Is Ischemic Pre-Conditioning Present in Patients with Acute Coronary Syndrome and ECG Derived Moderate Sleep Disordered Breathing?
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Is Ischemic Pre-Conditioning Present in Patients with Acute Coronary Syndrome and ECG Derived Moderate Sleep Disordered Breathing?

Abstract

Background: Sleep Disordered Breathing (SDB) has been found to be associated with anincreased risk of major cardiovascular events including Acute Coronary Syndrome (ACS). There is conflicting evidence that suggests SDB has a cardioprotective effect, via ischemic preconditioning, in patients with ACS when measured with cardiac troponin levels. This study was designed to examine whether troponin levels and or transient myocardial ischemia differed in patients with non-ST elevation (NSTE-ACS) with and without moderate SDB measured with 12-lead Holter electrocardiographic (ECG) data. Purpose: The purpose of this study was twofold: (1) examine the severity of myocardial injury using peak troponin levels between NSTEACS patients with and without Holter derived respiratory disturbance index (HDRDI) suggestive of moderate SDB; and (2) determine the frequency of transient myocardial ischemia between NSTE-ACS patients with and without a HDRDI suggestive of moderate SDB. Method: This was a secondary analysis from the COMPARE Study. A total of 110 hospitalized patients diagnosed with NSTE-ACS were included. SDB events were identified using 12-lead ECG Holter recordings using a combination of QRS, R-R intervals and the myogram. All 110 patients had at least eight hours of Holter recording. Moderate HDRDI suggestive of moderate SDB was defined as >15 HDRDI events per hour. Transient myocardial ischemia was defined as >1 millimeter (mm) of ST-segment ↑ or ↓, in > 1 ECG lead, > 1 minute. Results: Of the 110 NSTEACS patients included, 39% (n=43) had a HDRDI that was suggestive of moderate SDB. A higher proportion of males were in the moderate HDRDI group as compared to females (86% vs 14%; p=0.001). NSTE-ACS patients in the moderate HDRDI group had lower peak troponin levels than those without moderate HDRDI (6.8 ng/ml vs 10.2 ng/ml; p=0.037). There was a trend for fewer transient ischemic events in the moderate HDRDI group as compared to those without moderate HDRDI, however, this was not statistically different (16% vs 30%; p=0.081). Conclusions: NSTE-ACS patients with moderate HDRDI suggestive of SDB have less cardiac injury as compared to NSTE-ACS patients without moderate HDRDI. There was a trend for fewer transient myocardial ischemic events in the moderate HDRDI group compare to those without moderate HDRDI, but the groups were not different. These findings corroborate prior studies suggesting a possible cardioprotective effect of SDB via a precondition mechanism in patients with ACS. Future research is needed to explore the underlying physiologic mechanisms of this findings.

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