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IntroductionTo investigate the hypothesis that atorvastatin decreases blood pressure (BP) values and improves endothelial function assessed by flow-mediated dilation (FMD) in normolipidaemic hypertensive patients.Material and methodsFifty-six hypertensive patients were randomized in a 2 : 1 proportion to atorvastatin (80 mg/day/3 months; group A; n = 39) or previous standard anti-hypertensive therapy (group B), which means the patients were treated with angiotensin-converting enzyme inhibitors, diuretics, β-blockers, calcium antagonists and angiotensin receptor blockers. The study had a crossover design: after 3 months, both groups were changed (group A* stopped and group B* started atorvastatin treatment). Nitric oxide (NO), total antioxidant status (TAS), endothelin-1 (ET-1), and peroxide concentrations as well as FMD were measured before, after 3 and after 6 months of treatment. Atorvastatin added to existing treatment decreased BP in both groups.ResultsFlow-mediated dilation improved in both statin-treated groups, but only significantly in group B* (from 11.9 ±8.3% to 22.1 ±9.0%; p < 0.05). In patients with FMD improvement, there was a greater BP reduction. After treatment discontinuation, FMD significantly decreased (from 19.6 ±12.6% to 13.0 ±10.5%; p < 0.05), which was consistent with BP increase. Changes in FMD were not significantly related to the increase in NO and TAS concentrations and decrease in ET-1 and peroxides measurements.ConclusionsThe hypotensive effect of atorvastatin is associated with FMD improvement in normolipidaemic, hypertensive patients. Although this could be related to changes in oxidative stress and endothelial function, this was not demonstrated in this study and warrants further investigation.

Several minimally invasive modifications of endoscopic medial maxillectomy have been proposed recently, with the least traumatic techniques utilizing the lacrimal recess as a route to enter the sinus. The aim of the study was to analyze the anatomy of medial maxillary wall in the region of nasolacrimal canal and, thus, to determine the capability of performing minimally invasive approach to the maxillary sinus leading through the lacrimal recess. The course of nasolacrimal canal and the distance between the anterior maxillary wall and the nasolacrimal canal (the width of lacrimal recess) were evaluated in 125 randomly selected computed tomography (CT) head examinations. The proportion of cases with unfavorable anatomical conditions (lacrimal recess too narrow to accept a 4 mm optic) to perform minimally invasive middle maxillectomy was assessed. The width of lacrimal recess, measured at the level of the inferior turbinate attachment, varied between 0 and 15.2 mm and was related to slanted course of nasolacrimal canal. The more perpendicular the axis of the canal to the nasal flor, the narrower the lacrimal recess. In about 16% of cases, lacrimal recess width was less than 4 mm and in 14.4% it was missing. The endoscopic approach to maxillary sinus leading through lacrimal recess is possible in about 70% of patients. In the remaining group of patients when the lacrimal recess is too narrow, this type of approach may be difficult to perform without damaging the piriform aperture rim or bony framework of nasolacrimal duct, or it may be impracticable when lacrimal recess is missing.

Glycoprotein IIIa (GpIIIa) is a membrane receptor, found in various tissues, that has two alleles: A1 and A2. Signalling cascade of GpIIIa is modulated by enzymes called calpains, proteases that may also influence glucose metabolism. There is one small study that shows a high association of A1/A2 polymorphism with type 2 diabetes mellitus. In our research we planned to evaluate the association of A1/A2 polymorphism with type 2 diabetes in a population of patients with ST elevation acute myocardial infarction (STEMI). The study comprised 352 individuals. From the cohort of patients hospitalised for STEMI we chose 113 patients with diagnosed diabetes (diabetic group) and 118 patients with STEMI and normal glucose metabolism (non-diabetic group). The population group consisted of 121 persons. Genotyping was performed by the restriction fragments length polymorphism (RFLP) method. The frequency of alleles in all groups was in Hardy-Weinberg equilibrium. The percentage of A2 allele carriers was comparable among all groups : 20.4% (diabetic patients), 23.7% (nondiabetic) and 21.5% (control group) (p>0.05). There was no significant difference in frequency of A2 allele among the groups. We have not observed any association between GpIIIa polymorphism with either type 2 diabetes or STEMI.

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