There is increasing evidence that obstructive sleep apnea is an independent risk factor for arterial hypertension. Previous studies on the antihypertensive effects of positive airway pressure therapy on daytime blood pressure (BP) revealed inconsistent results.
The relations between the apnea/hypopnea index (AHI) and BP or heart rate (HR) were investigated in a cohort of 540 consecutive patients (age, 55.4 +/-11.1 years) with moderate or severe obstructive sleep apnea (OSA). The mean AHI was 28.2 +/- 22.0 events/h before OSA therapy. A group of 196 patients in whom antihypertensive medication was kept unchanged was followed for 6 months during bilevel or continuous positive airway pressure (Bi-/CPAP) therapy.
Significant associations were found between AHI and systolic BP (beta = 0.078, P = .014), diastolic BP (beta = 0.056, P = .003), HR (beta = 0.096, P < .001), and the prevalence of arterial hypertension (odds ratio = 0.015, P = .003), independent of age, body mass index, and gender. During the follow-up period with effective Bi-/CPAP therapy, the mean daytime systolic BP decreased from 130.7 +/- 15.5 mm Hg to 128.6 +/- 15.9 mm Hg (P = .051), diastolic BP from 80.2 +/- 9.3 mm Hg to 77.5 +/- 9.5 mm Hg (P = .001), and HR from 77.7 +/- 8.8 to 75.7 +/- 8.1 beats/min (P = .001). Multiple linear regression analysis revealed that the absence of antihypertensive drugs and the level of the initial BP are significant and independent predictors for the lowering effect of Bi-/CPAP therapy on systolic and diastolic BP.
This study confirms an independent relationship between the severity of OSA and BP/HR. Absence of BP-lowering medication and BP values before treatment are independent predictors for the reduction of BP with Bi-/CPAP therapy.
"Our fi ndings are consistent with those of others (for a review see Diogo and Monteiro 2014 ). Börgel et al. ( 2004 ) showed that the absence of AHD is an independent predictor of the lowering effect of CPAP therapy on systolic and diastolic BP. Furthermore, Dernaika et al. reported that the effects of CPAP therapy on BP regulation appear to be less evident in hypertensive patients simultaneously treated with AHD (Dernaika et al. 2009 ). "
[Show abstract][Hide abstract] ABSTRACT: Obstructive sleep apnea and hypertension are closely related diseases. The lowering effect of continuous positive airway pressure (CPAP) on blood pressure (BP) control is modest and concomitant antihypertensive therapy is still required. However, the best antihypertensive regimen for BP control in patients with OSA remains unknown. We aimed to investigate a hypothetical association between ongoing antihypertensive medication and BP control rates in patients with OSA. We conducted a prospective observational study in a cohort of 205 patients with OSA and hypertension who underwent a sleep study and 24-h ambulatory blood pressure monitoring (ABPM). Ongoing antihypertensive medication profile was recorded. Logistic regression models were used to investigate the association between antihypertensive regimen and BP control, before (n = 205) and, when applicable, after CPAP adaptation (n = 90). One hundred and fifty-five patients (155/205) were being treated with 31 different antihypertensive regimens. At baseline, the antihypertensive regimens and the number of antihypertensive drugs were not associated with BP control (p = 0.847; p = 0.991). After CPAP adaptation, a decrease in median night-time systolic and diastolic BP was observed (p = 0.001; p = 0.006). Nevertheless, the lack of association between antihypertensive regimens and the number of antihypertensive drugs and BP control remained (p = 0.864; p = 0.800). Our findings confirm that although CPAP improves nocturnal BP, this improvement is not sufficient to control blood pressure for 24 h. This study shows, for the first time, that in patients with OSA, there is no association between BP control and both the antihypertensive regimen and the number of antihypertensive drugs.
Advances in Experimental Medicine and Biology 08/2015; 860:201-9. DOI:10.1007/978-3-319-18440-1_22 · 1.96 Impact Factor
"Blood pressure Bixler et al. (2000), Suzuki et al. (1996), Borgel et al. (2004), Heitmann et al. (2004), Dhillon et al. (2005), Pepperell et al. (2002), Faccenda et al. (2001), Dernaika et al. (2009), Robinson et al. (2008), Patruno et al. (2007), Wilcox et al. (1993), Hui et al. (2006), Duran-Cantolla et al. (2010), Marrone et al. (2011) OSA is associated with elevated blood pressure that is attenuated by CPAP therapy; differences emerge regarding the level of reduction in BP after treatment , the circadian time at which reduction occurs (sleep/wakefulness), and whether the systolic or diastolic component is more affected Urine and blood catecholamine levels Fletcher et al. (1987), Baruzzi et al. (1991), Ziegler et al. (1997), Minemura et al. (1998), Loredo et al. (1999), Elmasry et al. (2002), Sukegawa et al. (2005), Drager et al. (2007), Kohler et al. (2008), Comondore et al. (2009), Zhang et al. (2011), Bao et al. (2002), Ziegler et al. (2001), Kohler et al. (2011) OSA patients demonstrate sustained elevation in catecholamine levels that are attenuated by treatment , and are elevated again by treatment "
[Show abstract][Hide abstract] ABSTRACT: Sleep is involved in the regulation of major organ functions in the human body, and disruption of sleep potentially can elicit organ dysfunction. Obstructive sleep apnea (OSA) is the most prevalent sleep disorder of breathing in adults and children, and its manifestations reflect the interactions between intermittent hypoxia, intermittent hypercapnia, increased intra-thoracic pressure swings, and sleep fragmentation, as elicited by the episodic changes in upper airway resistance during sleep. The sympathetic nervous system is an important modulator of the cardiovascular, immune, endocrine and metabolic systems, and alterations in autonomic activity may lead to metabolic imbalance and organ dysfunction. Here we review how OSA and its constitutive components can lead to perturbation of the autonomic nervous system in general, and to altered regulation of catecholamines, both of which then playing an important role in some of the mechanisms underlying OSA-induced morbidities.
Frontiers in Neurology 01/2012; 3:7. DOI:10.3389/fneur.2012.00007
"The patients were admitted to the hospital because of a history of apneas, snoring or hypersomnic symptoms like day time tiredness or impairment of cognitive functions. Detailed information about the determination of cardiac risk factors and polysomnography were described extensively in previous publications [12,13] The subjects of the other group (CAR group, N = 488) were consecutive patients encountered in the cardiac catheterisation laboratory in the St. Josef Hospital of the Ruhr-University Bochum from October 2001 to August 2002. The complete clinical history, including cardiovascular risk factors, was obtained from all study subjects by use of the same data collection method as in the OSA group (see above). "
[Show abstract][Hide abstract] ABSTRACT: Cytochrome P450 (CYP) enzyme 2J2, an epoxygenase predominantly expressed in the heart, metabolizes arachidonic acid to biologically active eicosanoids. One of the CYP2J2 products, 11, 12-epoxyeicosatrienoic acid, has several vasoprotective effects. The CYP2J2-G-50T-promotor polymorphism decreases gene expression and is associated with coronary artery disease. This association supports the vascular protective role of CYP-derived eicosanoids in cardiovascular disease. In the present study, we investigated the influence of this polymorphism on survived myocardial infarction in two study groups of patients with on average high cardiovascular risk profile.
The CYP2J2 polymorphism was genotyped in two groups of patients that were collected with the same method of clinical data collection. Data from 512 patients with sleep apnoea (group: OSA) and on average high cardiovascular risk profile and from another 488 patients who were admitted for coronary angiography (CAR-group) were evaluated for a potential correlation of the CYP2J2 polymorphism G-50T and a history of myocardial infarction. The G-50T polymorphism of the CYP2J2 gene was genotyped by allele specific restriction and light cycler analysis.
The T-allele of the polymorphism was found in 111 (11.1%; CAR-group: N = 65, 13.3%; OSA: N = 46, 9.0%). 146 patients had a history of myocardial infarction (CAR: N = 120, 24.6%; OSA: N = 26, 5.1%). Cardiovascular risk factors were equally distributed between the different genotypes of the CYP2J2 G-50T polymorphism. In the total group of 1000 individuals, carriers of the T-allele had significantly more myocardial infarctions compared to carriers of the wild type (T/T or G/T: 21.6%; G/G: 13.7%; p = 0.026, odds ratio 1.73, 95%-CI [1.06-2.83]). In the multivariate logistic regression analysis the odds ratio for a history of myocardial infarction in carriers of the T-allele was 1.611, 95%-CI [0.957-2.731] but this trend was not significant (p = 0.073).
In presence of other risk factors, the CYP2J2 G-50T failed to show a significant role in the development of myocardial infarction. However, since our result is close to the border of significance, this question should be clarified in larger, prospective studies in the future.
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