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Intracoronary thrombus formation on a guide wire: who is to blame?

Authors:
Kristina Maric Besic at University Hospital Centre Zagreb
Kristina Maric Besic
Zeljko Baricevic at University Hospital Centre Zagreb
Zeljko Baricevic
Maja Strozzi at University Hospital Centre Zagreb
Maja Strozzi
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Abstract

Case report: A 77-year-old man with stable angina and known left main coronary artery (LMCA) disease was admitted for elective percutaneous coronary intervention (PCI). Dual antiplatelet therapy with aspirin and clopidogrel had been instituted 7 days before the PCI, accompanied by administration of unfractionated heparin (UHF) during the procedure. For the PCI planning purpose, intravascular ultrasound was performed to evaluate the anatomy and the size of the LMCA and the morphology of the left anterior descending artery-first diagonal (LAD-D1) bifurcation lesion that had appeared only moderately stenotic on angiography. Minimal lumen diameter of the middle LAD segment and LMCA was 1.6 mm and 2.6 mm, respectively, indicating the severity of both lesions. After predilatation with the semicompliant balloon, a successful provisional stenting of the LAD-D1 bifurcation lesion using drug-eluting stent (DES) was performed, followed by high-pressure postdilatation to optimize stent deployment. At that time, the thrombus formation on a guide wire within the LMCA was noted, giving rise to distal LAD embolization. Direct stenting of the proximal LMCA with DES 4.0/9 mm was then performed and the intracoronary bolus of eptifibatide was given, leading to complete LMCA thrombus resolution, with residual thrombi seen in the distal LAD segments. Due to chest pain aggravation, a second-look angiography was performed 2 hours after the index procedure, showing non-occlusive dissection at the distal end of the LMCA stent. Additional DES 4.0/9 mm was implanted with optimal result and Thrombolysis In Myocardial Infarction 3 flow. Clopidogrel was replaced with ticagrelor. The 6-month follow-up was uneventful. Discussion: Pharmacotherapy during PCI is used to mitigate the sequel of iatrogenic plaque rupture and to reduce the risk of thrombus formation on intravascular PCI equipment. Iatrogenic damage to the endothelium leads to increased expression of tissue factor and activation of the coagulation cascade, ultimately leading to thrombus formation 1
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Cardiologia Croatica
2016;11(3-4):126.
VII. nacionalni sastanak o kardiovaskularnim intervencijama s međunarodnim sudjelovanjem
VI. sastanak intervencijskih kardioloških medicinskih sestara i tehničara
Case report: A 77-year-old man with stable angina and known left main coronary artery (LMCA) dis-
ease was admitted for elective percutaneous coronary intervention (PCI). Dual antiplatelet therapy
with aspirin and clopidogrel had been instituted 7 days before the PCI, accompanied by administration
of unfractionated heparin (UHF) during the procedure. For the PCI planning purpose, intravascular
ultrasound was performed to evaluate the anatomy and the size of the LMCA and the morphology of
the left anterior descending artery-rst diagonal (LAD-D1) bifurcation lesion that had appeared only
moderately stenotic on angiography. Minimal lumen diameter of the middle LAD segment and LMCA
was 1.6 mm and 2.6 mm, respectively, indicating the severity of both lesions. After predilatation with
the semicompliant balloon, a successful provisional stenting of the LAD-D1 bifurcation lesion using
drug-eluting stent (DES) was performed, followed by high-pressure postdilatation to optimize stent
deployment. At that time, the thrombus formation on a guide wire within the LMCA was noted, giving
rise to distal LAD embolization. Direct stenting of the proximal LMCA with DES 4.0/9 mm was then
performed and the intracoronary bolus of eptibatide was given, leading to complete LMCA thrombus
resolution, with residual thrombi seen in the distal LAD segments. Due to chest pain aggravation, a
second-look angiography was performed 2 hours after the index procedure, showing non-occlusive
dissection at the distal end of the LMCA stent. Additional DES 4.0/9 mm was implanted with optimal
result and Thrombolysis In Myocardial Infarction 3 ow. Clopidogrel was replaced with ticagrelor. The
6-month follow-up was uneventful.
Discussion: Pharmacotherapy during PCI is used to mitigate the sequel of iatrogenic plaque rupture
and to reduce the risk of thrombus formation on intravascular PCI equipment. Iatrogenic damage to
the endothelium leads to increased expression of tissue factor and activation of the coagulation cas-
cade, ultimately leading to thrombus formation1. Anticoagulation with UFH alone does not seem to
be sufcient for protection from ischemic sequel, such as periprocedural myocardial infarction. One
cause of these events is embolization of platelet aggregates that form as a result of platelet activation
induced by UFH2 and the prevention of thrombus formation strongly depends on platelet inhibition by
dual antiplatelet therapy. In cases with high-risk plaque features, a care has to be taken to recognize
iatrogenic damage in a timely manner. Usefulness of clopidogrel resistance testing before complex
PCI has yet to be shown.
Kristina Marić Bešić,
Željko Baričević*,
Maja Strozzi
University of Zagreb School
of Medicine, University
Hospital Centre Zagreb,
Zagreb, Croatia
KEYWORDS: percutaneous coronary intervention, intracoronary thrombus, guide wire.
CITATION: Cardiol Croat. 2016;11(3-4):126. | DOI: http://dx.doi.org/10.15836/ccar2016.126
*ADDRESS FOR CORRESPONDENCE: Željko Baričević, Klinički bolnički centar Zagreb, Kišpatićeva 12,
HR-10000 Zagreb, Croatia. / Phone: +385-1-2367-466 / E-mail: zbaricev@gmail.com
ORCID: Kristina Marić, http://orcid.org/0000-0002-4004-7271 • Željko Baričević, http://orcid.org/0000-0002-5420-2324
Maja Strozzi, http://orcid.org/0000-0003-4596-8261
Intracoronary thrombus formation on a guide wire: who is to
blame?
LITERATURE
1. Davie EW, Ku lman JD. An overvi ew of the structur e and function of th rombin. Semin Th romb Hemost. 2 006;32 Suppl 1 :3-15.
DOI: http://dx.doi.org/10.1055/s-2006-939550
2. Xiao Z, Th éroux P. Platele t activation with u nfractionate d heparin at thera peutic concent rations and comp arisons with a low -molecular-weig ht
hepari n and with a direct th rombin inhibito r. Circulati on. 1998;9 7:251-6. DOI: http://dx.doi.org/10.1161/01.CIR.97.3.251
Extended Abstract COMPLICATIONS IN PCI
RECEIVED:
February 7, 2016
ACCEPTED:
February 20, 2016
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Platelet Activation With Unfractionated Heparin at Therapeutic Concentrations and Comparisons With a Low-Molecular-Weight Heparin and With a Direct Thrombin Inhibitor
Article
  • Jan 1998
The growing use of heparin in acute thrombotic disorders, coupled with the availability of many new antithrombotic agents, emphasizes the need for adequate characterization of the platelet effects of the various anticoagulants. Controversial platelet effects have been reported with heparin (eg, enhanced platelet activation in vitro with high doses and no such effect in vivo at therapeutic doses). This study examined platelet receptor activation and platelet aggregation at therapeutic concentrations of unfractionated heparin (UFH), of enoxaparin, a low-molecular-weight heparin, and of argatroban, a direct thrombin inhibitor. Platelet P-selectin (CD62) and activated GP IIb/IIIa (PAC-1) expression on platelet membrane was quantified in whole blood as well as platelet aggregation in platelet-rich plasma in 43 patients with unstable angina before and during treatment with UFH or enoxaparin. Studies were also carried out in blood of seven normal volunteers after addition ex vivo of UFH (0.25 U/mL), enoxaparin (0.25 U/mL), argatroban (1 ng/mL), and normal saline. UFH in patients with unstable angina increased the percentage of circulating platelets positive to PAC-1 from 2.7+/-1.7% to 4.4+/-3.4% (P<.05) and to CD62 from 1.6+/-0.9% to 2.7+/-1.5% (P<.01). Platelets were also hyperresponsive to stimulation with ADP and with the thrombin-receptor agonist peptide. Aggregation to ADP increased from 6.8+/-4.6% to 11.2+/-7.0% and to TRAP from 5.2+/-3.5% to 11.1+/-6.0% (P<.001). The addition of UFH to blood of normal volunteers resulted also in activation of GP IIb/IIIa receptors, expression of P-selectin, and enhanced platelet aggregation. Enoxaparin had only minor effects on platelet activation in vivo and ex vivo, and argatroban, evaluated ex vivo, had no detectable effects. Therapeutic concentrations of UFH are associated with platelet activation.
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An Overview of the Structure and Function of Thrombin
Article
  • May 2006
The fundamental importance of thrombin in biology and medicine has made it one of the most extensively studied of all proteases. Thrombin performs essential functions in vertebrate biology as the central enzyme involved in blood coagulation and platelet aggregation, and as a mitogen and secretagogue for a variety of cell types. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade. Thrombin shares its general architecture and catalytic mechanism with those of pancreatic trypsin, the prototypical digestive serine protease. However, the specificity of thrombin toward substrates and cofactors, as well as its spatiotemporal regulation by effectors and inhibitors, is directed by features of the molecule that distinguish it from relatively nonspecific serine proteases like trypsin. Structural and functional studies have demonstrated the presence of surface loops that partially occlude the active site and make specific contacts with residues adjacent to the scissile bond of substrates. Specificity toward macromolecular substrates and cofactors is additionally enhanced by anion-binding exosites that are spatially distinct from the active site. More than five decades of multidisciplinary research on thrombin have produced an abundance of functional and structural information and provided a robust framework for understanding the role of thrombin in vertebrate biology.
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