29
AASM Membership Sections Newsletter
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Issue #6
an alternative therapy. Studies have suggested that the repetitive
cycles of hypoxemia and re-oxygenation that characterize OSA
may contribute to its association with increased cardiovascular
risk. Prospective data comparing CPAP to supplemental oxygen
for the reduction of cardiovascular risk is limited, however. The
recently published Heart Biomarker Evaluation in Apnea Treatment
(HeartBEAT) trial, which compared the impacts of CPAP versus
nocturnal oxygen supplementation on ambulatory blood pressure,
takes us one step further in our understanding of how best to
manage OSA (Gottlieb et al, N Engl J Med 2014;370:2276-85).
What did they do?
Patients aged 45-75 were recruited from four cardiovascular
practices. Of these, 318 who were found to have moderate to
severe OSA (apnea-hypopnea index of 15-50) on a portable sleep
study ultimately enrolled and randomized to one of three groups:
1) a control group receiving education about healthy sleep hygiene
and lifestyle modification, 2) nocturnal supplemental oxygen plus
education (without CPAP), or 3) CPAP plus education (without
supplemental oxygen). Patients’ 24-hour mean arterial pressure was
measured at baseline and again after 12 weeks of therapy.
What did they find?
Subject retention was high at 88%. Similar reductions in nocturnal
hypoxemia were seen between patients receiving supplemental oxygen
and those on CPAP, with both groups’ oxygen levels significantly
better than those of control patients. Patients wore supplemental
oxygen for significantly longer per night than those receiving CPAP
(4.8 hours vs. 3.5 hours). Most importantly, after 12 weeks, 24-hour
mean arterial pressure was significantly lower in patients receiving
CPAP than either those receiving supplemental oxygen or controls
(lower by 2.8 and 2.4 mmHg, respectively). Results persisted after
adjustment for age, sex, race, baseline body-mass index and AHI.
They did not find a significant difference in the effect of each therapy
on odds of nocturnal dipping in blood pressure (defined as a failure of
the mean to drop by at least 10% compared with the daytime value).
However, they did observe a dose-response relationship between
hours of CPAP use and increased odds of nocturnal dipping.
What are the implications for clinical practice?
While both CPAP and supplemental oxygen led to improvements
in nocturnal hypoxemia, only CPAP was associated with a reduction
in mean blood pressure. Until we have large randomized, controlled
trials powered to detect the impact of CPAP on clinical outcomes (e.g.
stroke, myocardial infarction, death) we must rely upon intermediate
markers of cardiovascular risk such as blood pressure to inform our
practice. This study further strengthens the literature suggesting that
the increased cardiovascular risk seen in OSA is driven by more than
simple nocturnal hypoxemia; a number of other factors including
sympathetic activation, oxidative stress and systemic inflammation are
likely at play.
A couple of points deserve emphasis. The magnitude of blood
pressure reduction in this study was similar to that seen in other
studies of CPAP for OSA. Although a 2 mmHg reduction in mean
arterial pressure may sound minimal, data from observational studies
suggests that even this small change may result in as much as a 10%
reduction in stroke mortality (Lewington et al, Lancet 2002;360:1903-
13). Furthermore, patients in this study were, on the whole, not very
sleepy (mean Epworth Sleepiness Scale was 8/24 in the CPAP group)
and therefore probably less adherent with CPAP than they would
otherwise have been. The relative benefits of CPAP over oxygen may
therefore be even greater in the (likely sleepier) population referred to
sleep centers whose use may be greater than was seen here.
In conclusion, although supplemental oxygen attenuates the
hypoxemia seen in OSA, CPAP should remain the mainstay of therapy
for patients who can tolerate it.
Clinical Case: Treatment-Emergent Central
Sleep Apnea
By Dr. Sreelatha Naik, MD
Case
A 70-year-old man is referred to the sleep clinic for suspected
obstructive sleep apnea hypopnea syndrome following a stroke two
years ago. He has excessive sleepiness with an Epworth Sleepiness
Score of 15/24. He has loud snoring and witnessed apnea by his wife.
He dozes off accidentally at his desk during work, despite a consistent
and adequate duration of sleep. He has no parasomnias or ancillary
symptoms to suggest narcolepsy. His medical history is notable for
hypertension, hyperlipidemia, cerebellar stroke two years ago and ST-
elevation myocardial infarction in 2009. On exam, his blood pressure
was 118/68, pulse 63, respiratory rate 14, SpO2 97% and BMI 30 kg/
(m2). His head and neck exam was notable only for Mallampati III,
and his neuro, cardiac and pulmonary exams were unremarkable.
Diagnostics
He underwent a split-night in-lab polysomnogram because
the apnea-hypopnea index (AHI) was 32 events/hour during the
diagnostic portion. Apneas during the baseline portion of the
study were obstructive events. (Figure 1) There were no central
apneas noted in the baseline portion of the polysomnogram. Once
continuous positive airway pressure (CPAP) titration was initiated,
there was the emergence of central apneas. (Figure 2) Optimal CPAP
that abolished obstructive events was CPAP of 7 cm H2O.
