on behalf of the Italian Society of Hypertension Left-ventricular hypertrophy (LVH) is a cardinal manifestation of hypertensive organ damage associated with an increased cardiovascular (CV) risk. We reviewed recent literature on the prevalence of LVH, as assessed by echocardiography, in order to offer an updated information on the magnitude of subclinical alterations in LV structure in contemporary human hypertension. A MEDLINE search using key words 'left ventricular hypertrophy', 'hypertension', 'echocardiography' and 'cardiac organ damage' was performed in order to identify relevant papers. Full articles published in English language in the last decade, (1 January 2000 --1 December 2010), reporting studies in adult or elderly individuals, were considered. A total of 30 studies, including 37 700 untreated and treated patients (80.3% Caucasian, 52.4% men, 9.6% diabetics, 2.6% with CV disease) were considered. LVH was defined by 23 criteria; its prevalence ranged from 36% (conservative criteria) to 41% (less conservative criteria) in the pooled population. LVH prevalence was not different between women and men (range 37.9 --46.2 versus 36.0 --43.5%, respectively). Eccentric LVH was more frequent than concentric hypertrophy (range 20.3 --23.0 versus 14.8 --15.8, respectively, Po0.05); concentric phenotype was found in a consistent fraction (20%) of both genders. Despite the improved management of hypertension in the last two decades, LVH remains a highly frequent biomarker of cardiac damage in the hypertensive population. Our analysis calls for a more aggressive treatment of hypertension and related CV risk factors leading to LVH. INTRODUCTIONLeft ventricular hypertrophy (LVH) secondary to arterial hypertension is a complex cardiac phenotype resulting from the response of myocyte and non-myocyte components to mechanical and neuro-humoral stimuli. 1 Although the mechanisms underlying this process remain incompletely understood, available evidence from the last two decades indicates that chronic haemodynamic overload has a driving role in activating LV myocardial growth; in turn, non-haemodynamic variables (that is, genetic, ethnic, environmental and hormonal factors) modulate the extent (and type) of the hypertrophic response. 2 --4 LVH in hypertensive patients may be regarded as a powerful, independent biomarker reflecting the impact of pressure overload as well as of several risk factors 5 on the heart.Routinely assessed LVH by electrocardiography or more accurately by echocardiography, is a strong determinant of cardiovascular (CV) prognosis over and beyond conventional risk factors in both population-based studies and in selected hypertensive cohorts. 6 --8 Initial levels of LV mass and mass reduction during antihypertensive treatment define CV risk related to subclinical cardiac damage 9 and influence therapeutic strategies. 10 In recent years, observational and interventional studies addressing hypertensive LVH performed worldwide 5 --9,11,12 offered us the opportunity to update available information o...

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.

In the presence of nocturnal hypertension, dippers have a similar subclinical cardiac and extra-cardiac organ damage as their nondipper counterparts. These data suggest that therapeutic strategies only addressing the nondipper pattern may be insufficient to protect hypertensive subjects against the dangerous effects of elevated nocturnal BP.American Journal of Hypertension, (2012); doi:10.1038/ajh.2012.49.

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.

Our analysis shows that LVH, as assessed by ECG, is present in a relevant fraction of the hypertensive population; these data highlight the role of ECG as a first-line examination for identifying subclinical organ damage and optimizing blood pressure control in hypertensive patients.

Extensive echocardiographic investigations performed in the past 3 decades have shown that hypertensive heart disease includes a variety of anatomic and functional alterations, such as left ventricular hypertrophy (LVH), systolic/diastolic dysfunction, myocardial fibrosis, and left atrial and aortic dilatations. [1][2][3][4][5] Among these manifestations of cardiac damage, particular attention has been devoted to LVH because this phenotype has been reported to be a powerful, independent predictor of cardiovascular (CV) events and all-cause mortality either in the general population or in hypertensive cohorts. 6,7 Although the pathogenesis of hypertensive LVH is not fully understood, a consistent body of evidence indicates that the severity of pressure overload, as better reflected by out-of-office than by in-office blood pressure (BP) levels, in combination with nonhemodynamic variables, including genetic, ethnic, and humoral factors, plays a pivotal role in its development. 8,9 Nonetheless, numerous reports have also shown that circadian variations in BP correlate to LVH independently of 24-hour ambulatory BP monitoring (ABPM) values. Furthermore, earlier studies suggested that daytime BP, in particular BP values recorded during working hours, is more closely associated with LVH compared with nighttime BP. 10 More recently, however, numerous studies have shown that nighttime BP and nocturnal BP fall are stronger correlates of LVH than daytime or average 24-hour BP. 11,12Although a blunted decrease in nighttime BP (ie, nondipping status) has been associated with unhealthy conditions, including diabetes mellitus, metabolic syndrome, sleep apnea, cardiac or extracardiac organ damage, resistant hypertension, and an increased risk of CV morbidity and mortality, 13-15 this issue remains a source of debate. It is worthy of mention that a systematic review by Hansen et al 16 which included 25 856 hypertensive patients and 9641 individuals randomly recruited from the population revealed that nondipping status and increased night-to-day BP ratio were associated with higher all-cause mortality and CV events but added a marginal prognostic value over and beyond 24-hour BP.

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.