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Obstructive Sleep Apnea Causes Myocardial Injury


OSA is associated with subclinical myocardial injury as indicated by increased high-sensitivity troponin T levels, according to this study.

Obstructive sleep apnea (OSA) is associated with subclinical myocardial injury as indicated by increased high-sensitivity troponin T levels, according to the first study to demonstrate an independent association between sleep apnea severity and this marker of early myocardial injury.

“Within each category of OSA severity, the presence and magnitude of high-sensitivity troponin elevation was significantly associated with a higher risk of incident heart failure. In OSA, higher-sensitivity troponin is associated with greater heart failure risk,” lead author Amil M. Shah, MD, MPH, of the Brigham and Women’s Hospital in Boston, told ConsultantLive.

The cross-sectional study included 1645 middle-aged and older patients in both the Atherosclerosis Risk in Communities Study and the Sleep Heart Health Study who were free of coronary heart disease and heart failure at baseline. All patients underwent overnight home polysomnography. They were monitored for a median of 12.4 years. OSA severity was categorized as none, mild, moderate, or severe using the respiratory disturbance index.

High-sensitivity troponin T levels-but not N terminal pro B-type natriuretic peptide levels, a marker for increased ventricular wall stress-were significantly associated with OSA after adjustment for the following potential confounders: age, sex, body mass index, smoking status, hypertension, diabetes mellitus, alcohol intake, pulmonary function variables (forced expiratory volume in 1 second and forced vital capacity), chronic obstructive pulmonary disease status, systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, insulin level, and estimated glomerular filtration rate.

The mechanisms linking OSA to subclinical myocardial injury reflected in higher high-sensitivity troponin levels are not yet defined. “Potential mechanisms include ischemia related to recurrent OSA-associated nocturnal hypoxemia, with associated sympathetic activation, hypertension, and tachycardia,” said Dr Shah. “Several publications have demonstrated ECG changes consistent with ischemia occurring in association with apneas. OSA may also cause myocardial stress and injury due to the increased load on both the right and left ventricles, resulting from marked swings in intrathoracic pressure during obstructed breathing, as well as associated paroxysmal nocturnal and more chronic systemic and pulmonary hypertension. Indeed, OSA has been associated with biventricular hypertrophy.”

Dr Shah pointed out that multiple epidemiological studies have demonstrated that high-sensitivity troponin levels are associated with incident heart failure, coronary heart disease, and cardiovascular mortality. “Data from our analysis demonstrate that this relationship also exists within each category of OSA severity. This association was particularly strong among those with severe OSA,” he said.

Future studies are necessary to determine whether high-sensitivity troponin levels can be used to identify high-risk OSA patients and help guide treatment decisions, he added.

“Our findings suggest that high-sensitivity troponin T may be an early marker of the adverse myocardial impact of OSA. Clinicians should continue to pay attention to appropriately diagnose and treat OSA,” said Dr Shah.

The findings were published online ahead of print publication in the American Journal of Respiratory and Critical Care Medicine.

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