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OSA may provide cardioprotection

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Results demonstrate ‘paradigm shift’ in OSA research

Although this study cannot definitively establish a clinically meaningful protective effect, it does provide important “preliminary evidence supporting the concept of OSA-induced cardioprotection” and challenges existing research, according to an editorial by Doron Aronson, MD, of the department of cardiology at Rambam Medical Center, Haifa, Israel, and coauthors (CHEST. 2018 Feb 153[2]:295-7. doi: 10.1016/j.chest.2017.07.036).

The results should be interpreted with caution, especially since accurate assessment of infarct size poses a challenge, they wrote.

“Myocardial infarct size is highly variable and is influenced by the duration of coronary occlusion, ST-segment elevation or non–ST elevation myocardial infarction, infarct location, residual antegrade infarct-related artery flow, collateral flow, the presence of non–culprit vessel coronary artery disease and myocardial metabolic demand,” they wrote. “Without accounting for these variables in a small study, results may be affected by variation in the characteristics of the patients.”

Though further study is needed, the findings may have “profound clinical implications regarding our therapeutic approach to patients with sleep apnea” if confirmed, the authors concluded.


 

Blood samples were collected from patients every 6 hours until two consecutive cTn-I measurements showed a decrease, with the highest measurement considered the peak cTn-I value.

Peak cTn-I value was significantly higher in non-OSA patients than in OSA patients. Median infarct size, measured by calculating the area under the cTn-I curve, was significantly different between the two groups (451 for non-OSA patients vs. 143 in OSA patients; P = .049), wrote Dr. Sánchez-de-la-Torre and her colleagues.

As cTn-I levels decreased, there was a trend toward increased OSA severity (P = .058). In the multivariable linear regression model used to assess OSA severity, patients with severe OSA had 61% lower cTn-I levels than non-OSA patients, the authors noted.

“The effects of chronic hypoxia in individual organ systems are not well understood. While chronic sustained hypoxia as seen with COPD may lead to pulmonary hypertension, chronic intermittent hypoxia (CIH) as seen predominantly in sleep apnea has been attributed to causing widespread effects ranging from systemic hypertension to metabolic dysfunction and systemic inflammation,” noted Krishna Sundar, MD, FCCP. “Despite these associations, an increased risk of major cardiovascular events from untreated OSA is yet to be definitively established.”

Dr. Krishna Sundar

In this article, a protective effect from OSA on myocardial ischemic events is demonstrated in a group of 127 consecutively admitted patients with acute coronary syndrome (ACS). While it is interesting that a high proportion of those admitted for ACS had OSA, there were no significant differences in the age, sex, BMI, usage of antihypertensive or antiplatelet agents, presence of hypertension, DM, dyslipidemia or smoking status between those with and without OSA. “OSA appeared to confer a protective effect on the size of myocardial injury with those having higher AHI values demonstrating lower peak cardiac troponin values,” said Dr. Sundar, who is an associate clinical professor of pulmonary, critical care and sleep medicine at the University of Utah.“An effect of age (mean age in this study being 64 years) and BMI (mean being 27) on the occurrence of preconditioning effects of OSA is not excluded given deleterious effects of untreated OSA on infarct size in other studies on obese or younger patients with ACS. Further understanding of molecular effects of chronic hypoxia exposure (high altitude, chronic lung disease, OSA) is required before the complex and often contradictory effects of chronic hypoxia can be affirmed as being protective or deleterious,” added Dr. Sundar, who is also medical director of the Sleep-Wake Center at the University of Utah and a member of CHEST Physician’s editorial advisory board.

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