The Journal of the American Society of Hypertension embarks on its second volume with this issue which includes three invited reviews from state-of-the-art lectures at the American Society of Hypertension’s most recent Annual sessions as well as four original research submissions.
The history of the development of antiplatelet drugs and the studies investigating their use in the prevention of stroke as well as the current role of such agents is critically reviewed by Dr. Philip Gorelick. This review provides a careful discussion of the rationale for selecting patients and agents for the most effective primary and secondary prevention of stroke, a common event in hypertensive patients.
Dr. Friedrich Luft and his colleagues describe the recognition of agonistic antibodies to a variety of receptors and their identification of such antibodies to the type 1 angiotensin II receptor in patients with pre-eclampsia. While such antibodies have been identified for several hormonal and adrenergic receptors, their possible role in the pathophysiology of pre-eclampsia which has eluded mechanistic definition for decades provides a new avenue of investigation and potential prevention and/or treatment of this mystifying problem.
Dr. Atsohira Ichihara reviews his intriguing observations regarding the prorenin receptor and its blockade by identifying angiotensin II-dependent and independent effects. Utilizing animal models of diabetes and of hypertension, he has shown that blockade of this receptor can prevent the development of end-organ disease typically associated with these abnormalities. The potential of this approach to the prevention and treatment of a variety of human disorders is very promising.
Dr. William White and colleagues provide information regarding the effect of an experimental progestin with anti-mineralocorticoid properties, drosperinone, in hypertensive, postmenopausal females. This agent induced a dose-dependent reduction in blood pressure that was especially prominent during the early morning hours when the risk for cardiovascular events is highest.
While peripheral blood pressure measurements have been the standard for decades, recent observations suggest that central blood pressure may differ from that measured at the periphery and may be more important as a determinant of cardiovascular disease. Dr. Michael O’Rourke provides a detailed assessment of central measurements in comparison to the peripheral determinations and how discrepancies between the two measures may be identified by clinicians. Future studies will elucidate the clinical relevance of this differentiation.
The TROPHY study was a novel and seminal approach to the evaluation of the potential benefit of blood pressure reduction with an angiotensin receptor blocker, candesartan, in a “prehypertensive” population in preventing or postponing the development of hypertension. This landmark study has provided answers to some questions but generated many more. One of the criticisms of TROPHY is that the criteria for the definition of hypertension used in the trial was the occurrence of a blood pressure greater than 140/90 on any three visits during the 4-year study. In this issue Dr. Stevo Julius and colleagues report the results of the study in terms of the criteria for hypertension advocated by JNC VII, specifically two consecutive visits with a blood pressure above that level. Applying these more stringent criteria reduced the number of subjects manifesting such changes but did not change the significance of the effect of candesartan on this endpoint.
The final paper in this issue provides a novel analysis of the NHANES database examining the frequency of uncontrolled hypertension in individuals without marked elevation of lipid levels and how that combination of factors impacts on cardiovascular risk. Applying the Framingham risk criteria to this population they found that this group could be expected to have 200,000 coronary events over a 4-year period, with almost two-thirds of that risk attributable to blood pressure and lipid levels. These observations provide a compelling rationale for the aggressive treatment of both risk factors even in those without markedly elevated values.
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