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Adrenergic hypersensitivity after beta-blocker withdrawal.

P J Ross, M J Lewis, D J Sheridan

    British Heart Journal
    |June 1, 1981
    PubMed
    Summary
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    Stopping beta-blocker medication for over a week can cause a significant rebound increase in heart rate. This sympathetic response rebound was not observed after short-term, four-day treatment.

    Area of Science:

    • Cardiovascular pharmacology
    • Autonomic nervous system function

    Background:

    • Beta-blockers are widely used to manage cardiovascular conditions.
    • Abrupt cessation of beta-blocker therapy may lead to adverse effects.
    • The potential for rebound sympathetic hyperactivity after beta-blocker withdrawal requires investigation.

    Purpose of the Study:

    • To determine if stopping beta-blocker treatment leads to a rebound increase in sympathetic response.
    • To assess the duration of beta-blocker treatment required to elicit a significant rebound effect.
    • To compare the magnitude of rebound heart rate increase across different beta-blockers and in specific patient populations.

    Main Methods:

    • Heart rate was measured under conditions of increased sympathetic drive (standing with vasodilatation, Valsalva maneuver).

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  • Beta-blocker treatment duration was varied (four days vs. one or more weeks).
  • Rebound heart rate was compared to control heart rate off beta-blockers.

    • Main Results:

    • Significant rebound increases in heart rate were observed after beta-blocker treatment for one or more weeks.
    • No significant rebound heart rate increase was noted after only four days of beta-blocker treatment.
    • The amplitude of rebound heart rate was comparable across propranolol, atenolol, oxprenolol, and acebutolol, and in hyperthyroid subjects.

    Conclusions:

    • Prolonged beta-blocker treatment (≥1 week) can result in a rebound sympathetic response upon cessation.
    • Short-term beta-blocker use (4 days) does not appear to cause a significant rebound effect.
    • The rebound phenomenon is consistent across various beta-blockers and is also observed in hyperthyroid individuals.