Pub Date: Monday, Jun 21, 2021
Author: David E. Winchester, MD, MS, FACC, FASNC, FACP
Affiliation: Malcom Randall VAMC, Gainesville FL; and University of Florida College of Medicine, Gainesville FL
Obstructive sleep apnea (OSA) is medical condition of disordered breathing familiar to many people in the public. Patients with OSA, or their family members, are likely aware that OSA causes people to snore and is often treated with bulky, uncomfortable machines to assist with breathing overnight. They are less likely to be aware that the condition affects several organ systems and induces an assortment of lifestyle limiting symptoms. Depending on gender and the criteria used for diagnosis, prevalence in the United States is between 5-30% and worldwide may affect close to a billion people.1 OSA is likely present in the majority of patients with other conditions such as congestive heart failure (CHF), hypertension (HTN), atrial fibrillation (AF), and coronary artery disease (CAD). Patients with OSA may experience daytime sleepiness, morning headaches, and snoring or choking during sleep. OSA is not limited to its frustrating symptoms; it is a risk factor for developing HTN and among patients with resistant HTN, the substantial majority may have underlying OSA as a contributor.2
In this American Heart Association Scientific Statement on OSA and cardiovascular disease (CVD), Dr. Yeghiazarians and the writing group have established the public health crisis that OSA represents by substantiating the remarkable prevalence of the disease and drawing linkages to a multitude of other medical conditions.3 The statement summarizes the impact of nonmodifiable risk factors including family history and craniofacial dysmorphisms and potentially modifiable risk factors, primarily overweight and obesity. A review of pathophysiologic mechanisms describes how OSA results from the relationship between upper airway anatomical abnormalities and sleep-related mechanical changes. The authors appraise options for testing and the potential value of population screening. The remainder of the statement explores the wide-reaching effects of OSA on a multitude of clinical conditions and mortality.
This statement is a useful document for public awareness and to inform policy makers; it should also be a clarion call for cardiologist and clinicians of all backgrounds and training. OSA is an excellent example of a condition that extends beyond the traditional organizational structure of most healthcare systems; it is not simply a “pulmonary”, “cardiology”, or “sleep medicine” problem. When patients with coronary disease present to clinic with a complaint of feeling tired, testing for myocardial ischemia may be warranted, but so is a thorough sleep history and potentially a screening test for OSA. Similarly, a patient with systolic blood pressure of 165 mmHg despite 4 medications may require higher doses or another agent, but they also need to have testing performed to determine any potential role of OSA.
The statement reviews the literature on relevant screening questionnaires such as the Epworth Sleepiness Scale, the Berlin Questionnaire, and the STOP-Bang. While the reported sensitivity and specificity of these instruments are clearly suboptimal, the prevalence in the general population and CVD population would suggest that we should be performing substantially more screening and testing for OSA. Clinicians definitely should make themselves aware of the diverse testing options. The original testing method of direct observation of apneic episodes during sleep was costly and time/resource intensive, substantially limiting patient access. Now, automated and semiautomated home testing options are widely available and facilitate a much broader screening approach. In the near future, wearable smart devices may further expand testing options. Despite these advancements, currently available evidence does not support a role for OSA screening as primary prevention. With fewer barriers and lower costs, primary screening may become a viable approach.
Other important limitations in our current understanding and treatment of OSA relate to the poor adherence to treatment and whether or not treatment actually affects outcomes. Table 3 in the statement provides a detailed description of the many available treatments ranging from airway management, to bariatric or airway surgeries, to repositioning and oral appliances, to lifestyle approaches to reduce obesity. Costs vary widely from hundreds to tens of thousands of dollars. Even more unfortunate are the treatment failure rates which may be 60-90%. These high failure rates undoubtedly contribute to the evidence summary provided by the statement authors which concludes that little or no evidence exists to show that treatment of OSA improves disease-specific outcomes or mortality.
Areas for future action are provided by the authors which include a call for more research on testing and treatment methods, especially those which allow personalized treatment plans to improve adherence and success. Research is also desperately needed in how race, ethnicity, and gender disparities affect all stages of OSA including prevalence, testing and diagnosis, treatments, and outcomes.4,5 As noted before, the other area for future action is for frontline clinicians. Over the past several years, cardiologists have embraced a multitude of new practice areas including cardiac amyloidosis, cardio-oncology, cardio-obstetrics, and cardiac intensive care. It is also time for cardiologists to embrace our role in the prevention, diagnosis, and treatment of OSA.
Yeghiazarians Y, Jneid H, Tietjens JR, Redline S, Brown DL, El-Sherif N, Mehra R, Bozkurt B, Ndumele CE, Somers VK; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Peripheral Vascular Disease; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Stroke Council; and Council on Cardiovascular Surgery and Anesthesia. Obstructive sleep apnea and cardiovascular disease: a scientific statement from the American Heart Association [published online ahead of print June 21, 2021]. Circulation. doi: 10.1161/CIR.0000000000000988
- Benjafield AV, Ayas NT, Eastwood PR, Heinzer R, Ip MSM, Morrell MJ, Nunez CM, Patel SR, Penzel T, Pépin JL, Peppard PE, Sinha S, Tufik S, Valentine K, Malhotra A. Estimation of the global prevalence and burden of obstructive sleep apnoea: a literature-based analysis. Lancet Respir Med 2019;7:687-698.
- Bock JM, Vungarala S, Karim S, Somers VK. Obstructive Sleep Apnea as a Cardiovascular Risk Factor - Beyond CPAP. Can J Cardiol 2021.
- Yeghiazarians Y, Jneid H, Tietjens JR, Redline S, Brown DL, El-Sherif N, Mehra R, Bozkurt B, Ndumele CE, Somers VK; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Peripheral Vascular Disease; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Stroke Council; and Council on Cardiovascular Surgery and Anesthesia. Obstructive sleep apnea and cardiovascular disease: a scientific statement from the American Heart Association [published online ahead of print June 21, 2021]. Circulation. doi: 10.1161/CIR.0000000000000988
- Jackson CL, Powell-Wiley TM, Gaston SA, Andrews MR, Tamura K, Ramos A. Racial/Ethnic Disparities in Sleep Health and Potential Interventions Among Women in the United States. J Womens Health (Larchmt) 2020;29:435-442.
- Chen X, Wang R, Zee P, Lutsey PL, Javaheri S, Alcántara C, Jackson CL, Williams MA, Redline S. Racial/Ethnic Differences in Sleep Disturbances: The Multi-Ethnic Study of Atherosclerosis (MESA). Sleep 2015;38:877-888.
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-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association --