Article

Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea.

Hypertension Unit, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 11.99). 10/2007; 176(7):706-12. DOI: 10.1164/rccm.200703-500OC
Source: PubMed

ABSTRACT Obstructive sleep apnea (OSA) is associated with adverse cardiovascular outcomes, including myocardial infarction and stroke. Atherosclerosis is a key mechanism for these cardiovascular events. Recent cross-sectional studies showed the presence of early signs of atherosclerosis in patients with OSA who were free of comorbidities.
To determine the impact of treatment with continuous positive airway pressure (CPAP) on atherosclerosis.
We randomly assigned 24 patients with severe OSA (age, 46 +/- 6 yr) who were free of comorbidities to receive no treatment (control, n = 12) or CPAP (n = 12) for 4 months. Carotid intima-media thickness, arterial stiffness (evaluated by pulse-wave velocity), carotid diameter, 24-hour blood pressure monitoring, C-reactive protein, and catecholamines were determined at baseline and after 4 months.
At baseline, all measurements were similar in both groups and did not change in the control group after 4 months. In contrast, a significant decrease occurred in carotid intima-media thickness (707 +/- 105 vs. 645 +/- 95 microm, P = 0.04), pulse-wave velocity (10.4 +/- 1.0 vs. 9.3 +/- 0.9 m/s, P < 0.001), C-reactive protein (3.7 +/- 1.8 vs. 2.0 +/- 1.2 mg/L, P = 0.001), and catecholamines (365 +/- 125 vs. 205 +/- 51 ng/ml, P < 0.001) after 4 months of CPAP. Carotid diameter did not change significantly. Regarding the whole group, changes in carotid intima-media thickness were correlated with changes in catecholamines (r = 0.41, P < 0.05). Changes in pulse-wave velocity were correlated with changes in C-reactive protein (r = 0.58, P < 0.01) and catecholamines (r = 0.54, P < 0.01).
The treatment of OSA significantly improves early signs of atherosclerosis, supporting the concept that OSA is an independent risk factor for atherosclerosis. Clinical trial registered with www.clinicaltrials.gov (NCT 00400543).

0 Bookmarks
 · 
97 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obstructive sleep apnea results in intermittent hypoxia via repetitive upper airway obstruction leading to partial or complete upper airway closure, apneas and hypopneas, respectively. Intermittent hypoxia leads to sympathetic nervous system activation and oxidative stress with a resultant systemic inflammatory cascade. The putative mechanism by which obstructive sleep apnea has been linked to numerous pathologic conditions including stoke, cardiovascular disease, hypertension, and metabolic derangements is through these systemic effects. Treatment of obstructive sleep apnea appears to reduce systemic markers of inflammation and ameliorates the adverse sequelae of this disease.
    Seminars in Respiratory and Critical Care Medicine 10/2014; 35(5):531-44. · 2.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypertension is a highly prevalent problem worldwide, affecting at least one third of the adult general population. Although the exact prevalence is uncertain, it is estimated that at least 15% to 20% of individuals with hypertension have resistant hypertension. Resistant hypertension has been shown to predict more adverse cardiovascular and renal outcomes. In 2003, the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure recognized obstructive sleep apnea (OSA) as an important cause of secondary hypertension. A large body of epidemiologic evidence has linked OSA to resistant hypertension, nondipping nocturnal blood pressure, as well as target organ damage, including left ventricular hypertrophy, arterial stiffness, and microalbuminuria. The importance of OSA as a risk factor for the development of hypertension independent of other confounding factors also was observed in a prospective longitudinal study. More importantly, OSA predicts an increased risk of adverse cardiovascular outcomes, mortality, and sudden cardiac death. This article discusses the associations between OSA and resistant hypertension and reviews the latest understanding on the pathophysiologic mechanisms of hypertension in OSA. Nocturnal continuous positive airway pressure therapy is regarded as the standard treatment for OSA. Prospective randomized controlled trials and meta-analyses of prospective randomized controlled trials within the past 10 years that have examined the effects of continuous positive airway pressure therapy on blood pressure control in patients with OSA with or without hypertension are reviewed and summarized. The majority of the trials suggest a modest but significant benefit on blood pressure control with continuous positive airway pressure therapy. Whether continuous positive airway pressure therapy may improve hard outcomes of patients with OSA and resistant hypertension warrants further investigation.
    Seminars in Nephrology 11/2014; · 2.94 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Traditionally, blood pressure measurements have been performed in office settings and have provided the basis for all diagnostic and therapeutic decisions. However, the develop-ment of a clinically relevant 24-hour blood pressure monitoring system has added greatly to the ability of blood pressure values to confer additional clinical information, including prognostic value. Mechanistically, the circadian rhythm of blood pressure is mediated by a complex pro-cess as a part of the neurohormonal cascade. Pattern recognition of blood pressure peaks and troughs over a 24-hour period has led to categorization into specific subsets namely, ie, dip-pers, nondippers, extreme dippers, and reverse dippers. Cardiovascular risk is associated with certain pattern types, as has been demonstrated in large observational and prospective studies. The development of therapies for the purpose of restoring more pathological patterns to normal ones continues to grow. These include both pharmaceutical and device therapy. This article describes the development of 24-hour blood pressure monitoring systems, the identification of circadian blood pressure patterns, and the treatment strategies studied thus far which affect these newer blood pressure parameters.