What are we missing? Hypertension and hypopneas

Citation:

Arora S, Collen JF. What are we missing? Hypertension and hypopneas. J Clin Sleep Med. 2020;16(10):1653–1654.

Modern medicine is grounded in accurate diagnostic information, contingent on cohesive sets of definitions. Sleep medicine is continuously refining its own diagnostic definitions to accurately capture outcome-based data and improve successful identification and severity categorization, impacting treatment decisions, public health, and research. With limited education regarding the diagnosis of OSA and access to care in vulnerable populations, there is a vast underestimation of the degree of sleep-disordered breathing in the United States. The vacillating definition of the hypopneas only adds to the confusion.

The controversy over the definition of the components of an OSA diagnosis is long-standing. The definition of hypopnea in 1999 concluded that hypopneas and apneas shared a similar pathophysiology; therefore, distinguishing them was unnecessary.¹ A revision to the definition in the 2001 American Academy of Sleep Medicine position paper suggested a ≥ 30% reduction in thoracoabdominal movement or airflow for ≥ 10 seconds accompanied by a decrease in oxyhemoglobin saturation of ≥ 4%.² This initial postulate had centered on high interobserver agreement. Later, with the advent of the first American Academy of Sleep Medicine scoring manual in 2007, the recommended hypopnea definition changed to a ≥ 30% reduction in nasal airflow and a ≥ 4% decrease in oxyhemoglobin saturation.³ In 2012, guidance switched to a ≥ 30% reduction in airflow and ≥ 3% arousal (3%A) with desaturation of ≥ 4% as an acceptable alternative for patients requiring Centers for Medicare and Medicaid Services reimbursement.⁴ Previous analyses such as those from Won et al⁵ have shown a rate of up to 37% negative Centers for Medicare & Medicaid Services diagnoses meeting OSA AHI criteria per the 3% arousal rule.

In the current (2020) issue of the Journal of Clinical Sleep Medicine, Budhiraja and colleagues primarily focus on 476 previously normotensive adults aged ≥ 40 years from the Sleep Heart Health Study who would be characterized as having OSA based on the use of the 3% arousal rule compared to those who would rate as negative for OSA if utilizing the Centers for Medicare & Medicaid Services criteria.⁶ The study used blood pressure (BP) screening at the time of an initial polysomnogram with an abbreviated follow-up visit 2 years later and a second sleep evaluation with a polysomnogram approximately 5 years after the initial screening. Results showed that approximately 40% of the cohort who were negative for OSA per Centers for Medicare & Medicaid Services standards went on to develop elevated BP or stage 1/2 hypertension per the 2017 American College of Cardiology/American Heart Association criteria by the time of their second evaluation.

The major strengths of the prospective study revolve around its well-characterized population, current hypertension definition, and adjustment for changes in age and body mass index. Moreover, the relatively long follow-up period of 5 years also helps in understanding the time frame between diagnosis and outcome.

The study does have some limitations but not enough to dampen the impact of its critical findings. The patients who were subsequently characterized in the hypertensive category (elevated BP + Stage 1/2 hypertension) were more likely to be older by a mean of 4.2 years, have a history of cardiovascular disease and stroke, and have moderate/severe OSA.⁶ Moreover, the article characterized a change in classification without the numerical mean difference in BP over 5 years for the newly hypertensive group.

The study’s adjusted bivariate analysis showed a β = 3.387 for the diastolic BP, suggesting a clinically significant independent increase in diastolic BP with each unit increase in AHI. The study also provided a glimpse of the average increase in AHI scoring based on the different thresholds (AHI = 7–8 events/h based on the 3% arousal criteria vs the 4% desaturation criteria). This finding was slightly higher than prior studies that reclassified patients based on different scoring rules.⁵

This article adds to the increasing body of literature showing that mild OSA may be independently associated with increased BP.⁷ There has been a long-standing debate as to whether arousals and associated sympathetic activation have enough of an impact on sympathovagal modulation to lead to a cardiovascular event. Theoretically, arousals leading to hyperpneas serve to counter episodic hypoxemia. These arousals are likely within the continuum of repetitive endothelial dysfunction, resulting in reductions in arterial elasticity that precede cardiovascular events. Other investigators have independently suggested an increase in diastolic BP because of repetitive arousals.⁸ Because hypertension is an insidious process, a 5-year window for this demographic of patients may not be enough to accurately capture the incidence of cardiovascular events.

The components of OSA diagnosis and classification should accurately reflect the complex pathophysiology surrounding sleep-disordered breathing and have the greatest predictability for adverse health outcomes. Exclusionary hypopnea criteria may reduce recognition of OSA in females and patients less than 65 years old, resulting in undertreatment.⁹ Utilizing the most up-to-date hypertension definitions and American Academy of Sleep Medicine scoring rules brings researchers and practicing physicians closer to the truth regarding the clinical impact of OSA.

DISCLOSURE STATEMENT

The authors report no conflicts of interest. The views in this commentary reflect those of the authors and do not constitute official policy of the United States Air Force, Army, or Department of Defense.