Journal of Sleep Disorders: Treatment and Care.ISSN: 2325-9639

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Review Article, J Sleep Disor Treat Care Vol: 2 Issue: 1

Obstructive Sleep Apnea in the Acute Myocardial Infarction Setting - Should I Treat My Patient?

Neomi Shah1,2*, Jorge R KizerShah1,2 and Vahid Mohsenin3
1Montefiore Medical Center, NY, USA
2Albert Einstein College of Medicine, NY, USA
3Yale University School of Medicine, CT, USA
Corresponding author : Neomi Shah
Associate Director, Pulmonary Sleep Lab-Montefiore Medical Center, Division of Pulmonary Medicine, NY, USA
Tel: 718-920-2105; Fax: 718-652-8590
E-mail: [email protected]
Received: December 12, 2012 Accepted: May 02, 2013 Published: May 06, 2013
Citation: Shah N, Kizer JR, Mohsenin V (2013) Obstructive Sleep Apnea in the Acute Myocardial Infarction Setting - Should I Treat My Patient? J Sleep Disor: Treat Care 2:1. doi:10.4172/2325-9639.1000109


Obstructive Sleep Apnea in the Acute Myocardial Infarction Setting - Should I Treat My Patient?

Obstructive sleep apnea is prevalent among patients with acute myocardial infarction. Epidemiological evidence supports an independent association between sleep apnea and myocardial infarction. Our current clinical practice is to recommend routine and immediate treatment for sleep apnea in patients with an acute myocardial infarction. However, emerging evidence from population based cohort studies does not support an independent role of sleep apnea in the development of incident coronary heart disease events. Furthermore, both animal and human studies suggest a potential cardioprotective role of intermittent hypoxia (as seen in sleep apnea) in the setting of an acute myocardial infarction. Routine treatment of withdrawing the intermittent hypoxia stimulus (such as positive airway pressure therapy for sleep apnea) may potentially adversely impact the myocardial recovery process post ischemic event. One potential mechanism may be due to hindrance of development of coronary collaterals due to reduced levels of vascular growth factors that are particularly sensitive and responsive to intermittent hypoxia stimulus. Treatment of sleep apnea in the immediate post-MI period appears to be debatable and clinical trials are needed to further delineate the role of sleep apnea and its associated intermittent hypoxemia in the myocardial recovery process post-acute myocardial infarction.


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