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Endothelial Functionality and Echocardiographic Parameters in Patients with Rhinitis and Nasal Polyps

Bulzis G, Carbonara R, Dentamaro I, Sasso N, Ricci G, Gelardi M, Iannuzzi A, Taliente S, Ciccone MM

Background: Chronic inflammation is associated with accelerated atherosclerosis, endothelial dysfunction and with early cardiovascular disease. Rhinitis and nasal polyps are inflammatory diseases and the local inflammation is often associated with systemic events that they see as a primary cause the endothelial dysfunction. Studies have shown a higher incidence of cardiovascular events such as stroke, intermittent claudication and myocardial infarction in patients with polyposis and/or rhinitis, but studies that have focused on myocardial injury are few and showed echocardiography as a subclinical deficiency of the right longitudinal functions in patients with nasal polyposis.

Methods and Results: Flow-mediated vasodilation (FMD), common carotid intima-media thickness (cIMT), echocardiographic parameters of left and right ventricular (LV and RV) function were studied in 44 subjects and compared with 42 subjects in the control group. Out of 44 patients, 35 had an allergic component and had mean values of FMD significantly lower (6.62 vs. 17.7, p=0.00), higher IMT even if they were normal values (0.68 mm vs. 0.61 mm, p=0.0429), a tricuspid Tei Index higher than the control group (1.28 vs. 0.44, p=0.0002).
Comparing patients suffering from polyposis with the control group, lower FMD values appeared (6.98 vs. 19.41, p=0.0017). The cIMT and Tei index were higher in patients with polyposis compared to patients with rhinitis but without polyposis (0.62 mm vs. 0.73 mm, p=0.0224; 0.74 vs. 1.68, p=0.0015).

Conclusions: The mechanisms responsible for accelerated atherosclerosis in patients with inflammatory diseases of the nasal cavity are related to the high degree of local inflammation which then becomes systemic inflammation. This leads to endothelial dysfunction through multiple mechanisms and still under study and it leads to a subclinical damage to the endothelium.