The relationship between plasma viscosity and endotel markers in patients with ascending aortic aneurysms: A pilot study A ortic aneurysms represent a leading cause of cardiovascular mortality and morbidity worldwide [1]. An aneurysm is defined as an irreversible dilation of a blood vessel accompanied by weakening of the vessel wall [2]. Ascending aortic aneurysms (AsAAs) are a well-known surgical entity, most commonly involving the ascending part of the aorta, and are morphologically defined as progressive dilatation of an aortic segment by more than 50% of its normal diameter [3]. Dilatation is associated with a propensity for dissection, rupture, and aortic valve insufficiency. Although most AsAAs are of unknown etiology, underlying physiological circumstances, such as the individual's age and body surface area are among the main determinants of the size of the ascending aorta [4, 5]. Aortic aneurysms are also associated with vascular remodeling, decreased capillary density, and increased left ventricular end-diastolic pressure, which may cause perfusion abnormalities and may result in an impairment of coronary flow hemodynamics [6]. Hemorheological parameters, such as blood and plasma viscosity (PV), and hematocrit (Hct) and fibrinogen values, which are in a continuous interplay with each other, have critical effects in Objectives: An ascending aortic aneurysm (AsAA) is fundamentally defined as the "ballooning" of the aorta at its exit site from the heart. The role of plasma viscosity (PV) and endothelial markers in AsAA is unknown. This study was designed to investigate AsAA in association with PV and the endothelial markers of fibrinogen, nitric oxide (NOx), and asymmetric dimethylarginine (ADMA). Methods: This study group consisted of 23 patients who underwent surgical repair for AsAA and 30 controls without diabetes, hypo-or hyperlipidemia, or heart disease. Several parameters, including plasma viscosity (PV), fibrinogen, NOx, and ADMA were assayed in both groups. Results: The preoperative PV in the patient group was significantly higher than that measured on postoperative day 7 and that of the control group (p<0.05). Fibrinogen and ADMA values were significantly higher in the control group than the preoperative values (p<0.001). Postoperative NOx results were lower than preoperative NOx (p<0.05). Conclusion: An increase in PV may cause an increase in permeability and glomerular capillary pressure. The fibrinogen level may have been lower in the preoperative AsAA group as a result of impaired production or increased consumption due to intravascular coagulation. The decrease in ADMA is associated with increased NOx, which is a potent inhibitor of platelet aggregation and adhesion to the vessel wall. A high preoperative level of NOx can be accounted for by impaired blood flow. Our results suggest that PV and oxidative stress parameters may play a crucial role in the diagnosis, treatment, and follow-up of patients with AsAA.