Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk

Abstract

Rationale We hypothesized increasing obstructive sleep apnea (OSA) severity would be associated with nondipping blood pressure (BP) in increased cardiovascular disease (CVD) risk. Methods Baseline data from 298 cardiology patients recruited for a multicenter randomized controlled trial were examined. Dipping was defined as a sleep-related BP or heart rate (HR) reduction of at least 10%. Logistic regression models were fit, adjusting for age, sex, race, BMI, CVD risk factors, CVD, and study site. Results There was a statistically significant 4% increase in the odds of nondipping SBP per 1-unit increase in both Apnea Hypopnea Index (AHI) and Oxygen Desaturation Index (ODI). There was no significant relationship between AHI and nondipping mean arterial pressure (MAP); however, a 3% increase in the odds of nondipping MAP per 1-unit increase in ODI was observed (odds ratio, OR =1.03; 95% confidence interval, CI 1.00–1.05). At severe OSA levels, a 10 and 4% increase in odds of nondipping DBP per 1-unit increase in AHI and ODI were observed, respectively. A 6% [OR =1.06; 95% CI (1.01–1.10)] increase in nondipping HR odds was observed with each increase in ODI until the upper quartile of ODI. Conclusion In patients at cardiovascular risk and moderate-to-severe OSA, increasing AHI and/or ODI were associated with increased odds of nondipping SBP and nondipping MAP. More severe levels of AHI and ODI also were associated with nondipping DBP. These results support progressive BP burden associated with increased OSA severity even in patients managed by cardiology specialty care.

Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms

“…Loss of this nocturnal dipping blood pressure pattern in both normotensive and hypertensive subjects is associated with a worse cardiovascular prognosis [10], which is particularly relevant in OSA because of the high likelihood of a nocturnal nondipping profile [3]. Data from the Wisconsin Sleep Cohort Study indicate a dose-response increase in the development of nondipping hypertension with severity of SDB at baseline when followed for 7 years [11], which was confirmed by a recent report demonstrating that in patients attending a cardiology clinic with known cardiovascular disease and moderate or severe OSA there is a 4% increase in the odds of having a nondipping blood pressure profile per unit increase in AHI [4]. Further recent data from the Wisconsin Cohort indicate that SDB during rapid eye movement sleep is particularly associated with a nondipping nocturnal blood pressure pattern [12].…”

“…OSA is recognised as an independent risk factor for systemic hypertension [3] and a nondipping nocturnal blood pressure profile is particularly likely in patients with OSA [4], even in the absence of significant hypertension. Furthermore, hypertension is increasingly recognised as an important predictor of prevalent OSA and appears to be more predictive than excessive day-time sleepiness in some settings [5].…”

Obstructive sleep apnea syndrome, continuous positive airway pressure and treatment of hypertension

“…In some instances, the surges in blood pressure that occur at the end of each apnea achieve levels greater than that recorded in the same individuals during wakefulness (31). There is therefore no doubt that OSA can elicit, acutely, a hypertensive surge (31) and a 'non-dipping' ambulatory blood pressure phenotype (32)(33)(34). The fundamental question, however, is whether these changes are sufficient to establish sustained daytime hypertension.…”

Role of autonomic nervous system in the pathomechanism of hypertension

“…It is necessary to mention obstructive sleep apnea as an important SNS activating disorder [44]. Although obstructive sleep apnea elevates SNS output due to multiple pathways, hypoxemia is suggested to be the main factor [45][46][47]. Intermittent hypoxia results in BP elevation that persist even after removal of hypoxemic factor [48].…”