Key result
Intermediate and poor CYP2D6 metabolizers had 2.1- to 4.6-fold greater plasma metoprolol concentrations compared to extensive metabolizers during early titration (P<0.0001).
Why the study?
Does CYP2D6 genotype modulate the pharmacokinetic and pharmacodynamic response to metoprolol CR/XL during dose titration in patients with systolic heart failure?
RCT (n=605)
Does CYP2D6 genotype modulate the pharmacokinetic and pharmacodynamic response to metoprolol CR/XL during dose titration in patients with systolic heart failure?
Effect estimate: 2.1-/4.6-fold greater
p-value: p=<0.0001
Although CYP2D6 genotype modulates metoprolol pharmacokinetics and pharmacodynamics during early titration in heart failure patients, the standard titration schedule remains recommended for all patients.
No takes yet. Share an insight, caveat, or question.
CYP2D6 genotyping should not yet alter metoprolol titration in systolic HF; leaves open whether genotype-guided dosing improves outcomes.
Batty et al. (2013) conducted an RCT in Systolic heart failure (n=605). Metoprolol CR/XL (intermediate or poor CYP2D6 metabolizers) vs. Metoprolol CR/XL (extensive CYP2D6 metabolizers) was evaluated on Plasma metoprolol concentrations (2.1-/4.6-fold greater, p=<0.0001). Intermediate and poor CYP2D6 metabolizers had 2.1- to 4.6-fold greater plasma metoprolol concentrations compared to extensive metabolizers during early titration (P<0.0001).
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