OSA Is Associated With Enhanced Coronary Collateral Circulation and Reduced Myocardial Injury During Acute Coronary Syndromes.
retrospective_cohort · Level III
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- Record sourced from PubMed, PMID 41802590.
- Also identified by DOI 10.1016/j.chest.2026.02.015.
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Abstract
Some evidence suggests that OSA may attenuate myocardial injury and reduce infarct severity during acute coronary syndromes (ACSs), potentially through stimulation of coronary collateral circulation (CCC). However, the relationship between OSA and collateral development, and their combined impact on ACS event severity, remains unclear. What is the relationship between OSA and coronary collateral development and what is their combined impact on ACS severity? Post hoc analysis of the ISAACC trial, including patients with first-time ACS with CCC assessment using the Cohen-Rentrop scale (CRS), where a score of ≥ 2 (CRS grade 2 or 3) indicated well-developed collaterals. OSA was diagnosed via respiratory polygraphy performed within 24 to 72 hours of hospitalization. Associations between OSA and CRS grade 2 or 3 were evaluated using adjusted logistic regression. Peak creatine kinase (CK), peak cardiac troponin I (cTnI), and left ventricular ejection fraction (LVEF) were analyzed as ACS severity markers. Of 185 participants included, 79.5% had OSA. Participants were mainly middle-aged male individuals and demonstrated a high comorbidity burden. OSA was associated with greater odds of well-developed collaterals with an adjusted OR of 2.84 (95% CI, 1.24-7.19; P = .019), with a dose-response increase across OSA severity categories. Among patients with OSA, the presence of robust collaterals was associated with significantly lower peak CK and cTnI levels during the ACS episode, but not with improved LVEF. Our research shows that in patients with first-time ACS, OSA was associated with a higher prevalence of well-developed coronary collaterals. Among patients with OSA, robust collateralization was associated with less myocardial injury during ACS, supporting the hypothesis that OSA may promote adaptive vascular remodeling, which warrants further mechanistic investigation. ClinicalTrials.gov; No.: NCT01335087; URL: www. gov.