Cost–Benefit of Home Blood Pressure Monitoring (page 891)
Previous research has confirmed that self-measured blood pressures taken at home are well accepted by patients, yield more accurate readings, and have better predictive value than blood pressures obtained by a clinician in a medical setting. However, home blood pressure monitoring continues to be underutilized, in part, because most insurers do not reimburse the cost of the monitor. In this issue of Hypertension, a decision-analytic model using insurance claims data shows for the first time that insurers who pay for home monitors can expect to reap positive short- and long-run economic returns on their investment. In the first year, estimated returns range from $0.85 to $3.75 per dollar invested in blood pressure monitors. Returns are higher when used for diagnosis of hypertension in nonelderly adults (20–64 years) and when used to monitor hypertension treatment in the elderly (≥65 years). Previous economic evaluations have ignored the private-payer perspective, opting instead for the more conventional societal perspective. By highlighting the economic gains that potentially can be realized by private insurers, this analysis indicates that it would make business sense for insurers to pay for home blood pressure monitors, and that health systems should develop strategies to increase provider adoption and use of this low-cost technology.
Autoimmunity Underlies the Development of Hypertension (page 792)
It is now widely recognized that both human and experimental hypertension are linked to activation of the innate and adaptive immune system. Experimental models have allowed investigators to determine the relative importance of immune cell subsets, inflammatory cytokines, and proinflammatory signaling pathways to regulate blood pressure through renal, central, and vascular mechanisms. In humans, small clinical studies suggest that targeting the immune system can benefit hypertensive patients, particularly those with concurrent chronic inflammatory diseases. Through these studies, a concept has emerged that the underpinnings of hypertension may be autoimmune in nature. This is partly supported by growing evidence that autoantigens are initiators of experimental hypertension, and that circulating autoantibodies are associated with human essential hypertension. In this issue of Hypertension, Mathis et al used an experimental mouse model of autoimmune disease (systemic lupus erythematosus) to address the question of whether autoimmunity per se underlies the development of hypertension. The results show that administration of a mouse anti-CD20 antibody (the equivalent of rituximab, used to deplete B lymphocytes in humans with chronic inflammatory disease) at an age preceding the development of systemic lupus erythematosus prevents the development of the hypertension and renal disease associated with this model. These data extend our understanding of the role for adaptive immunity in hypertension and further support the concept that autoimmunity can be an important factor in the pathogenesis of hypertension.
11β-Hydroxysteroid Dehydrogenase Type 2 and MicroRNA (page 860)
Salt sensitivity is best defined as a significant decrease in blood pressure when dietary salt intake is lowered. In this view, dietary salt restriction is the oldest antihypertensive therapy. The overall mechanism explaining salt sensitivity is complex and not entirely understood. Early work using severe salt restriction indicated that not all patient’s blood pressure reacted satisfactorily and the range of response might be variable from 20% to 70%. One mechanism involved in salt sensitivity is the activity and regulation of the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). This enzyme is selectively expressed in aldosterone target tissues and is implicated in the regulation of the mineralocorticoid receptor by glucocorticoids. A diminished activity of 11β-HSD2 causes salt-sensitive hypertension by specifically increasing sodium reabsorption in the mineralocorticoid responsive cortical collecting duct in the kidney. The mechanism of the variable and distinct 11β-HSD2 gene expression in this specific renal tubule segment is poorly understood. We analyzed, for the first time, the expression of microRNAs in 11β-HSD2 expressing renal tubules of 2 animal models diverging in 11β-HSD2 activity and salt-sensitive hypertension and highlighted differential expression of microRNAs modulating 11β-HSD2. We think that function and differential regulation of microRNAs at a specific renal tubular level may contribute to the molecular mechanisms underlying the development of salt-sensitive hypertension. Better understanding of these microRNAs and their regulation at a specific tubular level will not only give new insight to one of the mechanisms acting in salt-sensitive hypertension but might well represent a specific target for clinical intervention in hypertension therapy.
- © 2014 American Heart Association, Inc.