Obstructive sleep apnea (OSA) is a condition characterized by cessation of respiration due to obstruction of the upper airway during sleep. Its prevalence is approximately 4% in males and 2% in females in the adult population. It is seen frequently in patients with morbid obesity, cardiac, neurological, renal, and respiratory diseases. Although it is known for a long time that incidence of cardiovascular diseases (CVDs) is high in OSA patients, the underlying mechanisms of high incidence of CVDs in OSA have not been elucidated yet. When we searched the literature to find the reasons leading to higher incidence of CVDs in OSA, we found limited and conflicting information regarding risk predictors for CVDs in OSA patients. Therefore, we performed a study to investigate and identify potential risk predictors for CVDs in newly diagnosed OSA patients without manifest CVDs.  

We enrolled 60 OSA patients (13 moderate and 47 severe) diagnosed with polysomnography and 26 healthy volunteers into our study after receiving their written informed consent and local ethical approval. We selected seven parameters and measured them as potential biomarkers for CVDs in OSA patients such a plasma ischaemia-modified albumin (IMA), copeptin level, myeloperoxidase (MPO) activity, soluble tumor necrosis factor receptor-1 (sTNF-R1), advanced oxidation protein products (AOPP), total oxidative status (TOS),  total antioxidative capacity (TAC). 

To our surprise, we found significantly lower copeptin levels in the OSA patients compared to the controls. We tried to find out the underlying mechanism leading to unexpected low copeptin levels in the OSA patients. This might be due to the repetitive episodes of complete or partial upper airway obstruction in OSA causing increased negative intrathoracic pressure and venous blood flow to the heart and resulting with distention of right atrium and ventricle. From the cardiac atrium and ventricle, brain-type atrial natriuretic peptide (ANP) is released for compensation. It is known that ANP inhibits the secretion of ADH. As copeptin is a portion of ADH and related to ADH level, this might be the main reason of low copeptin levels in the OSA patients. Thus, we consider that reduced copeptin level is related with disturbed ADH secretion in OSA patients rather than reflecting a reduced risk for CVDs. In contrast to copeptin, we found a high oxidative stress in OSA as indicated by increased TOS and decreased TAC levels causing increased AOPP levels without causing an increase in IMA. Our findings of elevated plasma MPO activity and sTNF-R1 levels in the OSA patients indicate increased systemic inflammation which might contribute to the higher incidence of CVDs. According to the results of our study, we recommend measurement of plasma MPO activity, sTNF-R1, TOS, TAC and AOPP levels in the OSA patients as potential risk predictors for CVDs.