Obstructive sleep apnea syndrome (OSA) is an independent risk factor for atherosclerosis. Chronic intermittent hypoxia (CHI) causes atherosclerosis in the occurrence of a pre-existing hyperlipidemia. A new pathway, in animal models, is demonstrated that CIH significantly increased atherosclerotic lesion sizes, mRNA levels of COX-1 and thromboxane synthase (TXBS). Lesion size is correlated to COX-1 and TXBS mRNA levels. COX-1 inhibition reduced lesion progression in intermittent hypoxia mice. This study has demonstrated, that the activation of the COX pathway exposed to CIH is associated with increased atherosclerotic lesions in mice, highlighting early atherosclerosis markers in OSA patients.