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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.



The presence of obstructive sleep apnea (OSA) may have a protective effect in patients with acute coronary syndromes, according to researchers.

In a study of 127 patients presenting with acute coronary syndromes (ACS), median peak cardiac troponin-I (cTn-I) values were significantly higher in patients without obstructive sleep apnea, compared with OSA patients (10.7; interquartile range: 1.78-40.1, vs. 3.79; IQR: 0.37-24.3, respectively; P = .04 ). The findings were published Feb. 5 in CHEST.

The study comprised 89 OSA patients and 38 non-OSA patients who were admitted to a hospital for acute coronary syndromes. The OSA group had a median apnea-hypopnea index (AHI) of 32, while the non-OSA group had a median AHI of 4.8. There was no significant difference between the two groups in gender, age, or cardiovascular risk factors such as hypertension, diabetes mellitus, body mass index, dyslipidemia, and smoking.

The cohort was part of the Continuous Positive Airway Pressure (CPAP) in Patients With Acute Coronary Syndrome and Obstructive Sleep Apnea (ISAACC) study, a prior randomized, controlled trial that evaluated the effect of CPAP treatment on new cardiovascular events in patients with an episode of ACS and OSA, reported Alicia Sánchez-de-la-Torre, PhD, of the respiratory department at Hospital Universitari Arnau de Vilanova and Santa Maria in Catalonia, Spain, and her coauthors.

Respiratory polygraphy was performed in the first 24-72 hours after hospital admission, and patients with an AHI of at least 15 events per hour were considered to have OSA. Those with an AHI less than 15 events per hour were included in the non-OSA group.

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The OSA patients were randomized to conservative or CPAP treatment. An obstructive apnea “episode” was defined as a complete cessation of airflow for 10 seconds or longer, and an episode of hypopnea was defined as a reduction in airflow for at least 10 seconds associated with a greater than 4% decrease in arterial oxygen saturation.

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.

“These results suggest that patients with higher AHI are significantly more likely to have low cTn-I levels than patients without evidence of OSA, which could imply that patients with elevated AHI, particularly those with severe OSA, may experience less severe myocardial injury,” the authors said in the report. The findings “suggest that OSA has a protective effect in the context of MI,” they added.

Limitations of the study include exclusion of patients with severe ACS, exclusion of sleepy subjects, and assessment of myocardial injury using cTn-I as a biomarker, without further data to determine infarct size.

“The possible role of OSA in cardioprotection should be explored in future studies,” the authors concluded.

The authors disclosed relationships with ResMed Inc., Spanish Ministry of Health, Spanish Respiratory Society, Catalonian Cardiology Society, and ALLER. No other disclosures were reported.

SOURCE: Chest. 2018 Feb 5;153[2]:329-38. doi: 10.1016/j.chest.2017.06.046

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