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TDI-detected LV diastolic dysfunction is accompanied by increased aortic stiffness in newly diagnosed essential hypertension, suggesting that there may be a common pathophysiological pathway linking these two entities.

In hypertensive patients free of cardiovascular disease, CKD and LVH are both independent prognosticators of the composite end point of all-cause death and cardiovascular morbidity, whereas LVH but not CKD is a major predictor for stroke.

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.

Increased LAVI, closely associated with LV mass index and BNP, was still found in the early stages of essential hypertension. However, the clinical significance of these findings remains to be elucidated in future studies.

The role of serum uric acid (SUA) in the context of adverse cardiovascular events in hypertensive subjects is controversial. Additionally, the relationship between SUA and indices of target organ damage is not well defined in this setting. Towards this end, we studied 842 consecutive nondiabetic patients with stage I-II essential hypertension (office blood pressure ¼ 148/95 mmHg, aged 53.4 years), referred to our outpatient hypertensive unit within a period of 4 years. According to the urinary albumin excretion (UAE), the study population was classified into those with microalbuminuria [MA( þ ), UAE ¼ 20-200 mg/24 h, n ¼ 222] and those without MA [MA (À), UAEo 20 mg/24 h, n ¼ 620]. Moreover, according to the presence of left ventricular hypertrophy (LVH) the participants were subdivided into two additional groups: [LVH ( þ ), n ¼ 305 and LVH (À), n ¼ 537]. SUA levels were higher by 0.4 mg/dl, (P ¼ 0.04) in group MA ( þ ) compared with the group MA (À), while no difference was observed between groups LVH ( þ ) and LVH (À) (P ¼ NS). In the entire population, SUA was correlated with body mass index (BMI) (r ¼ 0.17, Po0.001), waist/hip ratio (r ¼ 0.3, Po0.001), office systolic blood pressure (SBP) (r ¼ 0.14, Po0.05), triglycerides levels (r ¼ 0.25, Po0.001), UAE (r ¼ 0.35, Po0.001) and HDL (r ¼ À0.26, Po0.001). Multiple regression analysis demonstrated that SUA was significantly related with BMI, office SBP and UAE (Po0.05). In conclusion, increased SUA levels are associated with MA but not with LVH in essential hypertensive subjects. Whether these inter-relationships may elucidate the clinical positioning of augmented SUA in this setting remains to be clarified in future studies.

Radial artery (RA) occlusion (RAO) remains the Achilles heel of transradial coronary procedures. Although of silent nature, RAO is relatively frequent, results in graft shortage for future coronary artery bypass surgery, and may occur even after short-lasting, 5F coronary angiography (CAG). The most frequent predictors of RAO are RA size, body size, female gender, and periprocedural anticoagulation intensity. Methods to detect RAO are variable, of which the Barbeau test and ultrasonography have similar diagnostic accuracy. Data indicate that late RAO recanalization may occur. Meticulous handling of RA and the use of appropriate hemostatic devices and techniques along with sufficient heparin dose appear important measures to reduce RAO rates. Recent contradictory studies indicate that the decreasing incidence of RAO overtime is not as uniform as previously thought. In 2 meta-analyses, the benefit of higher over lower anticoagulation intensity became evident. As "it may all be appropriate anticoagulation" for a simplified approach against RAO, the results of an ongoing trial comparing 100 with 50 IU/kg body weight in transradial CAG are eagerly awaited.

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