Continuous positive airway pressure treatment: good for obstructive sleep apnea syndrome, maybe not for hypertension?

Obstructive repose apnea syndrome (OSAS) is definitely considered single of the major health issues in the Western world. Besides the moot points with daily life functioning, like as hypersomnolence, decreased cognitive functions, motor vehicle crashes, and reduc quality of life, the greatest in quantity relevant medical issue is related to the able-bodied association of OSAS with cardiovascular, cerebrovascular, and metabolic diseases. (1)

Several studies (1-3) have pointed on the outside that OSAS is an independent risk factor for almost all cardiovascular diseases, of that kind as atrial fibrillation, congestive heart failure, coronary atherosclerosis, myocardial infarction, and unanticipated death. Namely, the last Joint National Committee report (4) for prevention and treatment of hypertension considered OSAS as the first identifiable cause of hypertension. Being the prevalence of this syndrome is for a like reason high in the general population, correct therapeutic strategies are important.

Continuous positive airway crushing (CPAP) ventilation is the treatment of choice for mild-to-severe OSAS. (5) Indeed, CPAP treatment is capable not sole of reducing OSAS symptoms and its ends but it has also been associated with the reduction of several of the so-called "intermediate mechanisms" linking OSAS to cardiovascular diseases, like as nighttime and daytime sympathetic hyperactivity, inflammation, and endothelial and metabolic dysfunction. (1) The ultimate convincing evidence supporting the protective issues of CPAP treatment of OSAS patients upon cardiovascular outcomes has been freshly published by Marin et al, (6) who studied snorers, mild OSAS patients, sharp OSAS patients without CPAP, and harsh OSAS patients under CPAP therapy. After a 10-year follow-up the patients with harsh OSAS without CPAP had a significant increase in fatal and nonfatal cardiovascular facts while the patients with morose OSAS receiving CPAP had a risk of facts similar to control subjects.

However, in their placebo-controlled trial evaluating the results of 4 weeks of treatment with CPAP upon ambulatory BP in hypertensive OSAS patients, published in this issue of CHEST (see page 1459) Campos-Rodriguez and coworkers (7) did not notice significant changes in daytime or nighttime BP This latter finding may of course raise a certain quantity of concern about the capability of CPAP treatment of reducing BP To this regard, data near in the literature are many times controversial. In addition to the articles quot by dint of this study reporting an issue or no effect of CPAP upon BP, a study by Mills and coworkers (8) has not long ago reported that 2 weeks of CPAP treatment was able to increase norepinephrine clearance and bring BP in a group of OSAS patients, half of whom were hypertensive. They did not measure ambulatory BP on the other hand only in-hospital daytime values. Moreover, they did withdraw antihypertensive therapy for the 2 weeks of application of mind at variance with the close attention of Campos-Rodriguez et al. (7) As discussed through the authors, (7) this might be a lock opener factor explaining the lack of decrease in BP in a collection of well-controlled hypertensive subjects. In support of this hypothesis are the observations that CPAP treatment reduc 24-h ambulatory BP in a assemblage of subjects with uncontrolled resistant hypertension despite therapy (9); and that 6-month and 1-year, on the contrary not 1-month, CPAP therapy was able to bring daytime sympathetic nerve activity in obstructive doze apnea (OSA) normotensive patients without affecting BP and heart rate. (10) Hence, CPAP may act by means of normalizing the mechanisms underlying high BP namely sustained sympathetic activation, without a clear event on BP (and heart rate as well), which is the arise of multiple neural, humoral, and vascular factors. These results would require longer-term CPAP therapy than 4 weeks as in the research of Campos-Rodriguez, (7) as recognized by means of the authors. Another issue that is not usually taken into account in this kind of trial is the duration of the hypertensive state. Since hypertension has a multifarious origin, (11) vascular remodeling is likely to show the last, and maybe definitive factor that contributes to the maintenance of hypertension despite the reduction of all neurohumoral, inflammatory, endothelial, metabolic, and other promoting factors. (12)

To this regard, we should have to bewilderment whether a different effect upon BP could be obtained starting the CPAP treatment as presently as hypertension is diagnosed in patients with concomitant OSA. Thus, a possible design for time to come randomized, placebo-controlled trials should include a population of OSA patients with newly diagnosed hypertension, in which CPAP treatment is compared to placebo. Last on the contrary not least, we should consider that CPAP is the optimal treatment for OSA, improving symptoms and cardiovascular issues but it is not by means of se an antihypertensive therapy. It works through improving overall neural cardiovascular regulation, which is rather composed of several elements during sleep, (13) through decreasing chemoreflex activation, increasing baroreflex sensitivity, and decreasing peripheral sympathetic drive, in addition to improve endothelial function, (114) all factors involved in the progression of the atherosclerotic proces and its events In this sense, CPAP acts indirectly by dint of improving the features that meet to the establishment and/or maintenance of arterial hypertension. Therefore, the investigation by Campos-Rodriguez et al (7) has the abysmal merit of not definitely establishing the potential antihypertensive events of CPAP, but vice versa of stimulating more extensive trials in order to evaluate the impact of this treatment upon BP in OSAS patients.