to the editor: I read with interest the article on hypertension in patients with diabetes mellitus. The authors did not mention the effect of beta blockers on lipid profile. Patients with diabetes and hypertension may have metabolic syndrome, which is a common disorder. Long-term administration of beta blockers in such patients could increase triglyceride levels and decrease high-density lipoprotein levels,1 which are also features of metabolic syndrome. This might complicate lipid status and require further unnecessary antihyperlipidemic agents.
in reply: We thank Dr. Kittisupamongkol for his commentary. Administration of beta blockers has been associated with alterations in the lipoprotein profile, namely an increase in triglycerides and a decrease in high-density lipoprotein (HDL) cholesterol. However, the effects do not appear to be significant enough to recommend against the use of beta blockers in patients with diabetes mellitus.
A meta-analysis that examined 315 trials of beta-blocker antihypertensive therapy concluded that beta blockers, on average, were associated with a 30 mg per dL (0.34 mmol per L) increase in triglycer-ides and a 4 mg per dL (0.10 mmol per L) decrease in HDL cholesterol.1 In a subset of trials in which the duration of beta-blocker therapy was greater than one year, there was no significant change in triglycerides, suggesting that some effects on the lipid profile may be transient. A Veterans Affairs Cooperative Study observed similar results.2 After one year of maintenance therapy with atenolol (Tenormin), triglyceride levels did not differ significantly from patients randomized to receive hydrochlorothiazide, captopril (Capoten), clonidine (Catapres), diltiazem (Cardizem), prazosin (Minipress), or placebo.2 The 2.9 mg per dL (0.08 mmol per L) reduction in HDL cholesterol levels observed in patients receiving atenolol was not statistically significant compared with the other treatment groups.2
One proposed theory for the lipoprotein effects of beta blockers is that suppression of beta-adrenergic activity leads to unopposed alpha-adrenergic stimulation. In turn, alpha-adrenergic stimulation leads to a decrease in peripheral lipoprotein lipase activity and a subsequent reduction in catabolism of very low-density lipoprotein and triglycerides.3 Antagonism of peripheral beta-adrenergic receptors is much less with the cardioselective beta blockers, and lower doses of these agents have negligible effects on lipoprotein parameters. Thus, for patients who need a beta blocker, a cardioselective agent is preferred.3,4
It is important to remember that hypertension in patients with diabetes is often difficult to manage, and most patients require multiple medications to reach the blood pressure target of less than 130/80 mm Hg.4,5 Many times a beta blocker will need to be included as part of the antihypertensive regimen to achieve adequate blood pressure control. Current evidence-based guidelines for the management of hypertension in patients with diabetes do not mention concerns about lipoprotein changes with beta-blocker therapy, and continue to recommend beta blockers as an alternative treatment for hypertension in patients with diabetes.4,5 For this reason, we chose not to mention the lipoprotein effects of beta blockers in the article. However, we did address the more critical concern of the potential for beta blockers to blunt the signs of hypoglycemia and worsen glucose intolerance.
Controlling blood pressure is integral to reducing cardiovascular risk in patients with diabetes.4,5 Therefore, if it is a choice between adding a beta blocker to gain adequate control of blood pressure or avoiding beta blocker use to minimize the possibility of slight changes in the lipoproteins, the choice should be to use the beta blocker. The benefits of blood pressure control in patients with diabetes outweigh the relatively minor risk of alterations in the lipid profile with beta blocker use.