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Ischemic Preconditioning in NSTE-ACS Patients With Obstructive Sleep Apnea
Quick Takes
- Non–ST elevation acute coronary syndrome (NSTE-ACS) patients with moderate obstructive sleep apnea (OSA) have lower peak troponin levels compared to NSTE-ACS patients without moderate OSA.
- Compared to NSTE-ACS patients without OSA, NSTE-ACS patients with moderate OSA do not have a significant increase in transient myocardial ischemia events in early phase of presentation.
- Ischemic preconditioning may have a cardioprotective effect in NSTE-ACS patients with moderate OSA.
Study Questions:
Can moderate obstructive sleep apnea (OSA) have a cardioprotective effect in patients with non–ST elevation acute coronary syndrome (NSTE-ACS)?
Methods:
A secondary analysis was performed using the COMPARE study data, which evaluated transient myocardial ischemia (TMI) in patients with suspected ACS. This study enrolled 110 of these patients who presented with NSTE-ACS as defined by a positive troponin I level >0.04 ng/mL. A Holter monitor was applied throughout the hospital admission to analyze 12-lead electrocardiogram (ECG) recordings and to generate a novel high-resolution 12-lead ECG (Holter-derived respiratory disturbance index [HDRDI]) algorithm that assesses the severity of OSA using changes in QRS morphology, heart rate, and ECG-derived myogram signals that are associated with inspiratory and expiratory volume changes during respirations. OSA with moderate OSA was defined as ≥15 HDRDI events/hour and OSA without moderate as <15 HDRDI events/hour. TMI events were assessed using 12-lead ECG recordings demonstrating ST-segment changes ≥1 mm in 1 or more ECG lead lasting ≥1 minute. Three troponin I samples were drawn over the initial 24-hour time frame to compare the highest peak values between patients with and without moderate OSA. Data were reviewed after discharge and not used for clinical decision-making during admission.
Results:
Two groups were assigned based on the HDRDI algorithm; 67 (61%) of whom were diagnosed without OSA and 43 (39%) with moderate OSA. The average length of hospitalization was 88 hours ± 86. No statistical difference was found between groups for age, body mass index, or race; however, the presence of moderate OSA was significantly higher in NSTE-ACS patients with a previous history of angina (58% vs. 36%; p = 0.022), significantly lower when heart rate on admission averaged 75 versus 82 bpm (p = 0.026), and significantly lower in patients with diabetes (19% vs. 37%; p = -.037). NSTE-ACS patients with moderate OSA had significantly lower peak troponin levels (6.8 vs. 10.2 ng/mL; p = 0.037). Although there was a trend for lower TMI events assessed in NSTE-ACS patients with moderate OSA patients, there was no significant difference (16% vs. 30%; p = 0.081).
Conclusions:
This study found that peak troponin I levels were lower in NSTE-ACS patients with concomitant moderate OSA compared to those without moderate OSA. Although not statistically significant, the frequency of TMI events in NSTE-ACS patients with moderate OSA was lower. These findings suggest that OSA may play a cardioprotective role as ischemic preconditioning during NSTE-ACS.
Perspective:
This study aimed to examine conflicting evidence from previous studies regarding the association between OSA and ischemic preconditioning. Using objective measurements of troponin levels, ST-segment changes, and a composite of physiological data with a novel HDRDI algorithm, the study found that moderate OSA may play a cardioprotective role in patients who present with NSTE-ACS and concomitant moderate OSA. Despite known physiological responses to OSA that may exacerbate hypoxia, oxidative stress, sympathetic activation, and hypercoagulability, this study found that moderate OSA did not have a significant effect on myocardial damage during the early phase of presentation of NSTE-ACS as compared to those patients without moderate OSA.
There are some limitations of this study. The emerging HDRDI method of assessing OSA severity still requires further validation. The pre-existing history of either central or obstructive sleep apnea was not reported. It is also unclear whether the cardioprotective association or frequency of TMI events persists over a longer period of time during post-discharge recovery or if similar responses occur across the ACS spectrum.
Clinical Topics: Acute Coronary Syndromes, Cardiovascular Care Team, Prevention, Stable Ischemic Heart Disease, Vascular Medicine, Stress, Sleep Apnea, Chronic Angina
Keywords: Acute Coronary Syndrome, Angina Pectoris, Body Mass Index, Diabetes Mellitus, Electrocardiography, Ischemic Preconditioning, Myocardial, Myocardial Infarction, Myocardial Ischemia, Non-ST Elevated Myocardial Infarction, Oxidative Stress, Patient Care Team, Patient Discharge, Respiration, Secondary Prevention, Sleep Apnea, Obstructive, Thrombophilia, Troponin I
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