[Antiaggregation therapy after percutaneous coronary intervention in a patient with thrombocytopenia: case report]

Dual antiaggregation (antiplatelet) therapy is mandatory in patients having received a stent during percutaneous coronary intervention. This therapy usually consists of acetylsalicylic acid (100 mg per day) and clopidogrel (75 mg per day) for at least 6 to 12 months (depending on the type of stent). Such therapy has been shown to reduce significantly unwanted clinical events, although slightly increasing the risk of bleeding. Coronary stents must rarely be implanted in patients who have or develop thrombocytopenia. In such patients, the risk of bleeding is increased manifold. On the other hand, the risk of potentially fatal thrombotic events is unknown. In this case report, we present a patient who developed thrombocytopenia shortly (one month) after the stent had been implanted. After thorough clinical workup, we could not find the remediable cause of thrombocytopenia. Because of the potential of acetylsalicylic acid to induce thrombocytopenia, it was excluded from therapy and a double dose of clopidogrel (150 mg per day) was introduced. Then we decided to evaluate platelet function with the ADP aggregation test (which indicates the degree to which the function of platelets is blocked by clopidogrel) and aspirin resistance test (which indicates the degree to which the function of platelets is blocked by acetylsalicylic acid). In the first set of tests, the patient was shown to be hyperreactive to both substances. We then lowered the dose of clopidogrel to the standard dose and evaluated the function of platelets with the same tests two weeks later and the results were the same. Because the patient was without obvious and laboratory signs of bleeding, we decided not to change the prescribed antiplatelet therapy because of fear from potentially fatal thrombotic events. The use of dual antiplatelet therapy in patients with thrombocytopenia is particularly challenging. We believe that in such patients, firstly, the cause of thrombocytopenia should be sought for by thorough clinical investigation. If not found, as in our patient, tailoring of such therapy should be done using currently available aggregation tests. In such a way, patients could be protected from both excessive bleeding and potentially devastating thrombotic events. Unfortunately, this is a sole example and definite conclusions could only be made on larger studies.