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Communications to the Editor |

Sleep, Breathing, Oxygen, and Heart FREE TO VIEW

Rohit Budhiraja; David Hudgel
Author and Funding Information

Henry Ford Hospital Detroit, MI

Correspondence to: David Hudgel, MD, FCCP, Professor of Medicine, Chief, Section Head, Sleep Disorders and Research Center, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202; e-mail: dhudgel1@hfhs.org



Chest. 2004;125(4):1596. doi:10.1378/chest.125.4.1596
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Published online

To the Editor:

We read with interest the recent report by Hayashi et al (September 2003)1 proposing a relationship between sleep-disordered breathing (SDB) and coronary artery disease (CAD).

There are several deficiencies in the study that negate the authors’ conclusions that “repetitive NOD [nocturnal oxygen desaturation] due to SDB is an important and independent risk factor for the development of coronary atherosclerosis.” First, a statistically significant correlation coefficient between NOD and CAD score does not necessarily reflect a causal relationship, as was assumed by the authors. Second, the degree of sleep hypoxemia experienced by these subjects appears to be relatively mild. There was no significant difference between the less and the more severe CAD groups in the time spent at < 90% oxygen saturation. While the lowest oxygen saturation readings were significantly lower in patients with more severe CAD, the total duration (and thus, the relevance) of such episodes is not stated. The authors’ hypothesis about the role of hypoxemia in “triggering” the coronary vascular disease process is also inaccurate since the study did not reveal any significant hypoxemia in patients with angiographically proven CAD of lesser severity (group N in the study). Furthermore, the basic premise that NOD would reflect obstructive sleep apnea in a cohort with lean body habitus, and thus, a low pretest probability of having obstructive sleep apnea, is faulty, as was appropriately pointed out by Dr. Sin in his editorial.2

From a health-care perspective, the more significant finding in the study appears to be the gross underutilization (8.4% of all patients) of therapy with β-blockers in these patients with proven coronary vascular disease.3

In conclusion, we believe that the authors’ assertion about the role of SDB in the genesis of coronary vascular pathology is an overstatement of the actual results of the study and has the risk of being taken at face value by readers of CHEST.

References

Hayashi, M, Fujimoto, K, Urushibata, K, et al (2003) Nocturnal oxygen desaturation correlates with the severity of coronary atherosclerosis in coronary artery disease.Chest124,936-941. [CrossRef] [PubMed]
 
Sin, DD Sleep-disordered breathing: a heart-changing experience?Chest2003;124,778-780. [CrossRef] [PubMed]
 
Frishman, WH, Cheng, A Secondary prevention of myocardial infarction: role of beta-adrenergic blockers and angiotensin-converting enzyme inhibitors.Am Heart J1999;137,S25-S34. [CrossRef] [PubMed]
 

Figures

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References

Hayashi, M, Fujimoto, K, Urushibata, K, et al (2003) Nocturnal oxygen desaturation correlates with the severity of coronary atherosclerosis in coronary artery disease.Chest124,936-941. [CrossRef] [PubMed]
 
Sin, DD Sleep-disordered breathing: a heart-changing experience?Chest2003;124,778-780. [CrossRef] [PubMed]
 
Frishman, WH, Cheng, A Secondary prevention of myocardial infarction: role of beta-adrenergic blockers and angiotensin-converting enzyme inhibitors.Am Heart J1999;137,S25-S34. [CrossRef] [PubMed]
 
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