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Clinical Investigations: SLEEP AND BREATHING |

Cardiac Troponin T in Obstructive Sleep Apnea

Apoor S. Gami, MD; Anna Svatikova, BA; Robert Wolk, MD, PhD; Eric J. Olson, MD, FCCP; Carolyn J. Duenwald, BS; Allan S. Jaffe, MD; Virend K. Somers, MD, PhD
Author and Funding Information

*From the Division of Cardiovascular Diseases (Drs. Gami, Wolk, Somers, and Ms. Svatikova), Cardiovascular Physiology Laboratory (Ms. Duenwald), Division of Pulmonary and Critical Care Medicine (Dr. Olson), Department of Laboratory Medicine and Pathology (Dr. Jaffe), Mayo Clinic and Foundation; Rochester, MN.

Correspondence to: Virend K. Somers, MD, PhD, Mayo Clinic, 200 First St SW, Rochester, MN 55905; e-mail: somers.virend@mayo.edu



Chest. 2004;125(6):2097-2100. doi:10.1378/chest.125.6.2097
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Study objectives: Obstructive sleep apnea (OSA) is associated with nocturnal angina and ST-segment depression, which are relieved by treatment with continuous positive airway pressure (CPAP). We tested the hypothesis that severe nocturnal hypoxia in patients with OSA causes myocyte necrosis as evidenced by increases in cardiac troponin T.

Design: Prospective cohort study.

Setting: Cardiovascular physiology and sleep research laboratory.

Participants: Fifteen male volunteers with coronary artery disease (CAD) and moderate or severe OSA (apnea-hypopnea index [AHI] > 15).

Measurements and results: Polysomnography and measurement of serum cardiac troponin T before sleep, after 4 h of untreated OSA, and in the morning after 4 h of treatment with CPAP. The mean AHI for the group was 41 (SD 16), and the mean oxygen saturation nadir during sleep was 83% (SD 8%). All measurements of cardiac troponin T were < 0.010 ng/mL.

Conclusions: Despite the fact that some patients with OSA may experience nocturnal ischemia, this study shows that patients with severe OSA and coexisting CAD do not have nightly episodes of myocardial injury detectable by the current-generation cardiac troponin T assay.


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