We investigated whether the type of left ventricular (LV) geometry is associated with left atrial (LA) size as determined either by LA diameter or by volume, indexed for body surface area, in essential hypertensives. A total of 339 consecutive, untreated, hypertensives (aged 51.8 years, 234 males) underwent 24-h ambulatory blood pressure (BP) monitoring and estimation of LA diameter and volume, as well as LV structure and function by echocardiography. LV hypertrophy was present in 130 (38.3%) patients whereas normal geometry (LV-NG), concentric remodeling (LV-CR), concentric hypertrophy (LV-CH) and eccentric hypertrophy (LV-EH) represented 34.5, 27.1, 25.7 and 12.7%, respectively. Patients with either LV-CH or LV-EH had increased LA diameter index compared with those with either LV-NG (by 1.1 mm m -2 , Po0.01 and 1.4 mm m -2 , P ¼ 0.003, respectively) or LV-CR (by 1.3 mm m -2 , P ¼ 0.003 and 1.6 mm m -2 , P ¼ 0.001, respectively). Similarly, patients with either LV-CH or LV-EH had significantly increased LA volume index compared with those with either LV-NG (by 3.2 ml m -2 , Po0.001 and 3.4 ml m -2 , Po0.005, respectively) or LV-CR (by 4.5 and 4.7 ml m -2 , respectively, Po0.001 for both). Multiple linear regression analysis showed that the independent predictors of both LA volume and diameter index were LV mass index, 24-h pulse pressure and E/Em.LA size assessed either by its diameter or by volume is closely related only to LV mass index and not to any specific LV geometric pattern in the early stages of essential hypertension.

The clinical relevance of nocturnal hypertension (NH) in comparison with non-dipping status has not been clarified yet, as regards subclinical target organ damage. We aimed to elucidate whether NH or dipping status reflects better organ damage. The study population included 319 newly diagnosed hypertensive patients. Subclinical organ damage was evaluated to all participants. On the basis of nocturnal blood pressure (BP) levels the population was divided into two groups: NH and nocturnal normotension. Also, individuals were defined as dippers and non-dippers according to systolic BP fall. Patients with NH were characterized by increased arterial pulse wave velocity (PWV; 9.1±1.7 vs 8.4±1.5 m s(-1), P=0.0001) and carotid intima-media thickness (0.77±0.18 vs 0.69±0.15 mm, P=0.016) compared with normotensive subjects. Notably, they also exhibited higher values of left ventricular mass index (88.1±22.9 vs 82.8±16.6 g m(-)(2) P=0.043). On the contrary, non-dipping status was associated only with differences in PWV (9.26±0.2 vs 8.64±0.2 m s(-1), P=0.031, 8) and in creatinine clearance (95±3 vs 106±4, P=0.025) in the group of NH. The presence of NH is accompanied by subclinical atherosclerosis, as well as structural abnormalities of the left ventricle. Therefore, NH rather than non-dipping status could be preferably integrated with the risk of organ damage.

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.