Sleep Apnea, Hypertension Together Significantly Increase Arteriosclerosis Risk

A study by Guangxi Chen and colleagues in Jiangxi, China, which recently appeared in the American Journal of Translational Research, explores the association between obstructive sleep apnea-hypopnea syndrome (OSAHS), hypertension, and arteriosclerosis, emphasizing the value of polysomnography (PSG) parameters and clinical biomarkers in predicting cardiovascular risk. OSAHS is a common sleep disorder marked by repeated episodes of upper airway obstruction during sleep, often resulting in intermittent hypoxia and fragmented sleep. Hypertension is a prevalent comorbidity in patients with OSAHS, with reported incidence rates between 50% and 60%. This relationship is largely due to the physiologic effects of repeated oxygen deprivation and disrupted sleep architecture, which trigger sympathetic nervous system hyperactivation. The resulting vasoconstriction elevates BP and contributes to long-term vascular damage.

Arteriosclerosis is a major consequence of this combined pathology and is known to progress through mechanisms such as endothelial dysfunction, proliferation of vascular smooth muscle cells, and lipid accumulation in arterial walls. The study highlights that both OSAHS and hypertension independently contribute to arteriosclerosis, and their coexistence intensifies the risk. Intermittent hypoxia and reoxygenation cycles in OSAHS increase oxidative stress and inflammatory responses, accelerating endothelial damage. Hypertension further compounds this damage by promoting lipid infiltration and plaque formation in arterial walls.

The primary aim of the study was to examine the predictive relationship between PSG parameters and arteriosclerosis in patients with OSAHS and hypertension. The findings revealed that 27.86% of the study population had arteriosclerosis, indicating a significantly elevated risk. Among the most relevant contributing factors were fasting blood glucose (FBG), triglycerides (TG), low-density lipoprotein cholesterol (LDL), apnea-hypopnea index (AHI), minimum oxygen saturation (minSpO₂), systolic BP, and intima-media thickness (IMT). These indicators reflect both metabolic and cardiovascular stress. For example, elevated FBG, TG, and LDL levels signal metabolic dysfunction, which exacerbates endothelial injury and plaque development. AHI and minSpO₂ are key PSG-derived markers that reflect OSAHS severity. Higher AHI suggests more frequent respiratory disturbances, and lower minSpO₂ indicates greater hypoxemic burden, both of which are associated with increased cardiovascular strain.

Statistical analyses, including logistic regression and Pearson correlation, confirmed that FBG, TG, LDL, AHI, SBP, and IMT are positively correlated with arteriosclerosis risk. In contrast, minSpO₂ was negatively correlated, suggesting that reduced nocturnal oxygen saturation is a significant contributor to vascular deterioration. Receiver operator characteristic curve analysis further assessed the predictive utility of these factors. Intima-media thickness and the total composite risk score had the highest predictive accuracy (area under the curve [AUC] of 0.805 and 0.922, respectively), whereas AHI and minSpO₂ showed moderate but still meaningful predictive value (AUC of 0.690 and 0.636, respectively).

The study authors conclude that PSG indicators, particularly when combined with clinical biomarkers, can be valuable in assessing arteriosclerosis risk in patients with OSAHS  and hypertension. However, the research is limited by its single-center design and relatively small sample size. Future studies should involve larger populations and more diverse cohorts to validate and refine the prediction model. Long-term follow-up and the inclusion of additional biomarkers are also recommended to enhance prediction accuracy and clinical applicability. Overall, early identification and comprehensive intervention strategies are essential to prevent arteriosclerosis progression and improve cardiovascular outcomes in this high-risk patient group.