Obstructive Sleep Apnoea in Acute Coronary Syndrome Patients: Prevalence and Influence on Vascular Function
Authors List
Benjamin K. Tong1, Hasthi Dissanayake1, Sally McClintock1, Kate Sutherland1, Seren Ucak1, Sanjay Patel2, Brendon Yee3, Peter A. Cistulli1,4
1 Sleep Research Group, Charles Perkins Centre, University of Sydney, Camperdown, NSW, Australia
2 Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
3 Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
4 Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, St Leonards, NSW, Australia
Obstructive sleep apnoea (OSA) is known to be associated with a range of cardiovascular diseases, including coronary artery disease, atrial fibrillation, and heart failure. Repetitive intermittent hypoxia, oxidative stress, endothelial dysfunction as a result of OSA has been suggested to contribute to acute coronary syndrome (ACS). Previous studies suggest a prevalence of OSA in patients with ACS of up to 70%, however OSA in this population remains under recognised and under-studied. Accordingly, in this study we aim to estimate the prevalence of OSA in patients with ACS within a hospital setting and compare the differences in arterial stiffness in ACS patients with and without OSA.
70 patients with ACS (age: 58[52,63] years, BMI: 27[24,30]kg/m2) were recruited and studied from the Coronary Care Unit at Royal Prince Alfred Hospital and Royal North Shore Hospital. A level 2 home sleep apnoea test was initially conducted to confirm OSA diagnosis (AHI ≥ 15 events/h) approximately 6 weeks after discharge from hospital. Participants were instrumented with a brachial blood pressure cuff for pulse wave analysis (PWA). Participants were also instrumented with a femoral blood pressure cuff and carotid arterial tonometry (ATCOR SphygmoCor® XCEL PWA/PWV) was performed to measure carotid femoral pulse wave velocity (cfPWV). Triplicate measures of PWA and cfPWV were made while participants were
lying supine at quiet wakefulness.
67% of patients in our study were found to have moderate-severe OSA (AHI ≥ 15 events/h) and 40% of patients have severe OSA (AHI ≥ 30 events/h). Moderate-severe OSA was highly prevalent in males (72% vs. 46%) and obese individuals (79% vs. 64%). cfPWV was higher in patients with OSA (7.3±1.4 vs. 5.9±1.5 m/s, p<0.001). cfPWV remained significantly different between patients with and without OSA after adjusting for age (p=0.03) and BMI (p=0.003). In addition, a weak linear correlation was present between pulse wave velocity and OSA severity (Y = 0.02248*X + 6.227, R2 = 0.08172, p=0.0268). Aortic augmentation index did not differ between patients with and without OSA (23.3[14.8,30.1] vs. 19[10.3,26.8]%).
OSA is highly prevalent in patients with ACS especially in males and obese individuals. Arterial stiffness as measured by cfPWV is elevated in OSA patients with ACS w ith a weak positive relationship with OSA severity. These findings highlight the need for robust screening of sleep disordered breathing in patients with ACS.
Research funding source: ResMed Foundation, Colin Sullivan Research Fellowship (HD)
Benjamin K. Tong1, Hasthi Dissanayake1, Sally McClintock1, Kate Sutherland1, Seren Ucak1, Sanjay Patel2, Brendon Yee3, Peter A. Cistulli1,4
1 Sleep Research Group, Charles Perkins Centre, University of Sydney, Camperdown, NSW, Australia
2 Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
3 Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
4 Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, St Leonards, NSW, Australia
Obstructive sleep apnoea (OSA) is known to be associated with a range of cardiovascular diseases, including coronary artery disease, atrial fibrillation, and heart failure. Repetitive intermittent hypoxia, oxidative stress, endothelial dysfunction as a result of OSA has been suggested to contribute to acute coronary syndrome (ACS). Previous studies suggest a prevalence of OSA in patients with ACS of up to 70%, however OSA in this population remains under recognised and under-studied. Accordingly, in this study we aim to estimate the prevalence of OSA in patients with ACS within a hospital setting and compare the differences in arterial stiffness in ACS patients with and without OSA.
70 patients with ACS (age: 58[52,63] years, BMI: 27[24,30]kg/m2) were recruited and studied from the Coronary Care Unit at Royal Prince Alfred Hospital and Royal North Shore Hospital. A level 2 home sleep apnoea test was initially conducted to confirm OSA diagnosis (AHI ≥ 15 events/h) approximately 6 weeks after discharge from hospital. Participants were instrumented with a brachial blood pressure cuff for pulse wave analysis (PWA). Participants were also instrumented with a femoral blood pressure cuff and carotid arterial tonometry (ATCOR SphygmoCor® XCEL PWA/PWV) was performed to measure carotid femoral pulse wave velocity (cfPWV). Triplicate measures of PWA and cfPWV were made while participants were
lying supine at quiet wakefulness.
67% of patients in our study were found to have moderate-severe OSA (AHI ≥ 15 events/h) and 40% of patients have severe OSA (AHI ≥ 30 events/h). Moderate-severe OSA was highly prevalent in males (72% vs. 46%) and obese individuals (79% vs. 64%). cfPWV was higher in patients with OSA (7.3±1.4 vs. 5.9±1.5 m/s, p<0.001). cfPWV remained significantly different between patients with and without OSA after adjusting for age (p=0.03) and BMI (p=0.003). In addition, a weak linear correlation was present between pulse wave velocity and OSA severity (Y = 0.02248*X + 6.227, R2 = 0.08172, p=0.0268). Aortic augmentation index did not differ between patients with and without OSA (23.3[14.8,30.1] vs. 19[10.3,26.8]%).
OSA is highly prevalent in patients with ACS especially in males and obese individuals. Arterial stiffness as measured by cfPWV is elevated in OSA patients with ACS w ith a weak positive relationship with OSA severity. These findings highlight the need for robust screening of sleep disordered breathing in patients with ACS.
Research funding source: ResMed Foundation, Colin Sullivan Research Fellowship (HD)
