β-blockers, once regarded as a mainstay for patients recovering from heart attacks, may not be as universally necessary or safe for all individuals as previously thought. Recent research out of Sweden indicates that these medications could heighten the risk of depression in heart attack survivors who maintain normal heart pumping function following their incident.
“At the same time, beta blockers have no life-sustaining function for this group of patients,” emphasized Philip Leissner, lead author of the study and a doctoral student in cardiac psychology at Uppsala University, in a news release. This revelation challenges a long-standing tradition in cardiology that routinely prescribed β-blockers to heart attack patients in a bid to reduce the likelihood of subsequent cardiac events.
As part of the REDUCE-AMI trial, this study, recently published in the European Heart Journal, casts a new light on the decades-old protocol. Historically, β-blockers have been prescribed universally to heart attack survivors, often resulting in a lifetime of medication. However, evidence is now suggesting that for those who do not experience heart failure post-attack, the ongoing use of β-blockers may correlate with an increase in depressive symptoms.
The study examined over 800 heart attack survivors who did not have heart failure, systematically dividing them into two groups: one receiving β-blockers, either metoprolol or bisoprolol, and the other group not receiving the medication. While hospitalized, those in the β-blocker cohort were started on either metoprolol or bisoprolol, with guidelines recommending a continuation of these medications following discharge. Physicians were encouraged to prescribe a minimum daily dosage of 100 mg of metoprolol or 5 mg of bisoprolol. The researchers monitored psychological outcomes over a duration of five years by utilizing the Hospital Anxiety and Depression Scale.
The researchers also explored the impact of β-blockers on anxiety, yet found no significant variations among the 27% of patients exhibiting anxiety symptoms at the start of the study.
One of the suggested reasons for the uptick in depressive symptoms relates to the medication’s interaction with neurotransmitters, which could subsequently influence the autonomous nervous system, guided by factors such as liposolubility and cardioselectivity. Furthermore, β-blockers may lead to reduced patient engagement in enjoyable pursuits, giving rise to symptoms of anhedonia—a prominent indicator of depression as measured by the Hospital Anxiety and Depression Scale.
Previous investigations have hinted at a correlation between these medications and mood disorders, including but not limited to depression, insomnia, and disturbing dreams. The recent findings bolster these concerns and suggest that the risk of developing depression could vary with dosage. Specifically, patients who had been using β-blockers prior to enrolling in the study exhibited even greater elevations in depressive symptoms, indicating a potential cumulative effect over time.
“Most doctors used to give beta blockers even to patients without heart failure, but as the evidence in favor of doing so is no longer so strong, this should be reconsidered,” Leissner asserted. “We could see that some of these patients appear to be more at risk of depression. If the drug doesn’t make a difference to their heart, then they are taking it unnecessarily and at risk of becoming depressed.”
A significant limitation of the study resides in the potential for baseline bias, as psychological assessments were taken post-treatment assignment. Selection bias may also have been introduced due to the exclusion of various eligible patients; the sample studied was generally healthier than the typical population affected by heart attacks. Moreover, utilizing the Hospital Anxiety and Depression Scale limited the evaluation to specific symptoms of depression and anxiety, potentially overlooking wider psychological effects.
References
- Leissner P, Mars K, Humphries S, et al. Short- and long-term effects of beta-blockers on symptoms of anxiety and depression in patients with myocardial infarction and preserved left ventricular function: a pre-specified quality of life sub-study from the REDUCE-AMI trial. Eur Heart J Acute Cardiovasc Care. Published online October 3, 2024. doi:10.1093/ehjacc/zuae112
- Patients may become unnecessarily depressed by common heart medicine. News release. Uppsala University. November 11, 2024. Accessed November 12, 2024. https://www.uu.se/en/press/press-releases/2024/2024-11-11-patients-may-become-unnecessarily-depressed-by-common-heart-medicine
- Watch: What are beta blockers and what do they do in your body? British Heart Foundation. Accessed November 12, 2024.
**Interview with Philip Leissner on the Risks of β-blockers in Heart Attack Survivors**
**Editor:** We’re joined today by Philip Leissner, lead author of a recent study from Uppsala University that challenges the traditional prescribing of β-blockers for heart attack survivors. Philip, thank you for being here with us.
**Philip Leissner:** Thank you for having me.
**Editor:** Your research suggests that β-blockers may not be as beneficial for all heart attack survivors as previously believed, particularly those who maintain normal heart function. Can you explain the key findings of your study?
**Philip Leissner:** Certainly. Our study examined over 800 heart attack survivors without heart failure and split them into two groups: one received β-blockers and the other did not. We found that the patients on β-blockers, despite having normal heart function, showed a significant increase in depressive symptoms over five years. This raises questions about the necessity of these medications for this specific group of patients.
**Editor:** That’s an eye-opening discovery. You mention in the study that β-blockers have no life-sustaining function for those with normal heart function. What implications does this have for current medical practices?
**Philip Leissner:** It suggests that we may need to reevaluate our approach. For years, the standard protocol was to prescribe β-blockers to all heart attack survivors. However, our findings indicate that this practice should be reconsidered, especially for those not at risk of heart failure, as the potential for increased depressive symptoms may outweigh the benefits.
**Editor:** Your research highlights a link between β-blockers and depressive symptoms. Can you elaborate on why this connection might exist?
**Philip Leissner:** One theory is that β-blockers affect neurotransmitters that play a role in mood regulation, thus influencing the autonomous nervous system. Additionally, by diminishing a patient’s engagement in enjoyable activities—often referred to as anhedonia—we may see an increase in depressive symptoms. Our study aligns with previous findings that suggest a broader relationship between these medications and mood disorders.
**Editor:** Were there any differences in psychological outcomes related to anxiety among the participants?
**Philip Leissner:** Interestingly, while we did explore the anxiety levels of patients, our results didn’t show significant differences in those exhibiting anxiety symptoms at the outset. This indicates that the relationship between β-blockers and mood disturbances may be more pronounced for depression rather than anxiety.
**Editor:** As a conclusion to our discussion, what steps do you think should be taken moving forward for doctors managing heart attack patients?
**Philip Leissner:** I believe it’s crucial for healthcare providers to critically assess whether β-blockers are necessary for each patient, particularly those without heart failure. More personalized approaches to treatment are essential, taking into account a patient’s overall mental health in addition to their physical condition.
**Editor:** Thank you, Philip, for sharing these important insights with us today. This research could potentially reshape the standard of care for heart attack survivors.
**Philip Leissner:** Thank you for having me. I hope it encourages more dialogue and research in this crucial area.
