Whether left ventricular mass (LVM) should be normalized to different indexes in relation to body size is still debated. We sought to evaluate the prevalence of left ventricular hypertrophy (LVH) defined by different indexation criteria in a cohort of hypertensive subjects categorized according to body mass index (BMI). A total of 2213 essential hypertensive subjects included in the Evaluation of Target Organ Damage in Hypertension (ETODH) were divided in three groups according to BMI thresholds (o25, 25-29.9 and X30 kg m À2 ). All patients underwent extensive investigations including quantitative echocardiography. LVH was defined as an LVM index equal to or higher than (1) 125 g m À2 in men and 110 g m À2 in women, (2) 51 g m À2.7 in men and 47 g m À2.7 in women. Overall, 687 out of 2213 patients (31.0%) were found to have LVH when LVM was indexed to body surface area (BSA) and 1030 (46.5%) when indexed to height 2.7 . A total of 845 patients (38.2%) had normal BMI, 954 patients (43.1%) were overweight and 414 (18.7%) were obese. Prevalence rates of LVH in the three groups were 25.1, 31.6, 41.2% by indexation to BSA and 29.9, 50.5, 71.8% by indexation to height 2.7 , respectively. LVM indexed to BSA markedly underestimates LVH prevalence in obese as well as overweight hypertensive patients. To avoid a systematic misclassification of cardiovascular risk, LVM should be routinely indexed to height 2.7 in overweight and obese patients representing a large percentage of the hypertensive population.

The classification of hypertensive subjects according to circadian blood pressure (BP) variations (i.e., dipping vs nondipping) is a useful means for reliable individual risk stratification and effective therapeutic decision-making. Increasing evidence, although not univocal, suggests that a reduced nocturnal BP fall relates to an excess of cardiovascular complications. The association between nondipping status with left ventricular hypertrophy (LVH) and its therapeutic implications are still debated; in this article we examined the studies published in the last decade on this controversial issue. The studies identified by a PubMed search were eligible for the analysis if they fulfilled the following criteria: full articles in English, published from 1 January 2000 to 31 December 2009, and inclusion of adult or elderly subjects. According to these criteria, 26 studies encompassing 3877 participants have been selected. A total of 17 studies for a total of 2497 subjects were positive for a link between nondipping and LVH, whereas the remaining nine studies were negative. Notably, three studies that accurately defined the nondipping status on the basis of two consistent ambulatory blood pressure monitoring sessions over a short time interval showed a significant association of this pattern with LVH; this suggests that a persisting nondipping pattern is associated with a more pronounced cardiac involvement. Preliminary data support the view that nondipping may be reverted to dipping by chronotherapy and by diuretics in salt-sensitive patients. Whether restoring the normal nocturnal BP dip in hypertensives with LVH regresses cardiac damage at present remains an untested hypothesis.

CUS is a highly specific and sensitive imaging technique. In referral centers, expert hands can use it as a reliable first-step screening for infants younger than 1 year, suspected to have a craniosynostosis, thus avoiding unnecessary exposure to ionizing radiation. The "golden age" to obtain the best CUS results is under 6 months of life. Because the method is operator-dependent and there is a learning curve, a case centralization is advisable.

RVH is commonly found in systemic hypertension and is associated with LVH (i.e., biventricular hypertrophy) in approximately one-fifth of the patients seen in a specialist setting. The clinical correlates of biventricular hypertrophy suggest that this phenotype is associated with a profile of very high cardiovascular risk.

The metabolic syndrome (MS) is associated with structural and functional alterations of the left ventricle (LV); no evidence is available on the impact of the MS on the right ventricle (RV). To assess whether MS, as defined by the ATP III report, is associated with biventricular hypertrophy, a total of 286 hypertensive subjects (mean age 58.7±12.2 years) attending our outpatient clinic underwent the following procedures: (1) physical examination and standard clinic blood pressure (BP) measurement; (2) routine laboratory investigations; (3) M-mode, two-dimensional and Doppler echocardiography. LV hypertrophy (LVH) was defined by LM mass index X51/47 g m À2.7 in men and women, respectively. Right-sided chambers were measured in parasternal long axis at the outflow tract and subcostal view; RV hypertrophy (RVH) was defined by anterior RV wall thickness X6.0/5.5 mm in men and women, respectively. Filling velocities of both ventricles were assessed by pulsed Doppler echocardiography. Structural cardiac alterations were more pronounced in hypertensive men and women with MS than in their non-MS counterparts and involved both ventricles as shown by the differences in continuous variables as well as in prevalence rates of LVH (58 and 48% vs 28 and 30%, respectively, Po0.01) and RVH (48 and 54% vs 25 and 35%, respectively, Po0.01). Both LV and RV filling in MS hypertensives were more dependent on the atrial systole. Our study shows that in human hypertension, structural and functional cardiac changes induced by MS are not limited to the LV but also involve the right one.