Recurrence of cardiovascular events from clopidegorel linked to genetic status
The recurrence risk of cardiovascular events and death following clopidogrel treatment is associated with CYP2C19 genetic status.
A number of recently published articles highlighted the importance of having a pharmacogenomic testing of CYP2C19 gene prior to clopidogrel treatment.
For clopidogrel to work, it requires CYP2C19 enzyme to convert it into its active metabolite which is responsible for the anti-platelet effect.
Individuals carrying certain common genetic variants that are associated with non-functional CYP2C19 gene have been shown to have reduced CYP2C19 enzyme function and do not effectively convert clopidogrel to its active metabolite compared to normal individuals. Consequently, clopidogrel has less effect on platelets and these individuals are at an increased risk of fatal or non-fatal cardiovascular events. This risk varies between 2 - 6 fold in different studies.
For individuals in this group, alternative medications may be suggested if testing for CYP2C19 gene is undertaken.
Meanwhile, other studies also have shown that individuals who carry increased function genes and are defined as ultrarapid metabolisers are at 4 times higher risk of bleeding from clopidogrel treatment. This is due to the increased conversion of clopidogrel to its active metabolite and therefore increased anti-platelet effect.
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