The Importance of Apneic Events in Obstructive Sleep Apnea Associated with Acute Coronary Syndrome

Abstract

Background Obstructive sleep apnea (OSA) is a potential cardiovascular risk factor. However, there is currently no prominent screening strategy for its diagnosis in patients with acute coronary syndrome (ACS). The aim of this study was to establish the impact of apneic events in case of OSA associated with ACS. Methods Between January 1st and June 30th, fifty-three subjects with ACS (first acute myocardial infarction) were prospectively evaluated for OSA. Each patient was evaluated by polysomnography (PSG) two months after the ACS. Results Mean age of 59±9,6 years, 81,1% males, BMI at 28,5±4,2 kg/m2, neck circumference of 42,5±12,6 cm, and waist circumference os 102,5±16,5 cm. The majority of patients (73,6%) had moderate to severe OSA (apnea-hypopnea index (AHI) ≥ 15/h and arousal index ≥ 10/h). We defined the apneic coefficient (AC) as the ratio between apnea index (AI) and AHI. We chose as cut-off the median value of apnea coefficient in our population which was at 37%. The patients with a higher AC (AC ≥ 37% versus AC < 37%) had higher levels of Troponin-I (63,4±63,2 versus 29,7±36,1 ng/mL, p=0,016), higher levels of NT-proBNP (1879,8±2141,8 versus 480±621,3 pg/mL, p=0,001), higher SYNTAX score (15,8±11,5 versus 10,2±5,9, p=0,049), and lower left ventricle ejection fraction (LVEF 53,3±11,4 versus 59,4±6,4%, p=0,023) and were more likely to have a STEMI (21 patients (77,7%) vesus 14 patients (53,8%), p=0,031). Conclusion An apneic coefficient (AI/AHI) ≥ 37% is correlated with more severe cardiac impairment, as well as higher hypoxemia and arousal index.

Baseline coronary artery stenosis severity is an independent predictor of subsequent poor sleep quality in patients with acute coronary syndrome

“…The pathophysiologic mechanism blamed for this relationship is based on endothelial dysfunction, coronary plaque burden, chronic inflammation and sympathetic activation secondary to intermittent hypoxemia [28].…”

“…Calcaianu et al . [28] performed polysomnography on patients with ACS 2 months after AMI and used the apneic coefficient (AC), defined as the ratio between apnea index and apnea-hypopnea index (AHI), as the main outcome. The results showed that the patients with a higher AC (≥37% vs. <37%) had higher baseline levels of troponin-I, N-terminal prohormone brain natriuretic peptide and higher SYNTAX scores, lower LVEF, and were more likely to have a STEMI.…”

“…OSA has significant effects on the cardiovascular system; it affects many systems. The pathophysiologic mechanism blamed for this relationship is based on endothelial dysfunction, coronary plaque burden, chronic inflammation and sympathetic activation secondary to intermittent hypoxemia [28]. Although several potential mechanisms have been proposed, the pathophysiology of the relationship between apnea-free sleep disorders and ACS remains unclear [5,38].…”

Adipokines and Inflammatory Markers in Acute Myocardial Infarction Patients with and without Obstructive Sleep Apnea: A Comparative Analysis

“…Nevertheless, it is worth noting that the relationship between OSA and myocardial markers is complex, with contradictory findings in the literature. Some studies have reported lower troponin levels in OSA patients presenting with AMI, suggesting a cardioprotective effect [31]. Additionally, meta-analyses have failed to identify significant differences in troponin, CK, and CK-MB levels between cardiovascular disease patients with and without OSA [32].…”

Association of Craniofacial and Upper Airway Morphology with Cardiovascular Risk in Adults with OSA

“…Calcaianu et al found that a higher frequency of apneic events (AI/AHI) is associated with increased levels of troponin-I and NT-proBNP in patients with acute coronary syndrome (ACS). 34 The association between apneic events and future CVD risk may be due to apnea leading to more severe SpO 2 desaturation than hypopnea. Additionally, compared with hypopnea, increased inspiratory efforts against a completely closed airway during apnea create greater negative intrathoracic pressures and elevated venous return, which in turn overloads the right ventricle and increases the afterload on the left ventricle.…”