Arterial hypertension is an established risk factor for acute coronary syndromes, and physical exertion may trigger the onset of such an event. The mechanisms involved include the rupture of a small, inflamed, coronary plaque and the activation of thrombogenic factors. Blood pressure (BP)-lowering treatment has been associated with beneficial effects on subclinical inflammation and thrombosis at rest and during exercise. This prospective study sought to compare the effect of different antihypertensive drugs on the inflammatory and thrombotic response during exercise. A total of 60 never-treated hypertensive patients were randomized to an angiotensin receptor blocker (ARB)-or non-dihydropyridine calcium channel blocker (CCB)-based regimen. Patients with inflammatory or coronary artery disease were excluded. Six months after pharmaceutical BP normalization, the patients underwent a maximal treadmill exercise testing. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cells (WBC), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), total fibrinogen (TF) and von Willebrand factor (vWF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity were measured in blood samples taken while the patients were at rest and during peak exercise. All of these biomarkers increased with exercise, except PAI-1, which decreased (Po0.05 for the difference between resting and peak exercise for all biomarkers). The ARB group had less marked (Po0.05) exercise-induced changes than the CCB group in hsCRP (5.8% vs. 7.7%), SAA (4.2% vs. 7.2%), WBC (46.8% vs. 52.6%), TNF-a (16.3% vs. 24.3%), TF (9.5% vs. 16.9%) and PAI-1 ( À9.5% vs. À12.3%) but a similar (P ¼ NS) change in IL-6 (39.4% vs. 38.6%) and vWF (29.2% vs. 28.6%). In conclusion, ARBs are most likely more effective than CCBs at suppressing the exercise-induced acute phase response. Potential protection against exercise-related coronary events remains to be elucidated.

Exercise had no effect on aortic and radial BP (p=NS for all). Walking for 30 min improved AIx (from 33.79 ± 0.91% to 31.73 ± 0.86%, p<0.001) and PWV (from 9.26 ± 0.95 m/s to 9.06 ± 0.21 m/s, p<0.001), while exercise for 60 min had adverse effects on vascular stiffness (for AIx: from 33.37 ± 0.93% to 33.73 ± 1.05%, p=NS and for PWV: from 9.25 ± 0.19 m/s to 9.37 ± 0.21 m/s, p < 0.05 mainly in older patients). Exercise for 60 min was associated with a significant 20% increase in MDA levels (p<0.05). Exercise had no effects on SOD1 levels, however it significantly increased SOD2 levels after 30 min (from 2.26 ± 0.22 ng/mL to 2.36 ± 0.18 ng/mL, p < 0.05) but not after 60 min (p=NS). Conclusion Shorter exercise duration was associated with favourable antioxidant and vascular effects, while longer exercise blunted these beneficial effects and was accompanied by adverse effects on vascular function, mainly in older coronary patients. Further studies are required to explore the hypothesis that a more individualised approach to the selection of the appropriate exercise programme should be considered for patients with CAD.

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Urine NGAL is potentially superior compared with conventional nephropathy markers in early CIN diagnosis after elective invasive cardiac procedures. Definition of clinically significant uNGAL changes with reference change value is probably a valuable supplement to statistically defined significant variations.

The emerging, from the present study, data raise the hypothesis that lower apelin and higher visfatin plasma levels in high normal BP subjects compared to normal or optimal BP individuals could partially explain the higher CV risk of the high normal BP group.