Abstract-Left ventricular (LV) mass (LVM) is the most important information requested in hypertensive patients referred for echocardiography. However, LV function also predicts cardiovascular (CV) risk independent of LVM. There is no evidence that addition of LV function significantly improves model prediction of CV risk compared with LVM alone. Thus, composite fatal and nonfatal CV or cerebrovascular events were evaluated in 5380 hypertensive outpatients (2336 women, 298 diabetics, and 1315 obese subjects) without prevalent CV disease (follow-up: 3.5Ϯ2.8 years). We compared 5 risk models using Cox regression and adjusting for age and sex: (1) LV mass normalized for height in meters 2.7 (LVMi); (2) LVMi, concentric LV geometry, by relative wall thickness (Ͼ0.43), ejection fraction, and transmitral diastolic pattern (by thirtiles of mitral deceleration index); (3) LVMi, LV geometry, midwall shortening, and mitral deceleration index thirtiles; (4) as No. 2 with the addition of left atrial dilatation (Ͼ23 mm); and (5) as No. 3 with the addition of left atrial dilatation. Individual hazard functions were compared using receiving operating characteristic curves and z statistics. Areas under the curves increased from 0.60 in the model with the sole LVMi to 0.62 in the others (all P values for differences were not significant). The additional information on systolic and diastolic function decreased the contribution (Wald statistics) of LVMi in the Cox model without improving the model ability to predict CV risk. We conclude that risk models with inclusion of information on LV geometry and systolic and diastolic function, in addition to LVMi, do not improve the prediction of CV events but rather redistribute the impact of individual predictors within the risk variance. (Hypertension. 2010;56:99-104.) Key Words: cardiac mass Ⅲ heart atria Ⅲ cardiovascular risk Ⅲ arterial hypertension Ⅲ prognosis Ⅲ outcome Ⅲ hazard models D espite the most common recommendation to perform echocardiographic examinations in hypertensive patients based on indications that might yield modifications of the management strategy 1,2 and the most recent guidelines that do not list echocardiography in the primary workup for arterial hypertension, 3,4 arterial hypertension remains one of the most frequent indications for echocardiography, especially in countries where the direct cost is not perceived as a direct charge for patients.The substantial reason for echocardiography in arterial hypertension is assessment of left ventricular (LV) mass, based on the broad evidence that LV hypertrophy (LVH) is one of the most important prognostic markers in hypertension, as well as in general populations. 3,4 However, following the reports on LVH, a large number of studies have indicated other echocardiographic markers of cardiovascular risk to be independent of LVH, including LV geometry 5,6 and systolic and diastolic function. [7][8][9][10] The demonstration of independence from LVH is usually obtained using multivariate Cox proportional hazard analysis, whi...

Background Fibro-calcification of the mitral annulus (MAC) has been associated with increased risk of ischemic stroke in general populations. This study was performed to assess whether MAC predicts incidence of ischemic stroke in treated hypertensive patients with left ventricular hypertrophy (LVH). Methods Baseline and follow-up clinical and echocardiographic parameters were assessed in 939 hypertensive patients with electrocardiogram (ECG) LVH participating in the Losartan Intervention for Endpoint reduction in hypertension (LIFE) echocardiography substudy (66±7 years; 42% women; 11% with diabetes) who did not have aortic or mitral valve stenosis or prosthesis. Results MAC was found in 458 patients (49%). Patients with MAC were older (68±7 vs. 65±7 years); were more often women (47% vs. 37%); had higher baseline systolic blood pressure (BP) (175±14 vs. 172±15mm Hg), left atrial diameter (4.0±0.5 vs. 3.8±0.6cm), and left ventricular mass index (58±13 vs. 55±12g/m(2.7)) and included more patients with proteinuria (30% vs. 21%; all P < 0.01). During a mean follow-up of 4.8 years, 58 participants had an ischemic stroke. Risk of incident ischemic stroke was significantly related to presence of MAC (log rank = 9; P < 0.01). In multivariable Cox regression analysis models, MAC was associated with increased risk of ischemic stroke (hazard ratio = 1.78-2.35), independent of age, baseline or time-varying systolic BP, prevalence or incidence of atrial fibrillation, history of previous cerebrovascular disease, and other well-recognized confounders, such as sex, time-varying left ventricular mass, left atrial diameter, and urinary albumin/creatinine ratio (all P < 0.05). Conclusions MAC is common in treated hypertensive patients with ECG LVH and is an independent predictor of incident ischemic stroke.

In treated hypertensive patients participating in the Campania Salute Network, higher PP/SVi is associated with carotid atherosclerosis independent of well-known clinical confounders.

The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular-vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricularvascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction. J Cardiovasc Med 2014, 15:773-787