterial lesions in the cerebral or coronary circulation, whereas only one of the eight patients demonstrating absent BP overshoot had coronary artery disease (70% vs. 12.5%, p = 0.025). Other clinical profiles, body mass index, frequency of obstructive pulmonary disease and valsalva ratio did not differ between patients featuring normal and absent BP overshoot. In conclusion, the pathogenesis of cough syncope could be different between patients with normal and abnormal VM responses. Patients who had no BP overshoot during VM sustained prolonged hypotension after cough. The VM helps in discriminating among pathogenic mechanisms and guiding investigation and treatment for cough syncope patients.

Background and Purpose-Asian patients with cerebrovascular diseases have more intracranial atherosclerosis and less extracranial carotid artery stenosis compared with white patients. We systemically evaluated the distribution of carotid arterial lesions in Chinese patients with transient monocular blindness (TMB), which was rarely reported. Methods-We prospectively evaluated 105 consecutive patients with TMB. All of the patients received ocular and physical examinations, blood tests for coagulation function and autoimmune diseases, and ultrasonography of cervical and intracranial arteries. All of the carotid lesions were confirmed by magnetic resonance angiography or cerebral angiography. Results-Of the 36 (34.3%) patients with significant carotid stenosis (Ն50%), 16 (15.2%) had extracranial carotid stenosis; 17 (16.2%) had carotid siphon stenosis; and 3 (2.9%) had both. The duration, onset, and patterns of visual loss were not different between patients with and without carotid arterial lesion. Conclusions-This

Background: The reliability of critical closing pressure (CrCP) estimates derived from peripheral blood pressure (BP) measurements is unclear. We attempted to evaluate the influences of peripheral circulation on determining CrCP. Methods: Twenty-five young healthy volunteers were studied. BP waves were obtained with plethysmography (Portapres) and carotid applanatory tonometry, respectively, for analysis. Transcranial Doppler was used to monitor cerebral flow velocity. Using linear regression analysis, beat-to-beat CrCP was calculated at rest, during voluntary hyperventilation and during 5% CO₂ inhalation. Results: Twenty of 25 participants demonstrating satisfactory tonometric tracings for both tests were included in the analysis. The systolic BP measured using plethysmography was higher than that derived from tonometry (139.4 ± 24.7 vs. 105.5 ± 29.6, p < 0.001). CrCP values derived from tonometry were all positive and higher than CrCP values derived from plethysmography (62.9 ± 19.9 vs. 11.1 ± 17.8, p < 0.001). The changes in CrCP induced by 5% CO₂ inhalation and hyperventilation had a correlation between two BP monitoring methods (r = 0.52, p = 0.001). Conclusions: Pressure waveform is an important determinant in calculating CrCP by linear regression analysis. The relative changes in CrCP induced by hemodynamic challenges remained a relevant indicator of cerebrovascular regulation regardless of the methods used for non-invasive BP recording.