METOPROLOL SUCCINATE Drug Interactions
Also known as: Metoprolol Succinate
METOPROLOL SUCCINATE (brand name: Metoprolol Succinate) is a Beta-Blockers. 1 INDICATIONS & USAGE Metoprolol succinate extended-release tablets, metoprolol succinate, beta-adrenergic blocker indicated for the treatment of: • Hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and non-fatal cardiovascular events, primarily strokes and…METOPROLOL SUCCINATE has 7 documented drug interactions in our database, including 0 contraindicated, 3 major, 1 moderate, and 3 minor interactions.
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Contraindicated
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Major
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Moderate
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Minor
Fluoxetine, a potent CYP2D6 inhibitor, can significantly increase plasma concentrations of metoprolol, a CYP2D6-metabolized beta-blocker. This can lead to an increased risk of adverse effects such as severe bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is primarily responsible for the metabolism of metoprolol. This pharmacokinetic interaction reduces metoprolol clearance, leading to higher systemic exposure.
Clinical Management
Avoid co-administration if possible. If concomitant use is necessary, closely monitor heart rate, blood pressure, and for signs of beta-blocker toxicity (e.g., bradycardia, dizziness, fatigue). A significant reduction in metoprolol dosage may be required, or consider switching to a beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, bisoprolol, nadolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
Fluoxetine can significantly increase the plasma concentrations of metoprolol, a beta-blocker. This interaction can lead to severe bradycardia, hypotension, and potentially heart block, increasing the risk of adverse cardiovascular events.
Mechanism
Fluoxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Metoprolol is primarily metabolized by CYP2D6, so fluoxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure of metoprolol.
Clinical Management
Avoid concurrent use if possible. If co-administration is necessary, closely monitor the patient for signs of bradycardia, hypotension, and other beta-blocker adverse effects. A significant dose reduction of metoprolol may be required, or consider switching to a beta-blocker with minimal CYP2D6 metabolism (e.g., atenolol, bisoprolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
The co-administration of paroxetine with metoprolol can significantly increase metoprolol plasma concentrations, leading to enhanced beta-blockade effects. This interaction can result in severe bradycardia, hypotension, and heart block, posing a significant risk to the patient.
Mechanism
Paroxetine is a potent inhibitor of cytochrome P450 2D6 (CYP2D6), the primary enzyme responsible for the metabolism of metoprolol. Inhibition of CYP2D6 by paroxetine reduces metoprolol clearance, thereby increasing its systemic exposure and pharmacodynamic effects.
Clinical Management
Avoid concurrent use of paroxetine with metoprolol if possible. If co-administration is necessary, consider using an alternative beta-blocker that is not significantly metabolized by CYP2D6 (e.g., atenolol, bisoprolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram). If the combination is unavoidable, initiate metoprolol at a much lower dose with careful titration, or significantly reduce the current metoprolol dose, and closely monitor the patient for signs of bradycardia, hypotension, and other symptoms of excessive beta-blockade.
Citalopram is a weak inhibitor of CYP2D6, which is the primary enzyme metabolizing metoprolol. This interaction can lead to increased plasma concentrations of metoprolol, potentially enhancing its beta-blocking effects and increasing the risk of bradycardia and hypotension.
Mechanism
Citalopram weakly inhibits cytochrome P450 2D6 (CYP2D6). Metoprolol is extensively metabolized by CYP2D6, so citalopram can decrease metoprolol's metabolic clearance, leading to elevated systemic exposure.
Clinical Management
Monitor patients for signs and symptoms of excessive beta-blockade, such as bradycardia, hypotension, and dizziness, especially when initiating or adjusting citalopram dose. A metoprolol dose reduction may be necessary if adverse effects occur. Consider using an alternative antidepressant with negligible CYP2D6 inhibition if close monitoring is not feasible.
Sertraline is a weak inhibitor of CYP2D6, the primary enzyme metabolizing metoprolol. While a theoretical increase in metoprolol levels is possible, it is generally not considered clinically significant.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Sertraline has minimal inhibitory effects on CYP2D6, leading to a small potential for reduced metoprolol metabolism and increased plasma concentrations.
Clinical Management
Generally, no specific dose adjustments are required when co-administering metoprolol and sertraline. Monitor patients for expected therapeutic effects of metoprolol and for signs of excessive beta-blockade (e.g., bradycardia, hypotension), especially if initiating sertraline or increasing its dose in a patient already on metoprolol.
Escitalopram is a weak inhibitor of CYP2D6, the primary enzyme metabolizing metoprolol. Therefore, a clinically significant increase in metoprolol plasma levels is generally not expected, unlike with potent CYP2D6 inhibitors such as fluoxetine or paroxetine. However, additive pharmacodynamic effects on heart rate and blood pressure are theoretically possible.
Mechanism
Escitalopram is a weak inhibitor of cytochrome P450 2D6 (CYP2D6), which is the main metabolic pathway for metoprolol. While pharmacokinetic interactions are unlikely to be significant, both drugs can independently cause bradycardia, leading to a potential additive pharmacodynamic effect.
Clinical Management
Routine co-administration of metoprolol and escitalopram generally does not require specific dose adjustments or enhanced monitoring for pharmacokinetic interactions. However, clinicians should monitor patients for signs of excessive beta-blockade, such as bradycardia or hypotension, especially when initiating or titrating either medication.
Fluvoxamine is not a significant inhibitor of CYP2D6, the primary enzyme responsible for metoprolol metabolism. Therefore, a clinically significant pharmacokinetic interaction leading to increased metoprolol levels is unlikely.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, but not CYP2D6. Thus, fluvoxamine is not expected to significantly alter the metabolism or plasma concentrations of metoprolol.
Clinical Management
No specific dose adjustments for metoprolol are typically required when co-administered with fluvoxamine. However, as both drugs can independently affect heart rate, general monitoring for bradycardia or hypotension is prudent, especially in sensitive patients. If adverse effects occur, consider alternative SSRIs with minimal CYP inhibition or monitor metoprolol levels if clinically indicated.
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