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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%), LVMI BSA (18.9%), and LVMI HT (22.3%) more than 10 years later. About a quarter developed LVH. The LVMI BSA change 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.

Background: Inconsistent evidence has assessed the impact of air pollution exposure on children’s growth trajectories. We investigated the role of 90-day average postnatal fine particulate matter (PM2.5) exposures by estimating the magnitude of effects at different ages, and the change in child weight trajectory by categories of exposure. Methods: We obtained weight values from electronic health records at each hospital visit (males = 1859, females = 1601) from birth to 6 years old children recruited into the Boston-based Children’s HealthWatch cohort (2009–2014). We applied mixed models, adjusting for individual and maternal confounders using (1) varying-coefficient models allowing for smooth non-linear interaction between age and PM2.5, (2) factor-smooth interaction between age and PM2.5 quartiles. Additionally, we stratified by sex and low birthweight (LBW) status (≤2500 g). Results: Using varying-coefficient models, we found that PM2.5 significantly modified the association between age and weight in males, with a positive association in children younger than 3 years and a negative association afterwards. In boys, for each 10 µg/m3 increase in PM2.5 we found a 2.6% increase (95% confidence interval = 0.8, 4.6) in weight at 1 year of age and a −0.6% (95% confidence interval = −3.9, 2.9) at 5 years. We found similar but smaller changes in females, and no differences comparing growth trajectories across quartiles of PM2.5. Most of the effects were in LBW children and null for normal birthweight children. Conclusions: This study suggests that medium-term postnatal PM2.5 may modify weight trajectories nonlinearly in young children, and that LBW babies are more susceptible than normal-weight infants.

Objective: Whether and to what extent the reported BP lowering effects of renal denervation (RD) are mediated by a sympathetic deactivation induced by the procedure is still largely undefined. We examined this issue by performing a meta-analysis of the microneurographic studies published so far based on the evaluation of the blood pressure (BP) and muscle sympathetic nerve traffic (MSNA) responses to RD. Design and method: The meta-analysis was based on 12 studies including a total of 394 patients with resistant hypertension underwent RD and followed up to 12 months. Evaluation was extended to the relationships of MSNA with heart rate (HR) and clinic or ambulatory blood pressure (BP) values (expressed such as mean and 95% confidence interval). Results: Baseline MSNA values amounted to 48.25 (43.86-52.64) bursts/minute, clinic HR to 66.35 (65.02-67.67) beats/minute and systo/diastolic clinic BP to 167.3 (157.6-177.01) and 90.54 (84.81-96.27) mmHg. RD caused a significant BP reduction at 3/6/12 months following the procedure amounting to 12.6 mmHg for systolic (range 20.9 to 4.39 mmhg, p = 0.003) and to 6.4 mmHg for diastolic BP (range -11.9 t0 0.9 mmHg, p = 0.02) respectively. No significant change in MSNA (-2.65, range -6.7 to 1.4 bursts/minute, P = NS) and HR (-0.58, range -3.98 to 2.81 b/min, P = NS) were concomitantly observed. No relationship was found between the number of renal ablations and the magnitude of the blood pressure or MSNA changes, this being the case also for HR. Conclusions: This meta-analysis, the first ever done on the MSNA responses to RD, shows that in a consistent number of patients underwent RD, the BP lowering effects of the procedure are not accompanied by any significant change in 2 adrenergic markers, i.e. MSNA and HR, and thus appear not to be mediated by any sympathetic deactivation.

Background: According to some guidelines, white-coat hypertension (WCH) carries little or no increase of cardiovascular risk in the absence of organ damage (OD), but no data are available on this issue. Methods: Using the population data from PAMELA (Pressioni Arteriose Monitorate E Loro Associazioni), we evaluated cardiovascular and total mortality over a median follow-up of 29 years in WCH (elevated office and normal 24-hour or home blood pressure [BP]) and normotensive controls (normal in- and out-of-office blood pressure) with no echocardiographic left ventricular hypertrophy and no reduction of estimated glomerular filtration rate. Patients with sustained hypertension (SH, in- and out-of-office blood pressure elevation) and normotensive, WCH, and SH with cardiac and renal OD served as controls. Results: In the 1423 subjects analyzed, there were 165 cardiovascular and 526 all-cause deaths. After adjustment for confounders, no-OD WCH exhibited a risk of fatal cardiovascular events lower than that of no-OD SH but greater than that of no-ODN (hazard ratio, 2.0 [95% CI, 1.1–3.6], P =0.02), this being the case also for all-cause mortality. Compared with no-OD normotensive, no-OD WCH also exhibited a greater 10-year adjusted risk to develop new SH or OD. Similar findings were obtained in normotensive, WCH, and SH with OD. Conclusions: The present study provides the first evidence that WCH with no OD is accompanied by a noticeable increase in long-term risk of mortality, new hypertension, and new OD, thereby differing from normotension.

Objective: SARS-CoV-2 infection could be complicated by serious autonomic imbalance caused directly by the virus or through secondary release of inflammatory cytokines. Some studies suggested that elevated resting heart rate (HR) and resting tachycardia, being markers of an increased adrenergic cardiac drive, are associated with poor prognosis in COVID-19 syndrome. Design and method: We performed a retrospective analysis in an inpatient cohort of 389 subjects diagnosed with SARS-CoV-2 infection to investigate the prognostic relevance of HR in predicting the maximum care intensity needed during hospitalization according to the following four severity outcome classes: I) no need for oxygen support/need for low flow oxygen therapy; II) need for high flow oxygen therapy/continuous positive airway pressure; III) transfer to the Intensive Care Unit; IV) death. HR assessments were recorded on admission and during the first 3 and 7 days of hospitalization. Results: For each class increase in maximum care intensity we observed a corresponding significant increase in HR, considering both data collected on admission (average HR value: 90.1 ± 17 beats/minute, p-value trend = 0.0397), and during the first 3 days (p-value trend < 0.0006) or 7 days (p-value trend < 0.0001) of hospitalization. The significant trend was maintained after adjustment for age, sex, comorbidities and fever and in the subpopulation of patients (n = 118) not receiving drugs potentially active on HR both before and during hospitalization. Kaplan-Meier curves for survival based on HR displayed a significant decreased survival in patients with higher HR. Conclusions: The assessment of HR during hospitalization provides information on the clinical outcome of patients affected by SARS-CoV-2 infection independently of other confounders. HR as an in-hospital prognostic marker can be obtained both through a first assessment at the admission or mean values over the course of hospitalization with an increase of its accuracy by a 7-days longitudinal evaluation. Further studies might elucidate the association between SARS-CoV-2 infection with multiple autonomic abnormalities.