The topic of antiplatelet therapy is one that starts preprocedure and is continued to postprocedure management. Aspirin (ASA) is the backbone of antiplatelet therapy. The importance of aspirin administration was highlighted by Barnathan et al. (1). The purpose of the study was to assess the role that oral antiplatelet agents played in controlling thrombosis post-PCI. In this study, done in the balloon angioplasty era, patients were stratified on the basis of whether aspirin and dipyridamole was administered: preprocedure, in the cath lab, or not at all. Patients were kept on the catheter table for a 30-minute postprocedure angiogram and evaluated for the presence of intracoronary thrombus. They found that when both agents were given preprocedure, there was no evidence of post-PCI thrombus compared with an 11.8% incidence with ASA with or without dipyridamole (a commonly used antiplatelet agent of that era, since abandoned for PCI use) given postprocedure and a 14.8% incidence when no ASA was given.

This study supports the recommendation that ASA should be started as soon as possible before PCI. If patients are not on ASA therapy, 325 mg should be given before PCI (2, 3). If patients are already taking daily ASA, then 81-325 mg should be given (2, 3). After the completion of the procedure, ASA therapy should be continued indefinitely at 81 mg or a higher dose (2, 4).

Thienopyridine use became increasingly important with the increased uses of both bare-metal stents (BMS) and drug-eluting stents (DES). Once a two-drug market (clopidogrel and ticlopidine) with clopidogrel being the drug of choice in the United States owing to its improved side effect profile (5), now several other drugs have come to market, leading to more choices for post-PCI management.

PCI-CURE, demonstrated improved outcomes associated with pretreatment with clopidogrel before PCI followed by long-term therapy (6). TRITON-TIMI 38 showed that in patients with acute coronary syndromes undergoing PCI, prasugrel therapy was associated with a significant reduction in ischemic events, including stent thrombosis with no significant reduction in overall mortality when compared with clopidogrel (7). An increased risk of major bleeding was also associated with prasugrel therapy (7). In PLATO, ticagrelor showed a significant reduction in rates of death from vascular causes, myocardial infarction, or stroke when compared with clopidogrel (8). There was no difference in the rates of major bleeding, but an increase in the rate of non-procedure-related bleeding (8).

In summary, careful consideration and patient education should be given before the procedure to determine your patient’s ability to tolerate and comply with antiplatelet therapy. After you are assured of your patient’s compliance with therapy, you should select your P2Y12 inhibitor (thienopyridine) of choice and continue it for 12 months in ACS patients (9). If the stent was delivered for a non-ACS indication, then clopidogrel, 75 mg, should be given for at least 12 months for patients receiving DES and a minimum of 1 month in patients receiving BMS (9). After completion of the procedure and before discharge, patients should once again be counseled on the importance of compliance with antiplatelet therapy and advised not to discontinue therapy without discussion with their cardiologist (9).

Intravenous glycoprotein IIb/IIIa receptor blocking agents (GP IIb/IIIa) have been demonstrated to be of substantial benefit in many patient subsets. With the advent of more potent oral antiplatelet regimens, their usage has declined, but still remains widespread. Data regarding selection of agent, dosage, and patient subsets are presented elsewhere in this book.

Relative to postprocedure management, the issues of greatest concern revolve around postprocedure bleeding and the need for urgent postprocedure surgery. Postprocedure bleeding may be related to access site problems (IV), but when it is related to gastrointestinal, retroperitoneal, genitourinary, or other cavitary or organ bleeding, cessation of GP IIb/IIIa therapy is generally immediately advisable.

When the patient develops an acute need for surgery postprocedure during the same time the GP IIb/IIIa is infusing or when effects of the drug are still present, then distinct management algorithms are needed. These algorithms are based on the stoichiometry of the drugs. If the agent used is the monoclonal antibody abciximab, the stoichiometry is such that there are fewer molecules of abciximab in the system than there are IIb/IIIa receptors. Therefore, there is no reservoir of free abciximab in the plasma. In this case, giving the patient platelet transfusions will dilute the receptor occupancy of the GP IIb/IIIa receptors and allow return of platelet function. Such transfusions should be given prior to beginning surgery if cardiopulmonary bypass is not to be used. If, however, cardiopulmonary bypass is planned, such transfusions should be deferred until the patient is ready to come off bypass. In this way,
the transfused platelets are not destroyed by the bypass itself and are immediately available and functional.

If, however, the GP IIb/IIIa agent is one of the small molecules (tirofiban or eptifibatide), the stoichiometry is different. In this case, there is a large plasma reservoir of the free GP IIb/IIIa blocking drug, and administered platelets will simply be inactivated by this free drug. Therefore, recovery of platelet function is best achieved by patient waiting. Given the half-life of these agents, recovery of platelet function can generally be expected in 3 to 5 hours’ postdrug discontinuance. Because both agents are dialyzable, in extreme cases, dialysis can be used to regain platelet function.

Thrombocytopenia is a postprocedure management issue occasionally seen and may be related to heparin or GP IIb/IIIa blocking agents. Abciximab is the only one that is a monoclonal antibody and has the highest reported incidence of postadministration thrombocytopenia. The incidence rate, defined as a platelet count falling below 100,000/mm³, has been reported to be between 2.5% and 6% in a number of clinical trials (10). In such patients, platelet transfusions were reported in 0.9% to 6% of patients. The other two intravenous GP IIb/IIIa agents are small molecules, relatively speaking. Eptifibatide is a cyclic heptapeptide, and has been associated with platelet counts <100,000 mm³ in 1.2% to 6.8% of patients in clinical trials. Tirofiban is a nonpeptide molecule and has the lowest reported frequency of platelet counts below 100,000 mm³, occurring in 0.2% to 0.5% of the study patients. Because all three agents may be associated with clinically significant thrombocytopenia, platelet counts should be monitored in any patient exposed to these agents. Baseline counts as well as counts 2 to 4 hours postexposure and 24 hours later should be obtained (10).

It is important to differentiate thrombocytopenia from pseudo-thrombocytopenia in such patients. Pseudothrombocytopenia is rare, and occurs as a result of artificial clumping of platelets in vitro. When processed through the standard platelet counters used in clinical laboratories, the result is a falsely low reported platelet count. The correct procedure to diagnose pseudothrombocytopenia and to differentiate it from true thrombocytopenia is to draw three tubes of blood, one each with citrate, heparin, and ethylenediaminetetraacetic acid (EDTA) as anticoagulants. Additionally, a smear should be sent for analysis. If the platelet count is normal in any one of the three tubes and the smear shows clumped platelets, pseudothrombocytopenia is diagnosed. Because this is a laboratory finding and not a true low platelet count, no therapy is needed.

Therapy for true thrombocytopenia is controversial. There is some evidence that intravenous corticosteroids may be of some benefit, but the data supporting the use of intravenous immunoglobin are conflicting. In general, corticosteroids alone or, in severe cases, in conjunction with IV immunoglobin is the recommended therapy (10). Of course, platelet transfusions should be considered if the count drops to very low levels. Unfortunately, there is no generally agreed-upon threshold to trigger platelet transfusion, partly because the process is seemingly immune-mediated. As such, exposure of banked platelets to the patient’s serum may inactivate them, and, if the drug is stopped promptly, restoration of platelet count is expected in 3 to 14 days with abciximab and 1 to 5 days with eptifibatide and tirofiban. Thus, the crucial elements are to check the platelet count postexposure, correctly diagnose true thrombocytopenia as described previously, and discontinue the offending agent immediately. It is worth noting that the risk of recurrent thrombocytopenia with reexposure of abciximab has been studied and found in about 50% of the original patients, and in many of them, a more severe degree of thrombocytopenia occurred (11).

Heparin administration is also a well-recognized complication of thrombocytopenia. Thrombocytopenia usually occurs 5 to 10 days after the initiation of heparin therapy (12). Heparin-induced thrombocytopenia (HIT) can be categorized into two types. Type I is of no clinical consequence, and is characterized by a decrease in platelets within 2 days after administration and will typically resolve with continued heparin administration (12). Type II HIT is an immunemediated disorder that is characterized by the formation of antibodies against heparin-platelet factor 4 complexes. The overall incidence of type II HIT is reported in one meta-analysis to be 2.6%. (13

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