Abstract-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, 43Ϯ7 years; body mass index, 28.8Ϯ3.0 kg/m 2 ) with untreated severe obstructive sleep apnea (apnea-hypopnea index, 56Ϯ22 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; nϭ18) or CPAP (nϭ18) 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 126Ϯ5 to 121Ϯ7 mm Hg; Pϭ0.001) and a trend for diastolic blood pressure (from 75Ϯ7 to 73Ϯ8 mm Hg; Pϭ0.08) as well as a significant decrease in daytime and nighttime systolic and diastolic blood pressure (PϽ0.05 for each comparison). There was a significant reduction in the frequency of prehypertension (from 94% to 55%; Pϭ0.02) and masked hypertension (from 39% to 5%; Pϭ0.04) 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.

Patients with OSA presented a higher unadjusted rate of masked hypertension than matched controls. Lowest oxygen saturation has an independent association with arterial stiffness.

INTRODUCTION:Serous carcinomas are the most frequent histologic type of ovarian and peritoneal cancers, and can also be detected in the endometrium and fallopian tubes. Serous carcinomas are usually high‐grade neoplasms when diagnosed, yet the identification of an associated precursor lesion remains challenging. Pathological examination of specimens obtained from prophylactic bilateral salpingo‐oophorectomies that were performed for patients harboring BRCA1/2 mutations suggests that high‐grade serous carcinomas may arise in the fallopian tubes rather than in the ovaries.OBJECTIVE:To investigate the presence and extent of fallopian tube involvement in cases of serous pelvic carcinomas.METHODS:Thirty‐four cases of serous pelvic carcinoma with clinical presentations suggesting an ovarian origin were analyzed retrospectively. Histologic samples of fallopian tube tissues were available for these cases and were analyzed. Probable primary site, type of tubal involvement, tissues involved in the neoplasia and vascular involvement were evaluated.RESULTS:Fallopian tube involvement was observed in 24/34 (70.6%) cases. In 4 (11.8%) of these cases, an intraepithelial neoplasia was present, and therefore these cases were hypothesized to be primary from fallopian tubes. For an additional 7/34 (20.6%) cases, a fallopian tube origin was considered a possible primary.CONCLUSIONS:Fallopian tubes can be the primary site for a subset of pelvic high‐grade serous carcinomas.

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. J Clin Hypertens (Greenwich). 2011;13:19–22. ©2010 Wiley Periodicals, Inc.