Different metabolic effects of selective and nonselective beta-blockers rather than mere heart rate reduction may be the mechanisms by which beta-blockade prevents cardiovascular events.

摘要

Thus, heart rate at baseline may have acted as a confounding factor in the analysis performed by Bangalore et al. (1). This suggests that reduction in heart rate may not be the main mechanism through which beta-blockers devoid of vasodilating properties, particularly atenolol, exert deleterious effects on the cardiovascular system, and demonstrate less effect than other antihypertensive agents for preventing cardiovascular events. Indeed, in contrast to vasodilating agents like calcium-channel blockers and renin-angiotensin system blockers, atenolol does not reduce total peripheral resistance and sympathetic drive, and fails to induce the long-term remodeling of large and small arteries that is required for structural improvement of arterial stiffness and resistance and the reduction in wave reflection and central aortic blood pressure.