Microparticles are small cell vesicles that are derived from the cell membrane in response to different biological processes. There is growing evidence supporting the association between microparticles and cardiovascular disease, as their pathophysiology commonly includes endothelial damage and chronic inflammation which also promote a prothrombotic state. The direct causal link between the release of the different subtypes of microparticles and their implications on physiological and pathological conditions is still not completely elucidated. However, evidence suggests microparticles released from platelets, leukocytes, and endothelium may help to evaluate vascular health as they have a relevant role in inflammation, endothelial function, and thrombosis. This review aims to provide a short overview of the biogenesis, characteristics, and detection methodology of microparticles with a special focus on their possible implication in cardiovascular settings.

Objective: Although the detrimental effect of increased mean blood pressure (BP) is well established, the role of the dynamic and circadian features of BP is less well defined but may be similarly important. In this prospective analysis of hypertensive patients from a tertiary hospital hypertension clinic, we investigated whether the presence of night-time systolic hypertension is associated with more pronounced end-organ damage as assessed by measures of pulse wave analysis (PWA) and pulse wave velocity (PWV). Methods: A cohort of 222 consecutive hypertensive patients underwent ambulatory blood pressure measurements, PWA, PWV testing and collection of routine clinical data. Group differences and group-effects of daytime and night-time hypertension on target organ damage and cardiovascular risk parameters were analysed. Results: Nocturnal hypertension was evident in more than half of the study population. PWV, central systolic, mean arterial and pulse pressure were higher in patients with nocturnal hypertension. Stratification into four groups according to daytime and night-time hypertension status revealed group differences in all outcome parameters. Posthoc testing for individual group differences demonstrated significant differences between fully controlled individuals and the group with high daytime and night-time BP. In a regression analysis for independent effects of categorical night-time and daytime hypertension, nocturnal hypertension was a significant predictor for all PWA and PWV outcomes. Conclusion: Nocturnal hypertension was a highly prevalent phenotype in this population and associated with increased central BP and more pronounced target organ damage as indicated by elevated PWV. Regression analysis confirmed the role of night-time hypertension as an independent explanatory variable for elevated PWV.

Purpose of Review The moderate glucose-lowering effect of sodium glucose co-transporter 2 (SGLT2) inhibitors is unlikely to explain SGLT2 inhibitor-mediated beneficial outcomes, and unravelling the underlying mechanisms is a high priority in the research community. Given the dominant pathophysiologic role of the sympathetic nervous system activation in conditions such as hypertension and perturbed glucose homeostasis, it is pertinent to postulate that SGLT2 inhibitors may exert their beneficial effects at least in part via sympathetic inhibition. Recent Findings SGLT2 inhibitors have shown enormous potential to improve cardiovascular outcomes in patients with type 2 diabetes, and their therapeutic potential is currently being investigated in a range of associated comorbidities such as heart failure and chronic kidney disease. Indeed, recent experimental data in relevant animal models highlight a bidirectional interaction between sympathetic nervous system activation and SGLT2 expression, and this facilitates several of the features associated with SGLT2 inhibition observed in clinical trials including improved glucose metabolism, weight loss, increased diuresis, and lowering of blood pressure. Summary Currently available data highlight the various levels of interaction between the sympathetic nervous system and SGLT2 expression and explores the potential for SGLT2 inhibition as a therapeutic strategy in conditions commonly characterised by sympathetic activation.