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...