Letter to the Editors

Statins do not affect platelet inhibition with clopidogrel during coronary stenting

Patients presenting for invasive cardiovascular procedures are frequently taking a variety of medications aimed to treat risk factors related to heart and vascular disease. During the procedure, antithrombotic, sedative, and analgesic medications are commonly needed, and after interventional procedures, new medications are often added for primary and secondary prevention of ischemic events. In addition to these prescribed medications, the use of over-the-counter drugs and supplements continues to rise. Most elderly patients, for example, are taking 5 or more prescribed medications and 1 or more supplements, and they often have some degree of renal insufficiency. This polypharmacy might result in drug–drug interactions that affect the balance of thrombotic and bleeding events during the procedure and during long-term treatment. Mixing of anticoagulants, for instance, might lead to periprocedural bleeding, and this is associated with an increase in long-term adverse events. Furthermore, the range of possible interactions with thienopyridine antiplatelets is of concern, because these drugs are essential to immediate and extended interventional success. The practical challenges in the field are great—some drug–drug interactions are likely present yet not well understood due to limited assays, whereas other interactions have well-described biological effects but seem to be more theoretical, because there is little to no clinical impact. Interventional providers need to be attentive to the potential for drug–drug interaction, the associated harm, and the appropriate action, if any, to minimize the potential for medication-related adverse events. This review will focus on drug–drug interactions that have the potential to affect procedural success, either through increases in immediate complications or compromising longer-term outcome.

Clopidogrel resistance has been used as one of the terms employed in the literature to describe different degrees of ex vivo low platelet inhibition after clopidogrel administration. In addition to the diverse nomenclature, the characterisation of clopidogrel resistance has also been problematic because different authors have given different definitions. The mechanisms responsible for this decreased platelet response are not yet clearly defined, some hypotheses have been put forward but not yet demonstrated.

Although there have been no large prospective studies demonstrating that the degree of platelet inhibition is directly related to clinical outcomes, several recent studies and reports have shown an association between less platelet inhibition and more adverse events after percutaneous coronary interventions with clopidogrel therapy suggesting that clopidogrel resistance may be a marker for increased risk of recurrent cardiovascular events. Larger scale investigations are needed to support these findings.