Endothelial dysfunction plays an important role in all stages of atherosclerosis, and is characterized by an increased activity of vasoconstricting factors, proinflammatory and prothrombotic mediators. The aim of the review is to evaluate the role of angiotensin II (Ang II) and especially of angiotensin type 1 (AT1) receptor in inflammation and endothelial dysfunction. Ang II with AT(1) receptor are through several mechanisms implicated in the progression of atherosclerosis. Stimulation of AT(1) receptor increases oxidative stress especially through activation of NADH/NADPH oxidase in the vascular cells. Oxidative stress is associated with activation of the inflammatory processes. Ang II via AT(1) receptor increases expression of adhesion molecules and stimulates the induction of monocyte chemoattractant protein-1 (MCP-1). AT(1) receptor enhances the activation of nuclear factor NF-kappaB, which stimulates the production of proinflammatory cytokines. Proinflammatory cytokines on the other side may induce acute-phase response in the liver. Activation of AT(1) receptor via inducible cyclooxygenase (COX)-2 promotes biosynthesis of matrix metalloproteinases (MMPs). Ang II is implicated in the process of angiogenesis. Via AT(1) receptor takes part in the regulation of vascular endothelial growth factor (VEGF), which is one of the most angiogenic factors and stimulates the activity of endothelial progenitor cells (EPC). Recently some patents were reported discussing role of different compounds for the treatment of cardiovascular disease, renovascular disease nephropathy, peripheral vascular disease, portal hypertension and ophthalmic disorders, are cyclooxygenase-2 inhibitors.

AIM Today we have not the established and single clinical mode to identifying hypertensive (HT) patients in risk for paroxysmal atrial fibrillation (pAF). Some non-invasive VCG and high-resolution VCG (Hi-Res) for P and QRS loops are available for ECG/VCG measurements in clinical practice via routinely used ECG/VCG equipment (General Electric). It is possible, that especially P wave and P loop values can reflect the abnormal status in atrial myocardium prior the pAF onset. MATERIAL AND METHOD We studied 276 HT patients in sinus rhythm: group I (n=133, without documented pAF), group II (n=129, with well-documented pAF) and group III (n=14, patients after successful radiofrequency ablation for AF or atrial flutter). ECG parameters were evaluated: (1) heart rate in SR; (2) VCG P loop and QRS loop non-filtered/filtered duration: nPd, fPd, nQRSd, fQRSd; (3) other Hi-Res P and QRS parameters: HFLAd, RMS(40)v; (4) angle between axes P-QRS and QRS-T loops; (5) echoCG parameters: LA dimension, LV ejection fraction, width of IVS ad posterior wall. RESULTS In group II a III the non-filtered parameters (nPd, nQRSd) and filtered parameters (fPd, fQRSd) were significantly longer than in group I (for nPd : 135.9 ms, 145.1 ms vs. 129.0 ms, p<0.05; for nQRsd : 104.2 ms, 110.0 ms vs. 99.0 ms, p<0.01; for fPd: 143.0 ms, 154.9 ms vs. 133.0 ms, p<0.005; for fQRSd 119.7 ms, 125.9 ms vs. 113.0 ms, p<0.005). P loop axis analysis is significantly higher in loop II and III vs. group I (+48.2 gr., +53.4 gr. Vs. 48 gr., p<0.01). Angle P-QRS is significantly wider in group II and III vs. group I (38.7 gr., 42.1 gr. Vs. 25.0 gr, p= 0.005. EchoCG parameters were not significantly different (LA dimensions for groups I,II,III: 39.8, 42.7 and 42.0 mm, n.s.; LVEF for groups I,II,III> 59.7, 57.8 and 58.1, ns.). CONCLUSIONS HT patients with verified pAF in documentation have more abnormal P and QRS wave/loop parameters than HT patients without history of pAF. According to our results, the most informative ECG and VCG factors for possible future pAF are: fPd, fQRSd, angle between loop axes P-QRS. ECG/VCG parameters (non-filtered and especially after filtration via to Hi-Res analysis) have potential to improve the risk stratification for possible future pAF.

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Objective: The study investigated the impact of renal sympathetic denervation on office blood pressure and ambulatory blood pressure monitoring in patients with resistant hypertension. We evaluated whether a decrease in blood pressure may improve local carotid stiffness and parameters of wave intensity. Methods: Renal sympathetic denervation was performed in 17 patients (age 55 ± 9 years) with true resistant hypertension. Measurements of carotid stiffness and wave intensity were performed using ultrasound combined with echo-tracking. Results: We found significantly improved office systolic blood pressure changes 1 month (p=0.023) and together with pulse pressure changes at the 6 month follow up (p=0.041; p=0.016). Changes in systolic blood pressure during the daytime were significantly decreased at 1 month and diastolic blood pressure changes during the daytime were significantly reduced at 1 and 3 months. Stiffness parameters beta stiffness and pressure-strain elastic modulus were significantly reduced (p=0.04; p=0.03) and arterial compliance was increased (p=0.03), especially 1 and 3 months. The changes in negative area were significantly reduced after 1 month (p=0.041) and the ejection period was significantly increased at the 6 month follow-up (p=0.011). According to linear regression analysis systolic blood pressure correlated positively with the beta stiffness, pressure-strain elastic modulus, pulse wave velocity, and negatively with arterial compliance. Conclusions: We found significantly lower office blood pressure as well as blood pressure from ambulatory blood pressure monitoring in patients with resistant hypertension 6 months after renal sympathetic denervation. The decrease in blood pressure was followed by improvement of carotid stiffness and wave intensity. That may be reflected in enhancement of ventricular-arterial coupling.

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