PCI complications: thrombocytopenia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Michael W. Tempelhof M.D.

Overview

Thrombocytopenia is defined as a platelet count of <100,000 cell/mm3. The morbidity and mortality associated with percutaneous coronary intervention (PCI) has substantially improved given recent advances in devices and pharmacotherapy.[1] Increased utilization of antiplatelet and antithrombin therapies has been associated with fewer postprocedure ischemic complications. Despite these benefits, there is also an increased risk of bleeding and hematologic complications. One such hematologic complication is thrombocytopenia. Both antiplatelet and antithrombin agents have been associated with a heightened risk of developing thrombocytopenia.[2] Furthermore, patients with pre-PCI thrombocytopenia are at an increased risk for mortality and hemorrhage as compared to patients without thrombocytopenia.[3]

Thrombocytopenia

Epidemiology and Demographics

The incidence of thrombocytopenia among patients with ischemic heart disease exposed to antiplatelet and antithrombin therapies varies widely and has been reported to be 3% to 16.5%.[4]

Differential Diagnosis of Thrombocytopenia in the Patient Undergoing PCI

  • Laboratory Related
  1. Laboratory error
  2. Thrombin-induced platelet clumping
  1. Platelet coagulation with Ethylene diamine tetra acetic acid (EDTA)
  2. Low specimen temperature
  1. Viral infections
  2. Alcohol toxicity
  3. Chemotherapy
  4. Vitamin B12 and folate deficiency
  1. Thrombotic Thrombocytopenic Purpura (TTP)
  2. Disseminated Intravascular Coagulation (DIC)
  3. Cardiopulmonary bypass graft surgery (CABG)
  4. Intra-aortic balloon pump (IABP) therapy
  1. Massive red blood cell transfusion
  1. Unfractionated heparin, low-molecular-weight heparin (includes heparin associated thrombocytopenia and heparin-induced thrombocytopenia)
  2. Glycoprotein IIb/IIIa inhibitors: abciximab, tirofiban, eptifibatide
  3. Thienopyridines: clopidogrel and ticlopidine
  4. Antibiotics (most commonly agents with a sulfa moiety)
  5. Thiazide diuretics

The most important clinical entities for the patient undergoing PCI (and the focus of this article) are:

  1. Pseudothrombocytopenia
  2. Drug-induced thrombotic thrombocytopenic purpura (TTP)
  3. Heparin-associated thrombocytopenia
  4. Heparin-induced thrombocytopenia (HIT) with or without thrombosis

Laboratory Error and Pseudothrombocytopenia

The importance of diagnosing pseudothrombocytopenia in the PCI patient cannot be overemphasized, as the discontinuation of antiplatelet therapies is inappropriate and may increase the risk for an adverse event.

Thrombotic Thrombocytopenic Purpura (TTP)

  • TTP is a rare disorder with an annual incidence of 4 to 11 cases per million in the US.
  • Although multiple systemic conditions are associated with the development of TTP, medications are implicated in up to 20% of cases.[8]

TTP occurs in one per every 5,000 patients exposed to thienopyridines and presents as thrombocytopenia usually within 2 to 4 weeks after exposure.[9]

Therapy
  1. Discontinuation of the thienopyridine and plasma exchange.
  2. Plasma exchange should be performed daily until the platelet count is normal, although the optimal duration of therapy is unknown.
  3. Whether thienopyridine therapy can be safely reinstituted in patients who have recovered from thienopyridine- associated TTP is unknown.

Drug-Induced Thrombocytopenia

The risk of developing drug-induced thrombocytopenia may be higher in patients undergoing PCI as antiplatelet and antithrombotic therapies have been strongly associated with drug-induced thrombocytopenia.[10]

Caveat for PCI patients with stent placement is that there will be an increased risk for stent thrombosis in the absence of thienopyridine therapy.

Treatment of Clopidogrel associated thrombocytopenia: methylprednisolone and platelet transfusions have demonstrated resolution.[11]

Other Causes of Drug-induced Thrombocytopenia

Glycoprotein IIbIIIa inhibitors (GPIs) and unfractionated or low-molecular-weight heparins.

  1. GPIs: abciximab, eptifibatide, and tirofiban.
Etiology

GPI-induced thrombocytopenia is analogous to the autoantibody– mediated pathogenesis previously described with thienopyridine- induced thrombocytopenia.

  • The [autoantibody|auto-antibodies]] to GPI are typically preformed and account for the acute presentation of thrombocytopenia.
Therapy
  • Subsequent administration of GPI in a patient who has previously developed GPI- associated thrombocytopenia may be reasonable provided that another agent is used.[15]

Heparin-Associated and Heparin-Induced Thrombocytopenia

Heparin-associated thrombocytopenia is a benign entity that occurs in approximately 5% of patients within 48 hours to 72 hours of exposure to UFH and results in mild thrombocytopenia that resolves despite continued heparin therapy.

  • No specific treatment is warranted.

HIT and its related clinical entity, heparin-induced thrombocytopenia with thrombosis syndrome (HITTS), are less begin as both can result in arterial and venous thrombosis, amputation, and death if not recognized and treated promptly.

Recognition is imperative as the 30-day mortality rate among HIT patients is 17% to 30%.[18]

Onset of HIT
  1. Typical-onset HIT occurs in 65% of reported cases and, in the heparin- naïve patient, develops 5 days to 10 days after heparin exposure.
  2. Rapid-onset HIT occurs 10 hours to 24 hours after heparin exposure and accounts for 30% of HIT cases.
  3. Delayed-onset HIT occurs in 2% of HIT patients 10 days to 40 days after the cessation of heparin therapy.
Diagnosis of HIT
  1. The serotonin release assay is based on the principle that antibodies from the blood of HIT patients will bind to and activate platelets from normal donors and lead to the release of serotonin.
  2. The heparin-induced platelet aggregation assay uses washed platelets from normal donors and measures platelet aggregation caused by the serum of a HIT patient in the presence of a heparin; this test is one of the most commonly used and is widely available.
  3. Platelet-rich plasma aggregation test and the antibody testing for anti-PF4 antibodies are less commonly utilized with poor sensitivities reported for both tests.
HIT Management
  1. Immediate discontinuation of all heparin-containing compounds.
  2. Identification of the HIT subtype.
  3. If anticoagulation is required (as in the clinical setting of PCI in a patient with a known history of HIT), one of three commercially available direct thrombin inhibitors (DTI)— lepirudin, argatroban, and bivalirudin should be used.

Conclusion

  1. Both pharmacological and mechanical interventional strategies can lead to decreased platelet counts in the patient undergoing PCI.
  2. Important medication-related causes include thrombotic thrombocytopenic purpura associated with thienopyridines, antibody-related platelet destruction seen with GPI and abciximab readministration, and HIT.
  3. If HIT is suspected or proven, DTIs are the agents of choice, with bivalirudin having the most supportive evidence.
  4. Early recognition of thrombocytopenia and rapid assessment of its cause can guide management and improve outcomes among PCI patients with thrombocytopenia.

References

  1. Singh M, Rihal CS, Gersh BJ, Lennon RJ, Prasad A, Sorajja P, Gullerud RE, Holmes DR Jr. Twenty-five-year trends in in-hospital and long-term outcome after percutaneous coronary intervention: a single-institution experience. Circulation. 2007;115:2835-41.
  2. Boersma E, Harrington RA, Moliterno DJ, White H, Théroux P, Van de Werf F, de Torbal A, Armstrong PW, Wallentin LC, Wilcox RG, Simes J, Califf RM, Topol EJ, Simoons ML. Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomized clinical trials. Lancet 2002;359:189-98.
  3. Berkowitz SD, Sane DC, Sigmon KN, Shavender JH, Harrington RA, Tcheng JE, Topol EJ, Califf RM, for the EPIC Study Group. Occurrence and clinical significance of thrombocytopenia in a population undergoing high-risk percutaneous coronary revascularization. J Am Coll Cardiol. 1998;32:387-392.
  4. Eikelboom JW, Anand SS, Mehta SR, Weitz JI, Yi C, Yusuf S. Prognostic significance of thrombocytopenia during hirudin and heparin therapy in acute coronary syndrome without ST elevation: Organization to Assess Strategies for Ischemic Syndromes (OASIS-2) study. Circulation. 2001;103:643-50.
  5. The EPIC Investigators. Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty. The EPIC Investigation. N Engl J Med. 1994;330:956-61.
  6. Sane DC, Damaraju LV, Topol EJ, Cabot CF, Mascelli MA, Harrington RA, Simoons ML, Califf RM. Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy. J Am Coll Cardiol. 2000;36:75-83.
  7. George, JN. Clinical practice. Thrombotic thrombocytopenic Purpura. N Engl J Med. 2006;354:1927-35.
  8. Andersohn F, Bronder E, Klimpel A, Garbe E. Proportion of drug-related serious rare blood dyscrasias: estimates from the Berlin Case-Control Surveillance Study.Am J Hematol. 2004;77:316-8.
  9. Bennett CL, Connors JM, Carwile JM, Moake JL, Bell WR, Tarantolo SR, McCarthy LJ, Sarode R, Hatfield AJ, Feldman MD, Davidson CJ, Tsai HM. Thrombotic thrombocytopenic purpura associated with clopidogrel. N Engl J Med. 2000;342:1773–1777.
  10. Aster RH, Bougie DW. Drug-induced immune thrombocytopenia. N Engl J Med. 200;357:580-7.
  11. Best PJ, Berger PB, Davis BR, Grines CL, Sadeghi HM, Williams BA, Willerson JT, Granett JR, Holmes DR Jr; PRESTO Investigators. Impact of mild or moderate chronic kidney disease on the frequency of restenosis: results from the PRESTO trial. J Am Coll Cardiol. 2004;44:1786-91.
  12. Topol EJ, Moliterno DJ, Herrmann HC, Powers ER, Grines CL, Cohen DJ, Cohen EA, Bertrand M, Neumann FJ, Stone GW, DiBattiste PM, Demopoulos L; TARGET Investigators. Do Tirofiban and ReoPro Give Similar Efficacy Trial. Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban and abciximab, for the prevention of ischemic events with percutaneous coronary revascularization. N Engl J Med. 344,1888-1894.
  13. ESPRIT Investigators. Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy. Novel dosing regimen of eptifibatide in planned coronary stent implantation (ESPRIT): a randomised, placebo-controlled trial. Lancet. 2000;356:2037-44.
  14. Tcheng JE, Kereiakes DJ, Lincoff AM, George BS, Kleiman NS, Sane DC, Cines DB, Jordan RE, Mascelli MA, Langrall MA, Damaraju L, Schantz A, Effron MB, Braden GA. Abciximab readministration: results of the ReoPro Readministration Registry. Circulation. 2001;104:870-5.
  15. Bougie DW, Wilker PR, Wuitschick ED, Curtis BR, Malik M, Levine S, Lind RN, Pereira J, Aster RH. Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa. Blood. 2002;100:2071-6.
  16. Greinacher A, Eichler P, Lubenow N, Kwasny H, Luz M. Heparin induced thrombocytopenia with thromboembolic complications: meta-analysis of 2 prospective trials to assess the value of parenteral treatment with lepirudin and its therapeutic aPTT range. Blood. 2000;96:846-851.
  17. Warkentin TE, Kelton JG. A 14-year study of heparin induced thrombocytopenia. Am J Med. 1996;101:502–507.
  18. Warkentin TE, Kelton JG. Temporal aspects of heparin-induced thrombocytopenia. N Engl J Med. 2001;344:1286- 92.
  19. Lincoff AM, Bittl JA, Harrington RA, Feit F, Kleiman NS, Jackman JD, Sarembock IJ, Cohen DJ, Spriggs D, Ebrahimi R, Keren G, Carr J, Cohen EA, Betriu A, Desmet W, Kereiakes DJ, Rutsch W, Wilcox RG, de Feyter PJ, Vahanian A, Topol EJ; REPLACE-2 Investigators. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trial. JAMA. 2003;289:853-63.
  20. Stone GW, McLaurin BT, Cox DA, Bertrand ME, Lincoff AM, Moses JW, White HD, Pocock SJ, Ware JH, Feit F, Colombo A, Aylward PE, Cequier AR, Darius H, Desmet W, Ebrahimi R, Hamon M, Rasmussen LH, Rupprecht HJ, Hoekstra J, Mehran R, Ohman EM; ACUITY Investigators. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006;355:2203-16.
  21. Mahaffey KW, Lewis BE, Wildermann NM, Berkowitz SD, Oliverio RM, Turco MA, Shalev Y, Ver Lee P, Traverse JH, Rodriguez AR, Ohman EM, Harrington RA, Califf RM; ATBAT Investigators. The anticoagulant therapy with bivalirudin to assist in the performance of percutaneous coronary intervention in patients with heparin-induced thrombocytopenia (ATBAT) study: main results. J Invasive Cardiol. 2003;15:611-6.



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