Beta blockers are even more powerful in reducing cardiac events in the patient with diabetes, than they are in others. This is because that in addition to lowering blood pressure, lowering heart rate, and acting as an anti-inflammatory, beta blockers, in the patient with diabetes, shift the metabolism of the myocardium away from fatty acid utilization and toward glucose utilization, which decreases the cardiac workload and reduces ischemia. Furthermore, hyperglycemia is a stimulus to myocardial remodeling, which is not only prevented but is reversed by beta blockade, and the incidence of heart failure that would otherwise be increased in the patient with diabetes, is reduced. The first and second generation beta blockers induce peripheral vasoconstriction and increase insulin resistance, causing an increase in serum glucose and triglycerides, and a decrease in HDL levels. These problems can be circumvented by using a third generation beta blocker, which are vasodilatory and reduce serum glucose and triglycerides, and increase HDL cholesterol. Therefore, the traditional and long-standing reluctance of endocrinologists to utilize beta blockade in the diabetic patient is unfounded and outdated due to the availability of later-generation beta blockers.
* Discuss the vulnerability of diabetic patients to heart disease and the rationale for administering beta-blockers to these patients.
* Relate the indications for, and the timing of beta-blocker treatment in type 2 diabetics with regard to coronary artery disease and heart failure.
* Summarize the risks of beta-blockade in diabetic patients and how they may be minimized.
Professor of Medicine and Director of Clinical Research, Division of Endocrinology and Metabolism, the University of Alabama at Birmingham School of Medicine, Birmingham, Alabama.
Chief Editor’s Note: This article is the 9th of 36 that will be published in 2003 for which a total of up to 36 Category 1 CME credits can be earned. Instructions for how credits can be earned appear following the Table of Contents.
Address correspondence and reprint requests to: David S. H. Bell, M.B., F.A.C.E., 1808 7th Avenue South, Room 802 Birmingham, AL 35294. E-mail: firstname.lastname@example.org
Dr. Bell has disclosed that he is the recipient of a research grant(s) from GlaxoSmithKline; is a consultant for GlaxoSmithKline; and is a member of the Speakers Bureau of GlaxoSmithKline.