METOPROLOL TARTRATE Drug Interactions
Also known as: METOPROLOL TARTRATE
Metoprolol Tartrate is a beta-blocker medication used to treat high blood pressure, chest pain (angina), and to improve outcomes after a heart attack. It works by relaxing blood vessels and slowing the heart rate, which helps to lower blood pressure and reduce the heart's workload.METOPROLOL TARTRATE has 10 documented drug interactions in our database, including 1 contraindicated, 3 major, 4 moderate, and 2 minor interactions.
1
Contraindicated
3
Major
4
Moderate
2
Minor
Combining a beta-blocker with verapamil can cause severe bradycardia, heart block, and cardiac arrest.
Mechanism
Both drugs independently slow AV node conduction. Combined use produces additive negative chronotropic and dromotropic effects.
Clinical Management
Contraindicated in most patients. If absolutely necessary, use only in a monitored setting with extreme caution.
Combining metoprolol and carvedilol, both beta-blockers, can lead to an additive effect, significantly increasing the risk of bradycardia, hypotension, and heart failure exacerbation. This combination is generally not recommended due to the heightened risk of adverse cardiovascular events.
Mechanism
Both metoprolol and carvedilol exert their primary therapeutic effects by blocking beta-adrenergic receptors, leading to decreased heart rate, myocardial contractility, and blood pressure. Their co-administration results in an enhanced pharmacodynamic effect, increasing the likelihood of profound beta-blockade.
Clinical Management
This combination should generally be avoided. If a patient requires more intensive beta-blockade, consider optimizing the dose of a single beta-blocker or exploring alternative drug classes. If co-administration is deemed absolutely necessary, close monitoring for bradycardia, hypotension, and signs of heart failure is crucial, and dosage adjustments of both agents may be required.
Fluoxetine is a potent inhibitor of CYP2D6, which is the primary enzyme responsible for the metabolism of metoprolol. This interaction can significantly increase metoprolol plasma concentrations, potentially leading to enhanced beta-blockade effects such as severe bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, thereby reducing the metabolic clearance of metoprolol, a substrate of CYP2D6. This pharmacokinetic interaction leads to elevated systemic exposure to metoprolol.
Clinical Management
If concomitant use is unavoidable, consider using an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or an alternative beta-blocker primarily cleared renally (e.g., atenolol, nadolol). If metoprolol and fluoxetine are co-administered, closely monitor the patient for signs and symptoms of excessive beta-blockade (e.g., bradycardia, hypotension, dizziness) and reduce the metoprolol dose as necessary.
The coadministration of metoprolol and paroxetine can lead to a significant increase in metoprolol plasma concentrations. This interaction can result in enhanced beta-blockade effects, potentially causing severe bradycardia, hypotension, or heart block, which may be life-threatening.
Mechanism
Paroxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Metoprolol is primarily metabolized by CYP2D6, so paroxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure of metoprolol.
Clinical Management
Avoid concurrent use if possible. If coadministration is necessary, closely monitor the patient for signs of bradycardia, hypotension, and heart block. A significant reduction in the metoprolol dose 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).
SSRIs can increase metoprolol plasma levels by inhibiting CYP2D6, potentially causing excessive beta-blockade.
Mechanism
Sertraline moderately inhibits CYP2D6, which is the primary metabolic pathway for metoprolol, increasing metoprolol AUC by 30–100%.
Clinical Management
Monitor for signs of excessive beta-blockade (bradycardia, fatigue, dizziness). Consider dose reduction of metoprolol.
Combining atenolol and metoprolol tartrate, both beta-blockers, can lead to additive pharmacodynamic effects. This increases the risk of excessive bradycardia, hypotension, and potentially heart block or exacerbation of heart failure symptoms. Patients may experience dizziness, fatigue, or syncope.
Mechanism
Both atenolol and metoprolol tartrate are beta-1 selective adrenergic receptor antagonists. When administered concurrently, their individual beta-blocking effects on the heart are additive, leading to a synergistic reduction in heart rate and blood pressure.
Clinical Management
Concurrent use of two beta-blockers is generally not recommended due to the increased risk of adverse effects without significant additional therapeutic benefit. If combination therapy is deemed necessary, close monitoring of heart rate, blood pressure, and cardiac function is essential. Dosage adjustments of one or both agents may be required, or an alternative antihypertensive or antiarrhythmic agent should be considered.
Fluoxetine significantly increases metoprolol plasma levels through CYP2D6 inhibition, increasing the risk of bradycardia and heart block.
Mechanism
Fluoxetine is a potent CYP2D6 inhibitor. Metoprolol is primarily metabolized by CYP2D6; inhibition increases metoprolol AUC by 3–5 fold.
Clinical Management
Monitor heart rate and blood pressure. Reduce metoprolol dose if bradycardia occurs. Consider using atenolol (not CYP2D6 substrate) as an alternative.
Coadministration of fluvoxamine with metoprolol may increase metoprolol plasma concentrations, leading to enhanced beta-blockade effects such as bradycardia, hypotension, and heart block. While fluvoxamine is primarily a CYP1A2 and CYP2C19 inhibitor, metoprolol is mainly metabolized by CYP2D6, suggesting a lower risk of significant pharmacokinetic interaction than with potent CYP2D6 inhibitors. However, both drugs can independently cause bradycardia, and additive pharmacodynamic effects are possible.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, and a moderate inhibitor of CYP2D6. Inhibition of metoprolol's metabolism by fluvoxamine's CYP2D6 inhibitory activity, even if moderate, can increase metoprolol plasma levels. Additionally, both drugs can cause bradycardia, leading to potential additive pharmacodynamic effects.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluvoxamine or metoprolol doses. Consider using the lowest effective dose of metoprolol or choosing an alternative beta-blocker with minimal CYP2D6 metabolism (e.g., atenolol, nadolol) if close monitoring is not feasible or if adverse effects occur. Dose reduction of metoprolol may be necessary.
Citalopram is not a significant inhibitor of CYP2D6, the primary enzyme metabolizing metoprolol. Therefore, a clinically significant pharmacokinetic interaction leading to increased metoprolol levels is unlikely. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible, though rarely clinically significant.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Citalopram is a weak or negligible inhibitor of CYP2D6, minimizing pharmacokinetic interaction. Both metoprolol (beta-blocker) and citalopram (SSRI) can cause bradycardia, suggesting a potential additive pharmacodynamic effect.
Clinical Management
Generally, no specific dose adjustment or enhanced monitoring is required for this combination due to the low interaction potential. However, clinicians should remain vigilant for signs of excessive bradycardia, especially in patients with pre-existing cardiac conditions or those on higher doses of metoprolol. If bradycardia occurs, consider assessing contributing factors.
Escitalopram has minimal inhibitory effects on CYP2D6, the primary enzyme metabolizing metoprolol. Therefore, a clinically significant pharmacokinetic interaction leading to increased metoprolol levels is unlikely. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Escitalopram is a weak or negligible inhibitor of CYP2D6, suggesting minimal pharmacokinetic impact on metoprolol clearance. Both metoprolol (beta-blocker) and escitalopram (SSRI, which can affect heart rate) can cause bradycardia through different pharmacodynamic pathways.
Clinical Management
Routine co-administration generally does not require specific dose adjustments. Monitor patients for signs of excessive bradycardia or hypotension, especially if they are sensitive to either medication or have pre-existing cardiac conditions. If bradycardia occurs, consider dose reduction of either agent or an alternative antidepressant with no CYP2D6 interaction.
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