Metoprolol (Dosage)

Metoprolol is a beta-blocker drug used in the treatment of cardiovascular diseases such as hypertension or acute myocardial infarction. However, the effect of these drugs may not be sufficient in some patients due to the presence of genetic variants in genes involved in their metabolization.

The β-blockers, such as metoprolol, are prescribed to reduce heart rate, blood pressure and contractility (heart strength), favoring cardiac diastole and thereby improving heart function and blood flow to the coronary arteries.

Metoprolol is used in the treatment of hypertension, angina pectoris and heart failure. Metoprolol selectively blocks β1-adrenergic receptors that are expressed mostly in cardiac tissue. Blockade of these receptors slows the heart rate and decreases the strength of muscle contractions. Metoprolol exerts its therapeutic action by reducing the impact of stimulation by catecholamines, hormones that are naturally produced by our body to maintain cardiac activity, but which, if exceeded, can lead to a reduction in the force of muscle contractions.However, if their action time is exceeded, they can cause damage such as an exaggerated increase in heart rate and hypertrophy of the myocytes (the contractile cells of the heart).



2nd and 3rd degree atrioventricular block, decompensated heart failure (pulmonary edema, hypoperfusion or hypotension), continuous or intermittent inotropic treatment that acts by antagonism with ß-adrenergic receptors; bradycardia, bradycardia and hypertension.rgic receptors; sinus bradycardia; sick sinus syndrome, cardiogenic shock, severe peripheral arterial disorder, myocardial infarction with heart rate < 45 bpm, a cardiac interval PQ>0.24 seconds or systolic pressure <100 mm Hg.


Severe hepatic insufficiency, asthma, heart failure, pheochromocytoma (administered together with an alpha blocker).

May aggravate symptoms of peripheral arterial circulatory disorders and rarely aggravate pre-existing moderate atrioventricular conduction disorders. If aggravation of bradycardia occurs, administer lower doses or gradually discontinue treatment.

Risk of coronary events during ß-blocker withdrawal, so cardiac monitoring is required.


Bradycardia, postural hypotension, cold hands and feet, palpitations, tiredness, headache, nausea, abdominal pain, diarrhea, constipation and dyspnea on exertion.


In association with clonidine, if it is necessary to discontinue treatment, first discontinue the ß-blocker several days before.

Metoprolol potentiates the negative inotropic and negative dromotropic effect of quinidine and amiodarone.

Cardiopressor effect increased with inhaled anesthetics.

The plasma concentration of metoprolol is decreased by concomitant treatment with rifampicin.

The plasma concentration of metoprolol may be increased by concomitant treatment with cimetidine.

The effect of metoprolol is reduced by indomethacin.

Metoprolol modifies glucose concentration in diabetics treated with hypoglycemic agents.

Metoprolol increases the toxicity of lidocaine.


  • Beloken ®
  • Lopressor ®

Genes analyzed



Collett S, Massmann A, Petry NJ, et al . Metoprolol and CYP2D6: A Retrospective Cohort Study Evaluating Genotype-Based Outcomes. J Pers Med. 2023 Feb 26;13(3):416.

Dean L. Metoprolol Therapy and CYP2D6 Genotype. 2017 Apr 4. In: Pratt VM, Scott SA, Pirmohamed M, Esquivel B, Kattman BL, Malheiro AJ, editors. Medical Genetics Summaries [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2012-.

Lymperopoulos A, McCrink KA, Brill A . Impact of CYP2D6 Genetic Variation on the Response of the Cardiovascular Patient to Carvedilol and Metoprolol. Curr Drug Metab. 2015;17(1):30-6.

Thomas CD, Johnson JA. Pharmacogenetic factors affecting β-blocker metabolism and response. Expert Opin Drug Metab Toxicol. 2020 Oct;16(10):953-964.

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