Beta blockers are first-line therapy in the control of symptoms in patients with chronic stable angina, particularly effort-induced angina. They are recommended for use in such patients in guidelines from the American College of Cardiology Foundation/American Heart Association/American College of Physicians/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society for Cardiovascular Angiography and Interventions/Society of Thoracic Surgeons (ACCF/AHA/ACP/AATS/PCNA/SCAI/STS) and from the European Society of Cardiology [1-3].
The major issues regarding the use of beta blockers in the medical management of the patient with stable angina and the evidence that these drugs are effective will be reviewed here. Their role, compared with other drugs, in the overall management of angina is discussed separately. (See "Overview of the care of patients with stable ischemic heart disease".)
MECHANISM OF ACTION
The physiologic effects of catecholamines (norepinephrine and epinephrine) are mediated by activation of specific alpha and beta adrenergic receptors. There are at least three distinct types of beta receptors [4-6]:
- Beta-1, which are found primarily in heart muscle. Activation of these receptors results in increases in heart rate, contractility, and atrioventricular (AV) conduction, and a decrease in AV node refractoriness.
- Beta-2, which are present in heart muscle but are more prominent in bronchial and peripheral vascular smooth muscle. Activation of these receptors results in vasodilatation and bronchodilatation.
- Beta-3, which are found in adipose tissue and the heart. Activation of these receptors may mediate catecholamine-induced thermogenesis and may reduce cardiac contractility [5,6].
Beta blockers act by competitively inhibiting catecholamines from binding to these receptors. Some are more selective for the beta-1 receptor. (See 'Cardioselectivity' below.)