"The 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 has been 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 demonstrated for the first time, 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."Read More
Obstructive Sleep Apnea
"Patients with obstructive sleep apnea syndrome (OSA) exhibit an early vascular remodelling and alterations of acid arachidonic pathway 2. Thromboxane A2 (TXA2) is a cycloxygenase (COX)-derived metabolite of AA involved in vascular remodelling."
"Atherosclerosis is a chronic inflammatory disease characterized by the activation of some components of the cyclooxygenase pathway. OSA is associated with activation of the thromboxane A2 (TXA2)-pathway, in which obesity seems to be a major confounding factor."
"Urinary excretion of 11-dTXB2 did not differ between OSA patients free of cardiovascular complications and healthy volunteers but increased in OSA patients with cormobidities compared to OSA patients without 694.0 (425.9-1235.6) versus 616.0 (354.3-838.2) pg/mg creatinine respectively; p=0.007). Finally, urinary 11-dTXB2 was increased by 30% in OSA Patients with cartoid hypertrophy (IMT>compared to OSA patients without carotid hypertrophy (783.0 (582.8-938.0) versus 592.9 (278.9-782.5) pg/mg creatinine, respect p=0.02)."Read More