From the Editor

It is with sadness that this issue begins with an In Memoriam for Dr. Thomas Pickering, who made many important contributions to our understanding of blood pressure (BP) variability as well as the interaction between the nervous system and BP in humans.

The recent reports of 2 massive genome-wide association studies of the genetics of human hypertension1, 2 have provided the rationale for an editorial on the topic of the genetics of hypertension by Dr. Stephen Harrap. Dr. Harrap has very elegantly placed the importance of these findings along with their limitations in proper perspective. In doing so, he has offered ideas for future studies which may provide additional information. He has appropriately reminded us that the traditional manner of measuring BP may not be optimal and has indirectly called for a more precise phenotype.

The following article, by Dr. Freitas and colleagues, describes a polymorphism of the HMG Coenzyme A-reductase gene that was found to be associated with BP. Moreover, they observed an association between urinary sodium:potassium ratio and BP in their study, suggesting a possible relationship to a known physiologic mechanism influencing BP.

Dr. Husain and colleagues provide a thoughtful consideration of the possible ways in which enhancing the activity of the GLP-1 incretin pathway by the use of DPP-4 inhibitors may provide cardiovascular benefits. While this is of obvious applicability to those with diabetes, individuals with the Metabolic Syndrome should also benefit from such treatment. It will be interesting to follow the investigative studies in this area with specific attention to multiple cardiovascular risk factors including BP and lipids as well as insulin sensitivity.

Dr. Fulop and colleagues examined a subgroup of the GENOA cohort receiving antihypertensive monotherapy. They observed differences in C-reactive protein levels among the different antihypertensive drug groups. While this cross-sectional observation is only suggestive, it provides evidence for a differential effect of these drugs on an important risk factor for cardiovascular events. Future prospective studies may provide more convincing information, perhaps if linked to outcome trials.

The next paper in this issue, by Dr. Faria and colleagues, addresses the issue of clinical inertia, a problem largely attributed to the lack of appropriate physician response. Their findings suggest that this focus may often be mis-directed and urge examination of all links in the therapeutic chain.

In the final paper, Drs. Weir and Townsend provide convincing evidence that simple measures of renal function such as estimated glomerular filtration rate and urinary albumin excretion are sensitive measures of cardiovascular disease risk. They offer clinically applicable and easy approaches to this assessment of an important independent risk factor for our patients.