Does it matter how blood pressure is lowered in patients with metabolic risk factors?

Abstract 

Abdominal obesity is an important cardiovascular risk factor. It is a primary driver of the metabolic syndrome, the cluster of metabolic risk factors that includes insulin resistance and dyslipidemia, and often occurs in association with hypertension. The aim of antihypertensive therapy in patients with metabolic risk factors is to reduce cardiovascular risk, but some antihypertensive agents can exert adverse metabolic effects. For example, beta-blockers produce significant weight gain, and are associated with an increased incidence of diabetes. By contrast, agents that inhibit the renin-angiotensin system (RAS), such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have been shown to be associated with a decreased risk of new-onset diabetes. This reflects the finding that increased activation of the RAS in obese individuals can contribute to the development of the metabolic syndrome. The ARB telmisartan has been shown to act as a selective peroxisome proliferator-activated receptor (PPAR)-γ modulator. It is known that PPAR-γ plays a role in the regulation of multiple genes affecting carbohydrate and lipid metabolism; however, the clinical significance of this remains to be established. The potential metabolic effects of RAS blockade should be considered in the choice of antihypertensive therapy for patients with metabolic risk factors, including obesity.

Keywords: Abdominal obesity, antihypertensive therapy, RAS, telmisartan