The Association of Remnant Cholesterol with Obstructive Sleep Apnea and Coronary Heart Disease: A Cross-Sectional Study.
Obstructive sleep apnea (OSA) is a significant risk factor for coronary heart disease (CHD), yet the precise pathophysiological mechanisms linking them remain incompletely understood. Remnant cholesterol (RC), as an atherogenic lipoprotein, is considered a key driver of residual cardiovascular risk. However, evidence regarding the role of RC in the association between OSA and CHD is still lacking.
In this single-center, cross-sectional study, we enrolled 368 consecutive patients with suspected coronary heart disease (CHD). All participants underwent overnight polysomnography (PSG) and were categorized into none/mild or moderate/severe obstructive sleep apnea (OSA) groups based on the apnea-hypopnea index (AHI). Coronary artery disease was assessed via angiography or computed tomography angiography (CTA), and its severity was quantified by the number of diseased vessels.
Compared to the none/mild OSA group, patients with moderate/severe OSA had a significantly higher prevalence of CHD (73.0% vs. 15.2%, p<0.001) and a greater proportion of multi-vessel disease (p<0.001). AHI was strongly positively correlated with the number of diseased vessels (overall population r=0.612, p<0.001). Multiple Linear Regression identified AHI as an independent determinant of the number of diseased vessels (β=0.804, p<0.001). Logistic regression confirmed that the number of diseased vessels was an independent risk factor for moderate/severe OSA (OR=3.575, p<0.001). While remnant cholesterol was not significantly correlated with AHI in the overall population (r=-0.051, p=0.327), it showed weak negative correlations with the number of diseased vessels in males (r=-0.120, p=0.036) and in the moderate/severe OSA subgroup (r=-0.130, p=0.035), which may be influenced by residual confounding factors.
This study demonstrates a strong and significant independent association between OSA severity and the presence and severity of CHD. Although remnant cholesterol showed no global association with OSA severity, its weak inverse correlation with coronary disease in males and severe OSA patients suggests a potential complex role, warranting further investigation into its mechanisms within specific populations.
In this single-center, cross-sectional study, we enrolled 368 consecutive patients with suspected coronary heart disease (CHD). All participants underwent overnight polysomnography (PSG) and were categorized into none/mild or moderate/severe obstructive sleep apnea (OSA) groups based on the apnea-hypopnea index (AHI). Coronary artery disease was assessed via angiography or computed tomography angiography (CTA), and its severity was quantified by the number of diseased vessels.
Compared to the none/mild OSA group, patients with moderate/severe OSA had a significantly higher prevalence of CHD (73.0% vs. 15.2%, p<0.001) and a greater proportion of multi-vessel disease (p<0.001). AHI was strongly positively correlated with the number of diseased vessels (overall population r=0.612, p<0.001). Multiple Linear Regression identified AHI as an independent determinant of the number of diseased vessels (β=0.804, p<0.001). Logistic regression confirmed that the number of diseased vessels was an independent risk factor for moderate/severe OSA (OR=3.575, p<0.001). While remnant cholesterol was not significantly correlated with AHI in the overall population (r=-0.051, p=0.327), it showed weak negative correlations with the number of diseased vessels in males (r=-0.120, p=0.036) and in the moderate/severe OSA subgroup (r=-0.130, p=0.035), which may be influenced by residual confounding factors.
This study demonstrates a strong and significant independent association between OSA severity and the presence and severity of CHD. Although remnant cholesterol showed no global association with OSA severity, its weak inverse correlation with coronary disease in males and severe OSA patients suggests a potential complex role, warranting further investigation into its mechanisms within specific populations.