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Do Beta Blockers Cause Depression?

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Do Beta Blockers Cause Depression? Medicine in Brief Do beta blockers cause depression? Andrew J. Muzyk, PharmD, and Jane P. Gagliardi, MD Principal Source: van Melle JP, Verbeek DEP, van den Berg ever, these reviews had major limitations, MP, et al. Beta-blockers and depression after myocardial such as inadequately defined methods for infarction: a multicenter prospective study. J Am Coll Cardiol. 2006;48(11):2209-2214. defining depression and lack of control for potential confounding factors. Mechanistically, peripheral effects of eyond their well-known role for treat- beta blockers on the heart and kidneys Bing cardiovascular disease, beta adren- lead to decreased chronotropy and inotro- Robert M. McCarron, DO ergic receptor antagonists—beta block- py as well as lower blood pressure. These Series Editor ers—are used for a variety of medical cardiovascular and hemodynamic changes conditions, including coronary artery dis- could cause fatigue, decreased energy, and ease, hypertension, migraines, and tremor. sexual dysfunction that may be interpreted Their usefulness makes them 1 of the most as symptoms of new-onset depression. commonly prescribed medication classes. Researchers found that beta-blocker Unfortunately, their increased use comes use was not associated with depression with increased reports of depression. Be- in a case-control study examining 4,302 ing able to sort fact from fiction will help New Jersey Medicaid records.3 Also, be- guide your care for patients taking beta cause most patients in this study received blockers who report new or worsening de- propranolol, the authors were unable to pressive symptoms. confirm a long-held belief that highly lipo- philic beta blockers (such as propranolol, Does research support a link? First reported in the 1960s, beta blocker- Practice Points induced depression was thought to re- • Although patients with cardiovascular sult from the drugs’ antagonistic effect on disease are at increased risk for developing norepinephrine at ß1 post-synaptic brain depression, there is no convincing receptors. Prompted by case reports of a evidence that adding beta blockers will further increase their risk. possible association between beta block- ers and depression, 2 prescription data- • Initiating beta-blocker therapy at the base reviews found that patients taking lowest possible dose and slowly titrating the dose over time could minimize adverse beta blockers were more likely to receive effects such as fatigue and sexual side a concurrent antidepressant prescription effects. than patients prescribed other cardiovas- cular and diabetic medications.1,2 How- • If a patient taking beta blockers develops signs of major depression, carefully evaluate and treat symptoms with Dr. Muzyk is a clinical pharmacist, Duke University Medical Center, and Dr. Galiardi is assistant professor of psychiatry appropriate psychotherapy, psychotropics, Current Psychiatry and behavioral sciences and assistant clinical professor of and monitoring. 50 May 2010 medicine, Duke University School of Medicine, Durham, NC. Medicine in Brief Table Beta blockers and depression: Is there a link? Study Methods Results Bright et al, Case-control study of 4,302 Beta-blocker use was not associated 19923 patients with new-onset depression with depression after controlling for confounding factors, although depressed patients were more likely to receive beta blockers van Melle et al, A prospective study of post- No significant differences in depressive 20064 myocardial infarction patients; 254 symptoms or incidence of depressive taking beta blockers, 127 controls disorder between beta-blocker users and nonusers Gerstman et al, New users of propranolol (n=704) Depression occurred no more frequently 19965 other beta blockers (n=587), among beta-blocker users than other angiotensin-converting enzyme subjects inhibitors (n=976), calcium channel blockers (n=742), and diuretics (n=773) Clinical Point Ko et al, 20026 Quantitative review of randomized Beta-blocker therapy was not associated trials that tested beta blockers in with a significant absolute annual increase Studies show no myocardial infarction, heart failure, in risk of depressive symptoms (6 per and hypertension 1,000 patients; 95% confidence interval, significant difference -7 to 19) in incidence of depression between metoprolol, and timolol) are more likely • indicators and risk factors for cardiac patients who received than hydrophilic beta blockers such as disease beta blockers and atenolol to produce depression. • baseline depressive symptoms A retrospective cohort study analyzed • benzodiazepine use. those who did not 381 patients from 2 myocardial infarc- In fact, after controlling for baseline de- tion (MI) trials who had been assessed pression, researchers found that beta-block- for depressive symptoms and severity.4 er users demonstrated significantly lower Researchers matched 254 subjects taking BDI scores 3 months post-MI than nonus- beta blockers during hospitalization for MI ers. Based on these results, the authors con- with 127 subjects not taking beta blockers. cluded that clinicians should not be deterred Patients in the study were well balanced on from prescribing beta blockers because the multiple baseline characteristics, including drugs’ benefit in reducing morbidity and demographics, history of depression, and mortality in cardiovascular disease greatly left ventricular ejection fraction, although outweighs the risk—if any—of new-onset those who did not take beta blockers had depression associated with beta-blocker use. a significantly higher incidence of chronic Two additional studies reported no sig- obstructive pulmonary disease, digoxin nificant difference in the incidence of de- use, and pre-MI beta-blocker use. Re- pression between patients who received searchers assessed depressive symptoms beta blockers and those who received other using the Beck Depression Inventory (BDI) antihypertensives or placebo.5,6 Future stud- at baseline and 3, 6, and 12 months post-MI ies assessing depression among subjects ran- and identified patients with depression us- domized to beta blockers vs placebo would ing a Composite International Diagnostic be helpful, though withholding beta block- Interview. They found no statistically sig- ers in some cardiac conditions is not justifi- nificant difference in BDI scores between able, and such studies may not be feasible. beta-blockers users and nonusers at dis- charge and at 3, 6, and 12 months post-MI after accounting for potential confounding Treatment for psychiatric patients factors, including: Evidence supports beta-blocker use in • contraindications for beta-blocker use coronary artery disease and congestive Current Psychiatry (other than history of depression) heart failure. Although patients with these Vol. 9, No. 5 51 continued on page 55 13209a5.qxd:A Size Spread 12/7/09 7:51 AM Page 3 Medicine in Brief continued from page 51 dose-dependent increase in the proportion of patients who developed sustained hypertension. Abnormal Bleeding- voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or SSRIs and SNRIs can increase the risk of bleeding events. Concomitant use of aspirin, other drugs that affect establish a causal relationship to drug exposure: Skin and subcutaneous tissue disorders – Angioedema. DRUG Related Resources platelet function, nonsteroidal anti-inflammatory drugs, warfarin, and other anticoagulants can add to this risk. INTERACTIONS: Central Nervous System (CNS)-Active Agents-The risk of using Pristiq in combination with • Rivelli S, Jiang W. Depression and ischemic heart disease: what have we Extended-Release Tablets Bleeding events related to SSRIs and SNRIs have ranged from ecchymosis, hematoma, epistaxis, and petechiae to other CNS-active drugs has not been systematically evaluated. Consequently, caution is advised when Pristiq is BRIEF SUMMARY. See package insert for full Prescribing Information. For further product information and life-threatening hemorrhages. Patients should be cautioned about the risk of bleeding associated with the taken in combination with other CNS-active drugs [see Warnings and Precautions (5.13)]. Monoamine Oxidase learned from clinical trials? Curr Opin Cardiol. 2007;22(4):286-291. current package insert, please visit www.wyeth.com or call our medical communications department toll-free concomitant use of Pristiq and NSAIDs, aspirin, or other drugs that affect coagulation or bleeding. Narrow-angle Inhibitors (MAOIs)- Adverse reactions, some of which were serious, have been reported in patients who have at 1-800-934-5556. Glaucoma-Mydriasis has been reported in association with Pristiq; therefore, patients with raised intraocular recently been discontinued from a monoamine oxidase inhibitor (MAOI) and started on antidepressants with • National guideline clearinghouse. Secondary prevention of coronary pressure or those at risk of acute narrow-angle glaucoma (angle-closure glaucoma) should be monitored. pharmacological properties similar to Pristiq (SNRIs or SSRIs), or who have recently had SNRI or SSRI therapy WARNING: Suicidality and Antidepressant Drugs Activation of Mania/Hypomania-During all MDD and VMS (vasomotor symptoms) phase 2 and phase 3 studies, discontinued prior to initiation of an MAOI [see Contraindications (4.2)]. Serotonergic Drugs- Based on the artery disease. www.guideline.gov/summary/summary.aspx?docid=14585. Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in
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