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Published on: August 14, 2013
Effects of beta-blockers on glucose and lipid metabolism
1Tulane University School of Medicine, New Orleans, LA, USA. vfonseca@tulane.edu
Insights
Vasodilating beta-blockers improve glucose and lipid metabolism in hypertensive patients, unlike nonvasodilating types. This may reduce coronary artery disease risk in high-risk individuals.
Area of Science:
- Cardiology
- Pharmacology
- Metabolic Syndrome
Background:
- Sympathetic nervous system (SNS) activation is linked to hypertension.
- Beta-blockers lower blood pressure but raise concerns about metabolic side effects.
- Physicians hesitate to prescribe beta-blockers due to potential impacts on glycemic control and lipid profiles.
Purpose of the Study:
- Review hypertension pathophysiology and metabolic effects of beta-blockers.
- Compare glucose and lipid metabolism effects of vasodilating vs. nonvasodilating beta-blockers.
- Assess impact on cardiovascular morbidity and mortality.
Main Methods:
- Literature search of PubMed (1980-2008) for randomized, controlled trials (≥100 patients).
- Focused on effects of specific nonvasodilating (atenolol, metoprolol, propranolol) and vasodilating (carvedilol, labetalol, nebivolol) beta-blockers.
- Analyzed impact on glucose and lipid metabolism parameters in hypertensive patients.
Main Results:
- Beta-blockers exhibit varied effects on glucose and lipid metabolism.
- Nonvasodilating beta-blockers may worsen glycemic and lipid control.
- Vasodilating beta-blockers demonstrate more favorable metabolic profiles compared to nonvasodilating agents.
Conclusions:
- Vasodilating beta-blockers show improved glucose and lipid metabolism.
- These metabolic improvements may decrease coronary artery disease risk.
- Beneficial for high-risk hypertensive patients.
Background:
Activation of the sympathetic nervous system (SNS) has been linked to hypertension. Beta-blockers, which decrease SNS activation via beta-adrenergic receptor antagonism, are effective in lowering blood pressure and reducing cardiovascular morbidity and mortality in several conditions, including post-myocardial infarction and heart failure. Despite these clinical benefits, many physicians are reluctant to prescribe beta-blockers because of perceived negative metabolic effects, including reduced glycemic control, masking of hypoglycemia, insulin resistance, and dyslipidemia.
Objective:
This article reviews the pathophysiology of hypertension and either insulin resistance or dyslipidemia as well as treatment effects from glucose- and lipid-lowering regimens on cardiovascular morbidity and mortality. Based on a PubMed literature search from January 1980 to December 2008, the effects of nonvasodilating (atenolol, metoprolol, and propranolol) and vasodilating beta-blockers (carvedilol, labetalol, and nebivolol) on parameters of glucose and lipid metabolism in hypertension are presented. Preference for clinical trial inclusion was given to randomized, controlled trials with at least 100 patients. Limitations of a drug class literature review may include trial inclusion bias with associated result skewing and underrepresentation of an individual agent, which may give different results.
Results:
Beta-blockers differ in terms of their mechanism of action and their effects on glucose and lipid metabolism. Nonvasodilating beta-blockers reduce blood pressure in association with a cardiac output reduction and may increase or have no appreciable effect on peripheral vascular resistance. As a result, nonvasodilating beta-blockers are associated with a worsening of glycemic and lipidic control. In contrast, vasodilating beta-blockers reduce peripheral vascular resistance but have little or no effect on cardiac output. Numerous studies have established that vasodilating beta-blockers are associated with more favorable effects on glucose and lipid profiles than nonvasodilating beta-blockers.
Conclusions:
Improvements in glucose and lipid metabolism mediated by vasodilating beta-blockers may help reduce coronary artery disease risk among high-risk patients with hypertension.
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