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Arterial hypertension is the most prevalent global modifiable risk factor for cardiovascular morbidity and mortality. Despite the availability of numerous pharmacologic treatments, many patients do not achieve guideline-recommended blood pressure targets. Therefore, renal sympathetic denervation (RDN), a process in which catheter-directed techniques are used to ablate portions of the renal artery to reduce sympathetic activity, has been extensively investigated as a complementary and nonpharmacologic approach for the treatment of arterial hypertension. This review seeks to discuss the pathophysiological rationale of this strategy, to survey its history and development, and to highlight the current clinical evidence and possible future directions of its employment. In sum, RDN has demonstrated itself to be a safe and well-tolerated endovascular intervention that can reliably contribute to improved blood pressure control and, perhaps ultimately, significant cardiovascular prognosis.

Introduction: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used for cardiovascular disease (CVD) prevention. Long-term use of statins has been linked to the development of diabetes mellitus (DM) which increases CVD risk. Areas covered: We discussed the reported incidence of DM in statin users, various possible mechanisms responsible for the development of DM and the clinical implications of this association on CVD risk. Relevant supporting literature was identified using MEDLINE/EMBASE search. Expert opinion: Data from available RCTs and observational studies suggest a 10-45% higher risk of new-onset DM with statin use compared to nonusers. Several cellular, molecular, and genetic mechanisms, and lifestyle changes have been studied and discussed as potential underlying mechanisms responsible for this elevated DM risk with statin therapy. The mode of the diabetogenic action of statins is still unclear and an interplay of pancreatic and peripheral effects in the pathogenesis of DM is a possibility. Despite these observations, the CVD preventative benefit of statin treatment outweighs the CVD risk associated with of development of new DM. There is a need for further research to identify the exact mechanisms involved so as to specifically target causative factors and individualize treatment.

3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors are ubiquitously prescribed for cardiovascular disease (CVD) prevention and treatment. However, the use of statins has been linked to the development of new-onset diabetes mellitus (NODM), which could possibly increase future CVD risk. This phenomenon necessitates a clear discussion of the possible etiologies of this relationship and its broader clinical consequences. We discuss the reported incidence of NODM in statin users through a rigorous review of data from metaanalyses of randomized control trials examining this association. We also highlight the various possible mechanisms responsible for the development of statin-induced diabetes mellitus. Finally, we examine the clinical implications of this effect on future CVD risk and identify specific patient factors that can be used for risk-stratification strategies. Data from 14 randomized control trials metaanalyses suggest a 9-33% higher risk of NODM with statin use. Several cellular, molecular, and genetic mechanisms, as well as lifestyle habits, have been identified as potential underlying factors responsible for this elevated risk. The principle mode of the diabetogenic action of statins is still unclear, though it is likely the result of a complex interplay of pancreatic and extrapancreatic effects. It is understood that patient populations with a greater predisposition to diabetes mellitus, and those with thicker epicardial adiposity are more at risk for the development of statin-induced NODM. Despite these observations, robust data from a variety of investigations suggest that the CVD preventative benefits of statin treatment significantly outweigh the risks associated with the development of NODM. Nevertheless, further study must better identify the causative mechanisms involved in this process, its natural history, and the unique factors that will help clinicians risk stratify and appropriately monitor patients on statin therapy.

OBJECTIVE: To evaluate whether equal volumes of oral rehydration solution (ORS) or intravenous saline provide similar improvements in cardiovascular status during controlled orthostatic challenge when administered to patients with postural tachycardia syndrome (POTS) with orthostatic intolerance. STUDY DESIGN: We studied the neurovascular response to fluid loading during orthostatic stress using lower body negative pressure (LBNP) in 10 subjects with POTS with OI and 15 controls, and on subsequent days before, and 1 hour after intravenous saline or ingestion of ORS. RESULTS: Subjects with POTS exhibited reduced tolerance (P < .0001) to LBNP compared with controls (Orthostatic Index of 35,715±3,469 vs. 93,980±7,977, respectively). In POTS, following ORS but not saline, cerebral blood flow velocity (CBF(v)) was significantly higher than no treatment (p