Antihypertensive Combination and Central BP Reduction
Antihypertensive Combination and Central BP Reduction
Not all blood pressure (BP)-lowering agents have the same effect on central BP, but we know that central BP, in itself, is a risk factor for cardiovascular diseases. Therefore, antihypertensive agents should ideally also have a central BP-lowering effect. In this paper the authors evaluate the effect of adding a calcium channel blocker to a β-blocker. The results show this combination does not reverse the lesser effect of β-blockers on central BP, and that the combination of valsartan plus amlodipine is more effective in lowering central BP than a combination of amlodipine plus atenolol.
In the management of hypertensive patients, a cornerstone of good clinical practice is to maintain blood pressure (BP) below the goals recommended by guidelines. Combination therapy of antihypertensive agents is often necessary to achieve such goals. However, do all the combinations have the same effect? Which combination is best? This article evaluates a recent paper by Boutouyrie et al. in which the authors evaluate the effect of different antihypertensive combinations on central BP, a prognostic factor of cardiovascular disease.
Since the publication of the Conduit Artery Function Evaluation (CAFE), a substudy of the Anglo–Scandinavian Cardiac Outcomes Trial (ASCOT), we know that antihypertensive agents, despite a similar impact on brachial BP, could have different effects on central BP. Furthermore, these findings could also explain the different clinical outcomes found between the two antihypertensive treatment arms in the ASCOT trial, which showed highly statistically significant reductions in the amlodipine/perindopril arm versus the atenolol/bendroflumethiazide arm on the combined end point, which included nonfatal myocardial infarction (MI) and fatal coronary heart disease.
Amlodipine is a calcium channel blocker and therefore acts as a vasodilator. The question that remained unanswered until the publication of the article under evaluation was if this vasodilation would dampen the deleterious effect of β-blockers on central BP. In this article, the authors have found an answer to that question.
Abstract and Introduction
Abstract
Not all blood pressure (BP)-lowering agents have the same effect on central BP, but we know that central BP, in itself, is a risk factor for cardiovascular diseases. Therefore, antihypertensive agents should ideally also have a central BP-lowering effect. In this paper the authors evaluate the effect of adding a calcium channel blocker to a β-blocker. The results show this combination does not reverse the lesser effect of β-blockers on central BP, and that the combination of valsartan plus amlodipine is more effective in lowering central BP than a combination of amlodipine plus atenolol.
Introduction
In the management of hypertensive patients, a cornerstone of good clinical practice is to maintain blood pressure (BP) below the goals recommended by guidelines. Combination therapy of antihypertensive agents is often necessary to achieve such goals. However, do all the combinations have the same effect? Which combination is best? This article evaluates a recent paper by Boutouyrie et al. in which the authors evaluate the effect of different antihypertensive combinations on central BP, a prognostic factor of cardiovascular disease.
Since the publication of the Conduit Artery Function Evaluation (CAFE), a substudy of the Anglo–Scandinavian Cardiac Outcomes Trial (ASCOT), we know that antihypertensive agents, despite a similar impact on brachial BP, could have different effects on central BP. Furthermore, these findings could also explain the different clinical outcomes found between the two antihypertensive treatment arms in the ASCOT trial, which showed highly statistically significant reductions in the amlodipine/perindopril arm versus the atenolol/bendroflumethiazide arm on the combined end point, which included nonfatal myocardial infarction (MI) and fatal coronary heart disease.
Amlodipine is a calcium channel blocker and therefore acts as a vasodilator. The question that remained unanswered until the publication of the article under evaluation was if this vasodilation would dampen the deleterious effect of β-blockers on central BP. In this article, the authors have found an answer to that question.
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