Lack of circadian variation of pulse wave velocity measurements in healthy volunteers.

Arterial stiffness is an independent marker of cardiovascular events. Pulse wave velocity (PWV) is a validated method to detect arterial stiffness that can be influenced by several factors including age and blood pressure. However, it is not clear whether PWV could be influenced by circadian variations. In the present study, the authors measured blood pressure and carotid-femoral PWV measurements in 15 young healthy volunteers in 4 distinct periods: 8 am, noon, 4 pm, and 8 pm. No significant variations of systolic (P=.92), mean (P=.77), and diastolic (P=.66) blood pressure among 8 am (113±15, 84±8, 69±6 mm Hg), noon (114±13, 83±8, 68±6 mm Hg), 4 pm (114±13, 85±8, 70±7 mm Hg), and 8 pm (113±7, 83±10, 68±7 mm Hg), respectively, were observed. Similarly, carotid-femoral PWV did not change among the periods (8 am: 7.6 ± 1.4 m/s, noon: 7.4±1.1 m/s, 4 pm: 7.6±1.0 m/s, 8 pm, 7.6±1.3 m/s; P=.85). Considering all measurements, mean blood pressure significantly correlated with PWV (r=.31; P=.016). In young healthy volunteers, there is no significant circadian variation of carotid-femoral PWV. These findings support the concept that it does not appear mandatory to perform PWV measurements at exactly the same period of the day.

The effects of continuous positive airway pressure on prehypertension and masked hypertension in men with severe obstructive sleep apnea.

Obstructive sleep apnea and hypertension are common conditions that frequently coexist. Continuous positive airway pressure (CPAP) reduces blood pressure in patients with obstructive sleep apnea and sustained hypertension. However, the impact of CPAP on patients with obstructive sleep apnea and prehypertension and masked hypertension, conditions associated with increased cardiovascular risk, is unknown. Thirty-six male patients (age, 43 ± 7 years; body mass index, 28.8 ± 3.0 kg/m(2)) with untreated severe obstructive sleep apnea (apnea-hypopnea index, 56 ± 22 events/hr on polysomnography) with diagnostic criteria for prehypertension and/or masked hypertension, based on office and 24-hour ambulatory blood pressure monitoring, respectively, were studied. The patients randomized to no treatment (control; n=18) or CPAP (n=18) for 3 months had similar frequency of prehypertension and masked hypertension at study entry. There were no significant changes in blood pressure in patients randomized to the control group. In contrast, patients randomized to CPAP presented significant reduction in office systolic (from 126 ± 5 to 121 ± 7 mm Hg; P=0.001) and a trend for diastolic blood pressure (from 75 ±7 to 73 ± 8 mm Hg; P=0.08) as well as a significant decrease in daytime and nighttime systolic and diastolic blood pressure (P<0.05 for each comparison). There was a significant reduction in the frequency of prehypertension (from 94% to 55%; P=0.02) and masked hypertension (from 39% to 5%; P=0.04) only in the CPAP group. In conclusion, effective CPAP therapy promotes significant reduction in the frequency of prehypertension and masked hypertension by promoting significant blood pressure reductions in patients with severe obstructive sleep apnea.

Obstructive sleep apnea, masked hypertension, and arterial stiffness in men.

BACKGROUND: Obstructive sleep apnea (OSA) is an established cause of hypertension. However, it is not clear whether the frequency of masked hypertension in patients with OSA and whether OSA have an independent role on arterial stiffness taking into account ambulatory blood pressure (BP) monitoring (ABPM). METHODS: We evaluated 61 male normotensive participants as determined by casual clinic BP level <140/90 mm Hg without clinical evidence of cardiovascular disease and on no medications (43 patients with moderate-to-severe OSA (apnea-hypopnea index (AHI) > or = 15 events/hour by polysomnography) and 18 age- and body mass index-matched controls without OSA (AHI <5 events/hour)). Pulse wave velocity (PWV), an index of arterial stiffness, and 24-h ABPM were performed in a blinded fashion. Masked hypertension was defined when abnormal daytime ABPM was > or = 135 or > or = 85 mm Hg. RESULTS: The AHI and lowest oxygen saturation were 2.6 +/- 1.6 and 90 +/- 2 vs. 52.8 +/- 21.0 events/hour and 75 +/- 10% for controls and OSA patients, respectively; P < 0.001. Compared with controls, patients with OSA had higher office systolic BP (113 +/- 9 vs. 118 +/- 10 mm Hg; P = 0.05) and a higher unadjusted proportion of masked hypertension (2 controls (11.1%) vs. 13 patients (30.2%); P < 0.05). PWV was 8.7 +/- 0.7, 9.4 +/- 1.0, and 10.6 +/- 1.1 m/s in the control, OSA without and with masked hypertension groups, respectively (P < 0.01 for each comparison). Multiple regression showed that systolic daytime ABPM and the lowest oxygen saturation were independently related to PWV (adjusted R2 = 0.34; P < 0.01). CONCLUSIONS: Patients with OSA presented a higher unadjusted rate of masked hypertension than matched controls. Lowest oxygen saturation has an independent association with arterial stiffness.