Published: Nov 5, 2013 | Updated: Nov 6, 2013
By Crystal Phend, Senior Staff Writer, MedPage Today

Full Story:  http://www.medpagetoday.com/Pulmonology/SleepDisorders/42734

Treating obstructive sleep apnea (OSA) modestly brought down some measures of resistant hypertension beyond what blood pressure medications could achieve alone, a small randomized trial showed.

Six months of continuous positive airway pressure (CPAP) treatment cut daytime ambulatory blood pressure by 6.5/4.5 mm Hg whereas it rose by 3.1/2.1 mm Hg among controls on medical therapy alone (P<0.05), Geraldo Lorenzi-Filho, MD, PhD, of the Heart Institute at the Universidade de São Paulo, Brazil, and colleagues found.

However, nighttime and 24-hour pressures didn’t differ significantly between groups, the researchers reported in the November issue of CHEST.

The impact of CPAP on blood pressures in these patients with confirmed resistanthypertension and moderate-to-severe OSAwas in the range of that expected from treating other causes of secondary hypertension, they noted.

Based on prior research, the magnitude of blood pressure reduction achieved with CPAP in the trial would be expected to reduce cerebrovascular events by more than 30% and cardiovascular events by more than 20%, Malcolm Kohler, MD, of University Hospital Zurich, and John R. Stradling, MD, from the NIHR Biomedical Research Centre in Oxford, England, noted in an accompanying editorial.

“Whether this beneficial effect of CPAP on blood pressure can be achieved over several years and can ultimately result in reduced vascular morbidity and mortality in patients with OSA remains to be proven,” they wrote.

However, no single intervention is likely to normalize blood pressure in this complex condition, Lorenzi-Filho’s group cautioned.

Even renal denervation, which achieves blood pressure reductions in the range of 28/10 to 32/15 mm Hg, leaves many resistant hypertension patients well above the threshold for hypertension.

Roughly 80% of resistant hypertension patients are estimated to have OSA, and the trial results support a causal link, Kohler and Stradling noted.

Patients presenting with resistant hypertension should be evaluated for OSA, they concluded.

The intermittent hypoxia and mechanical stress on the heart and arteries from OSA may contribute to elevated blood pressure via mechanisms like increased sympathetic activity, endothelial dysfunction, and such, the researchers explained.

Their trial included 40 patients with hypertension uncontrolled despite use of at least three medications, including a diuretic, newly diagnosed with moderate to severe OSA by full polysomnography (apnea-hypopnea index of at least 15 events/hour). Four patients were excluded from analysis because of poor medication adherence and one other because of acute myocarditis.

This group of predominately middle-age, obese (median body mass index 32 kg/m²) men was randomized to hypertensive medical therapy alone or with CPAP for 6 months.

The CPAP group averaged 6 hours a night on the machine. Medication regimens were not changed during the study.

Ambulatory 24-hour blood pressure monitoring showed that daytime averages went from 145.8/88.4 at baseline to 148.8/90.6 mm Hg at 6 months in the control group compared with from 148.4/85.4 to 141.9/80.9 mm Hg in the CPAP group.

But nocturnal averages increased slightly in both group without a significant difference, so the 24-hour average didn’t show a significant advantage to CPAP either.

Nighttime blood pressures went from 136.6/78.4 to 139.3/80.3 mm Hg in the control group and from 136.2/75.4 to 137.8/76.2 mm Hg in the CPAP group, respectively.

“The lack of a significant reduction in nocturnal blood pressure is surprising and against our initial hypothesis,” the researchers noted, although a prior trial in nonresistant hypertension showed the same to be true with CPAP.

“One possibility is that resistant hypertension is a hyperadrenergic condition that contributes to sleep disruption and poor blood pressure control during sleep, independent of OSA,” they suggested.

“Recurrent arousals produced by repetitive blood pressure measurements during the night may also contribute to this phenomenon.”

Six patients treated with CPAP got their blood pressure to the 140/90 mm Hg target compared with two control-group patients, but the difference didn’t reach statistical significance (32% versus 12%, P=0.18).

Nocturnal dipping didn’t change either. Nor were there correlations between blood pressure change and CPAP compliance.

Limitations included the large number of patients excluded due to the stringent criteria, particularly regarding adherence to antihypertensive medication, lack of a placebo treatment or blinding, and lack of data on sodium intake as a potential confounding factor.