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Background: Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular events, and evidence has been obtained that an increase of a normal left ventricular mass (LVM) or new-onset LVH over time augments cardiovascular outcomes. Methods: We addressed this issue in a sample of a general population at relatively low cardiovascular risk. We analyzed subjects with normal echocardiographic LVM enrolled in the PAMELA (Pressioni Arteriose Monitorate E Loro Associazioni) study to follow the increase of LVM over time and assess the prognostic impact of this change on the incidence of cardiovascular events (mean follow-up 18.5 years). Results: In 990 subjects with no LVH at baseline, there was a significant average increase of LVM (21.2%), LVMIBSA(18.9%), and LVMIHT(22.3%) more than 10 years later. About a quarter developed LVH. The LVMIBSAchange exhibited an association with the cardiovascular risk mortality during the following 18.5 years, and the association remained significant after adjustment for confounders (hazard ratio, 1.2 [1.0-1.5]). Similar findings were obtained for LVM in absolute values or indexed for height. The association was seen in both genders, but the link with the cardiovascular risk was statistically significant in males only. Conclusions: Thus, although over 10 years, the LVM increase does not reach a LVH status, it is associated with an augmented cardiovascular mortality risk. This suggests that it might be important to consider periodical LVM assessment, even when LVM is within the normal range, to timely detect its increase and cope with the need of cardiovascular risk restratification.

AIM: Evidence on the impact of blood pressure (BP)-lowering drugs on left ventricular (LV) mechanics in hypertension is still limited. We performed a meta-analysis of speckle-tracking echocardiographic studies in order to provide a new piece of information on this topic. METHODS: The PubMed, OVID-MEDLINE, and Cochrane library databases were analysed to search for articles published from the inception up to 31 October 2021. Studies were identified by using MeSH terms and crossing the following search items: 'myocardial strain', 'left ventricular mechanics', 'speckle tracking echocardiography', 'systolic dysfunction', 'left ventricular hypertrophy', 'systemic hypertension', 'BP lowering drugs,' 'antihypertensive therapy'. RESULTS: A total of 1140 hypertensive patients (mean age 55.4 years, 50% men, follow-up 6-36 months) were included in eight studies. Pretreatment and posttreatment pooled SBP/DBPs were 148.4 ± 3.5/88.7 ± 2 vs. 127.4 ± 1.9/77.8 ± 0.9 mmHg. Corresponding values for ejection fraction (EF), LV mass (LVM) index, and global longitudinal strain (GLS) were 64 ± 2.3 vs. 65.9 ± 1.7% (SMD: 0.14 ± 0.03, CI 0.08- 0.20, P = 0.001); 108.4 ± 11.2 vs. 100.2 ± 11.0 g/m2 (SMD: -0.27 ± 0.10, CI -0.46 to -0.08, P < 0.01); -17.7 ± 0.6 vs. -19.6 ± 0.4%, (SMD 0.26 ± 0.03, CI 0.20-0.32, P < 0.0001), respectively. A meta-regression analysis showed a significant relation between GLS improvement and the extent of reduction of LVMI (P = 0.0003), but not of SBP (P = 0.27). CONCLUSION: Our meta-analysis suggests that antihypertensive treatment has a clear beneficial effect on LV mechanisms, and the improvement in GLS is mainly related to the reduction in LVMI rather than SBP.

Aim:We sought to assess the long-term changes in aortic root diameter in a population-based sample, focusing on new-onset aortic root dilatation, as well as on the demographic and clinical variables independently related to this dynamic process.Methods:A total of 1122 participants with measurable echocardiographic parameters at baseline and after a 10-year follow-up were included in the analysis. Sex-specific upper limits of normality for absolute aortic root diameter, aortic root diameter indexed to body surface area (BSA) and to height were derived from 712 healthy normotensive PAMELA participants.Results:Over the 10-year follow-up, new aortic root dilatation occurred in 3.4% (aortic root /BSA), 4.4% (aortic root /height) and 7.3% (absolute aortic root), respectively. No substantial relationship was observed between baseline office and ambulatory blood pressure (BP) or their changes over time and incident aortic root /BSA and aortic root /height dilatation. Baseline aortic root diameter and left ventricular mass index (LVMI) emerged as important predictors of aortic root dilation, regardless of the diagnostic criteria used. This was also the case for the 10-year change in LVMI. The strength of association between nonhemodynamic variables and new-onset aortic root dilatation was variable, depending on the definition of the aortic phenotype.Conclusion:The incidence of aortic root dilatation in a general middle-aged population is a relatively infrequent but not so rare event and scarcely influenced by both office and out-office BP. On the contrary, it is strongly related to LVMI (and its variations over time). From a clinical perspective, this underlines that LVH prevention and regression can reduce the risk of aortic root dilatation in the community.

An increased 24-h blood pressure variability, expressed as SD of 24-h average ambulatory blood pressure values, is associated with target organ damage and cardiovascular risk in hypertension, while a physiological nocturnal blood pressure fall has been associated with reduced cardiovascular risk. Nocturnal blood pressure fall, however, may contribute markedly to the overall blood pressure variability. The aim of our study was to quantitatively assess the contribution of nocturnal blood pressure fall to 24-h blood pressure variability, and to propose,a new method for computing 24-h blood pressure variability correcting for nocturnal blood pressure fall. From a large database of ambulatory blood pressure recordings obtained in two hypertension centres (Milan, Italy and Krakow, Poland), we selected 1995 re cordings of a sufficiently high quality (>= 70% valid readings, >= 1 measure/h). We calculated (1) blood pressure variability, as SD of 24-h mean blood pressure, both directly from all 24-h individual readings and as a weighted mean of separately computed daytime and night-time blood pressure SD; and (2) the size of nocturnal blood pressure fall. The weighted mean SD of 24-h blood pressure was significantly lower than the corresponding direct 24-h SD of blood pressure. The size of the difference between direct SD and weighted mean SD was strongly correlated with the absolute size of nocturnal blood pressure fall (SD: r=0.89 and 0.86 for systolic and diastolic blood pressures, respectively, P<0.001 for all). The 24-h SD of blood pressure is markedly influenced by the size of nocturnal blood pressure fall, while the weighted mean SD is not. The inclusion of nocturnal blood pressure fall in the calculation of 24-h blood pressure variability may thus lead to the overestimating of this phenomenon. Given that blood pressure variability and fall at night may have opposite prognostic significance, it may be advisable to calculate 24-h SD as the weighted mean of daytime and n