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Author: Brent N. Reed, PharmD, BCPS-AQ Cardiology, FAHA

When I originally wrote this piece in 2013, I was compelled to do so after encountering my third patient in as many weeks who had to be hospitalized for symptomatic bradycardia — all secondary to the accumulation of atenolol in the setting of renal impairment.  While we were able to avoid the placement of a permanent pacemaker in two of these patients, the third had underlying conduction abnormalities that were revealed by the beta blocker overdose. Given the many agents available in this class, I continue to be surprised by the number of patients who are prescribed atenolol today. I hope to make a case here for why the drug should be avoided altogether.

Of the beta blockers, atenolol is the most dependent on renal clearance — nearly 50% of the drug is eliminated by the kidneys, making it problematic in patients with mild to moderate renal impairment. The risks are further compounded in older patients, where renal function is less predictable and only deteriorates with time.

There are some theoretical advantages of atenolol, which may explain why its use remains so prevalent, but these characteristics rarely translate into clinically meaningful differences in everyday practice. For example, the purported duration of beta blockade with atenolol is 24 hours, making once-daily dosing an attractive option compared to other beta blockers. However, its effects on heart rate and blood pressure do not often last the full day, and this variability may help explain the increased risk of stroke observed when atenolol is compared to other anti-hypertensive therapies (1). Some clinicians feel atenolol has greater anti-hypertensive effects compared to other beta blockers, but given the limited effects of the class overall (and poorer outcomes in certain subgroups), they have largely fallen out of favor in guidelines for the management of high blood pressure (2). Besides, for patients with compelling indications for beta blockade (e.g., myocardial infarction, heart failure), there are a myriad of other therapies that can be added to beta blocker therapy to assist with blood pressure control (e.g., ACE inhibitors, angiotensin II receptor blockers) rather than switching to atenolol. In fact, many of these drugs exert their benefits independently of their effects on blood pressure.

Otherwise, the evidence to support atenolol in patients who have had a myocardial infarction is no better than other beta blockers (3, 4), and many of these alternatives are better supported in other common comorbid conditions (e.g., metoprolol succinate in patients with heart failure) (5). Although the twice daily dosing strategy is a disadvantage of many beta blockers, there are numerous agents in the class that can be dosed once per day (e.g., metoprolol succinate, bisoprolol, carvedilol controlled-release, nebivolol). For patients requiring multiple doses per day, pharmacists can be especially helpful in identifying strategies to integrate these regimens into patients’ routines.

In summary, there is minimal, if any, evidence to support the use of atenolol over other beta blockers, and this is likely true in any clinical scenario where a beta blocker is indicated. Moreover, given its risk for accumulation and subsequent toxicity in specific patient populations (e.g., older patients, those with renal impairment), the disadvantages of atenolol far outweigh its purported benefits, which are largely theoretical at best.

P.S., If you’d like to change your patient to a different beta blocker, atenolol 50 mg once daily is approximately equal to metoprolol tartrate 50 mg twice daily or metoprolol succinate 100 mg once daily.

Brent N. Reed, PharmD, BCPS-AQ Cardiology, FAHA

Dr. Reed is an associate professor in the Department of Pharmacy Practice and Science at the University of Maryland School of Pharmacy, and practices as a clinical pharmacy specialist in advanced heart failure at the University of Maryland Medical Center in Baltimore, MD. Follow him on his website or on Twitter @brentnreed.

Note: the above entry initially appeared on Reed’s personal blog The Unit in 2013.


  1. Rothwell PM, Howard SC, Dolan E, et al; ASCOT-BPLA and MRC Trial Investigators. Effects of beta blockers and calcium-channel blockers on within-individual variability in blood pressure and risk of stroke. Lancet Neurol. 2010 May;9(5):469-80.
  2. James PA, Oparil S, Carter BL, et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507.
  3. First International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous atenolol among 16 027 cases of suspected acute myocardial infarction: ISIS-1.  Lancet. 1986 Jul 12;2(8498):57-66.
  4. Turi ZG, Braunwald E. The use of beta-blockers after myocardial infarction. JAMA. 1983 May 13;249(18):2512-6.
  5. MERIT-HF Investigators. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) Lancet. 1999 Jun 12;353(9169):2001-7.
Avoiding Atenolol

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2 thoughts on “Avoiding Atenolol

  • July 2, 2018 at 4:10 pm

    Dear Dr Reed,

    Recent Medical reports have indicated that besides atenolol, bisoprolol could be a molecule
    inducing atrial fibrillation in young patients with normal heart. Do you have ideas how to repalce the combo; flecainide plus a beta blocker, in order to avoid induction of AF.
    Thank you
    J. Gogusev M.D.

    • July 2, 2018 at 7:43 pm

      Dr. Gogusev,

      Could you please share those reports with us? Bisoprolol is not as commonly used in the US but it would be a reasonable choice for controlling ventricular rate in a patient with atrial fibrillation. However, it would be unusual for bisoprolol to cause/induce atrial fibrillation. I’d be happy to look at the literature you have on this phenomenon.



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