Perspective:

The following are 10 points to remember about drug–drug interactions (DDIs) in cardiovascular catheterizations and interventions:

1. Patients presenting for invasive cardiovascular procedures are frequently taking a variety of medications aimed to treat risk factors related to heart and vascular disease. The potential for DDIs to occur among interventional cardiology patients is high and increasing.

2. For percutaneous coronary intervention (PCI) procedures, it is recommended to develop an institution-specific protocol that allows for anticoagulant switching to occur in time frames based on pharmacological and clinical evidence.

3. For patients on dual antiplatelet therapy and oral anticoagulants with target international normalized ratio (INR) 2.0–3.0, it is recommended to use low-dose aspirin (75–81 mg daily) and consider gastric protection with proton pump inhibitors.

4. Drug–drug interactions with aspirin primarily exist in the form of pharmacodynamic interactions based on overlapping anti-hemostatic mechanisms. Regular-release aspirin should be administered before (30 minutes) or 8 hours after nonselective nonsteroidal anti-inflammatory drug (NSAID) therapy (e.g., ibuprofen, indomethacin, naproxen) in patients receiving continuous NSAID therapy.

5. Thienopyridines are prodrugs, requiring conversion by the liver via the CYP450 system before the desired clinical effect is achieved. Many theoretical DDIs with thienopyridines involve pharmacokinetic interactions that interfere with the metabolic conversion of the parent compound to the active metabolite.

6. Ticagrelor is eliminated through the liver, primarily via the CYP3A4 system. Administration of ticagrelor and strong CYP3A4 inhibitors (e.g., ketoconazole, voriconazole, clarithromycin, protease inhibitors) or strong CYP3A4 inducers (e.g., rifampin, dexamethasone, phenytoin, carbamazepine) is contraindicated.

7. Aspirin dose should not exceed 100 mg/day when used with ticagrelor.

8. Benzodiazepines and opiates are extensively metabolized by the liver and are therefore subject to potential DDI from agents that might affect liver metabolism.

9. Although some DDIs have the potential to induce harm in patients, many others are theoretical or exist only in pharmacokinetic form, with post-marketing registry reports as the ‘clinical evidence’ to support the relevance of the issue.

10. Interventional providers need to be aware of the potential for DDI and associated harm in cardiovascular patients and of the appropriate action to take, if any, to minimize the potential for medication-related adverse events.