Obesity is a growing global health concern, with a rapid increase being observed in morbid obesity. Obesity is associated with an increased cardiovascular risk and earlier onset of cardiovascular morbidity. The growing obesity epidemic is a major source of unsustainable health costs and morbidity and mortality because of hypertension, type 2 diabetes mellitus, dyslipidemia, certain cancers and major cardiovascular diseases. Similar to obesity, hypertension is a key unfavorable health metric that has disastrous health implications: currently, hypertension is the leading contributor to global disease burden, and the direct and indirect costs of treating hypertension are exponentially higher. Poor lifestyle characteristics and health metrics often cluster together to create complex and difficult-to-treat phenotypes: excess body mass is such an example, facilitating a cascade of pathophysiological sequelae that create such as a direct obesity-hypertension link, which consequently increases cardiovascular risk. Although some significant issues regarding assessment/management of obesity remain to be addressed and the underlying mechanisms governing these disparate effects of obesity on cardiovascular disease are complex and not completely understood, a variety of factors could have a critical role. Consequently, a comprehensive and exhaustive investigation of this relationship should analyze the pathogenetic factors and pathophysiological mechanisms linking obesity to hypertension as they provide the basis for a rational therapeutic strategy in the aim to fully describe and understand the obesity-hypertension link and discuss strategies to address the potential negative consequences from the perspective of both primordial prevention and treatment for those already impacted by this condition.

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has had a tremendous impact on health services; hundreds of thousands of healthcare workers (HCWs) have died from coronavirus disease 2019 (COVID-19). The introduction of the BNT162b2 mRNA vaccine in Italy provided recipients with significant protection against COVID-19 within one to two weeks after the administration of the second of the two recommended doses. While the vaccine induces a robust T cell response, the protective role of factors and pathways other than those related to memory B cell responses to specific SARS-CoV-2 antigens remains unclear. This retrospective study aimed to evaluate the determinants of serological protection in a group of vaccinated HCWs (N = 793) by evaluating circulating levels of antiviral spike receptor-binding domain (S-RBD) antibodies during the nine-month period following vaccination. We found that 99.5% of the HCWs who received the two doses of the BNT162b2 vaccine developed protective antibodies that were maintained at detectable levels for as long as 250 days after the second dose of the vaccine. Multivariate analysis was performed on anti-S-RBD titers in a subgroup of participants (n = 173) that were evaluated twice during this period. The results of this analysis reveal that the antibody titer observed at the second time point was significantly related to the magnitude of the primary response, the time that had elapsed between the first and the second evaluation, and a previous history of SARS-CoV-2 infection. Of importance is the finding that despite waning antibody titers following vaccination, none of the study participants contracted severe COVID-19 during the observational period.

The majority of patients with a standard indication for permanent pacing and normal LV function remained in a clinically stable condition after pacemaker implantation. However, ∼7% of patients developed new-onset HF over a period of follow-up of 27 months, and the presence of LBBB and LVEF <50% at the baseline predicted HF death or hospitalization.

RA-CA produces extensive damage to the RA. The lesions tend to heal with time but incomplete recovery of endothelial integrity and function is still present more than 30 days after the procedure. After RA-CA, the cannulated RA should not be used for CABG.