Abstract 1030: Links of Sleep Apnea Syndrome to Coronary Atherosclerotic Burden and Elevated Cardiac Biomarkers in Stable Coronary Artery Disease Patients
Objectives: This study sought to evaluate links of sleep apnea syndrome (SAS) to coronary arterosclerotic plaque burden and silent myocardial stress in the stable coronary artery disease (CAD) patients.
Background: SAS is highly prevalence in the population of cardiovascular diseases, though it is not clarified whether SAS has any linkage to the pathophysiology of coronary atheroscrelotic burden in the stable CAD.
Methods: We prospectively studied 105 consecutive patients who underwent diagnostic coronary angiography or scheduled percutaneous coronary intervention during September to December 2008. SAS was evaluated by ambulatory polygraphic monitoring device with electrocardiograms, nasal airflow, thoracic and abdominal effort, arterial O2 saturation to analyze proportion of central and obstructive SAS during sleep. Coronary atherosclerotic burden was evaluated by Gensini’s score, and myocardial stress/injury were assessed by measuring plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high sensitivity troponin T (hs-TnT).
Results: Patients with apnea hypopnea index (AHI) above 15/hour (n=42) showed significantly higher Gensini’s score (40.9 +/−42.7 vs. 25.3 +/− 28.7, p=0.039) than those below 15/hour (n=51). The higher AHI group revealed significantly higher hs-TnT levels (median level 0.011 ng/ml [0.008 – 0.016 ng/ml] vs 0.009 ng/ml [interquartile range, 0.007– 0.012 ng/ml], p=0.033). The longest obstructive apnea time was significantly longer in patients with chronic total occlusion (CTO) than those without CTO (36.8±23.4 vs. 55.5±33.3 seconds, p=0.01). The CTO group showed significantly higher levels of myocardial stress/injury biomarkers, NT-proBNP(971.4pg/ml [140.6 –1262.0 pg/ml] vs 96.9 pg/ml [41.3–255.3 pg/ml], p=0.002) and hs-TnT (0.016 ng/ml [0.010 – 0.022 ng/ml] vs 0.009 ng/ml [0.007– 0.011 ng/ml], p=0.005).
Conclusion: More severe SAS has profound linkage to the severity of coronary atheroscrelotic burden, especially presence of CTO. The prolonged apnea time and elevated cardiac stress/injury biomarkers in CTO patients suggested association of nocturnal periodic silent myocardial ischemia contributed to the pathogenesis of CTO in stable CAD patients.