Management of the thrombotic lesion

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Brian C. Bigelow, M.D.

Overview

The presence of angiographically apparent thrombus is associated with poorer outcomes in patients undergoing PCI. Thrombus often embolizes distally and causes no reflow and associated myonecrosis. There are two broad strategies to reduce thrombus burden: mechanical strategies and pharmacologic strategies.

Differentiating Thrombus from Other Angiographic Abnormalities

  • Coronary spasm can also lead to a focal narrowing of the lumen and should be treated with vasodilators
  • A dissection can cause a hazy appearance to the lumen and should be treated with intracoronary stenting

Goals of Treatment

Goals in the management of the thrombotic lesion include:

Step-By-Step Strategy in the Management of the Thrombotic Lesion

  • The first strategy is to prevent the occurrence of thrombus through the use of upstream antiplatelet and antithrombotic pharmacotherapies including aspirin, thienopyridines, and glycoprotein 2b3a inhibition.
  • The second strategy is to mechanically aspirate thrombus.
  • The third strategy is to direct stent the lesion without pre-dilation to minimize distal embolization.
  • The fourth strategy is to utilize intracoronary fibrinolytic therapy to dissolve clot that is refractory to other forms of treatment and dissolve clot inside branches that may be accessible to mechanical devices.
  • Alternate / additional strategies include the use of distal protection and saphenous vein grafts to minimize distal embolization.

Pharmacologic Therapy

Antiplatelet Therapy

  • The incidence of thrombus on the coronary angiogram can be reduced by and complications of the PCI procedure can be reduced by upstream pharmacologic therapy with antiplatelet therapy including aspirin, platelet glycoprotein IIb/IIIa receptor (GP IIb/IIIa) antagonists in patients who are troponin positive (abciximab, eptifibatide, tirofiban), and ADP receptor/P2Y12 inhibitors (plavix, ticagrelor, prasugrel)
  • Aspirin is a conventional therapy that reduces ischemic complications after PCI.
  • GP IIb/IIIa antagonists are used adjunctively to treat and prevent thrombus formation and decreases ischemic complications post-PCI in patients with angiographic evidence of or suspected thrombus. In patients with STEMI undergoing primary PCI, GP IIb/IIIa antagonists have been shown to reduce mortality in meta-analyses. There is an ongoing debate as to the optimal timing of their administration (upstream vs in-lab administration).

Antithrombin Therapy

Thrombolytic Therapy

  • Thrombolytic Therapy: Urokinase (UK), tissue plasminogen activator (tPA) for STEMI when other pharmacologic and mechanical treatments are not successful. Caution: intracoronary administration of fibrinolytic agents is an "off label" the use of these agents (this mode of administration is not been approved by the FDA, but fibrinolytic agents are an FDA approved drug). The total dose of tPA is 20 mg which is approximately the 1/5 of that generally used for systemic fibrinolysis. tPA can it be administered 2 mg at a time to evaluate its efficacy.

Mechanical Therapy

  • Aspiration Catheter: (Export, Pronto) is the choice prior to the other interventions listed below
  • Percutaneous Coronary Intervention (PCI): Bare metal or drug-eluting stent, particularly direct stenting without pre-dilation by conventional balloon angioplasty
  • Distal Protection: (Percusurge guardwire, Triactive, Spider wire, Proxis), particularly in saphenous vein grafts
  • Transluminal Extraction Catheter (TEC)
  • Rheolytic Thrombectomy (Possis Angiojet)

Management of No Reflow

You should also treat the patient for potential spasm or no-reflow with a calcium channel blocker, adenosine (100 mcg IC) or nitroprusside (100 mcg IC).

References

  1. White HD, Braunwald E, Murphy SA; et al. (2007). "Enoxaparin vs. unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction in elderly and younger patients: results from ExTRACT-TIMI 25". Eur. Heart J. 28 (9): 1066–71. doi:10.1093/eurheartj/ehm081. PMID 17456482. Unknown parameter |month= ignored (help)


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