Intraprocedural stent thrombosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammed Salih, M.D.


Synonyms and Keywords: IPST

Overview

Intraprocedural stent thrombosis (IPST) is the formation of a new, increasing, or reappearing occlusive or non-occlusive thrombus of grade ≤2 that occurs before the completion of the percutaneous coronary intervention (PCI) procedure, and is specifically located within the recently deployed stent or immediately adjacent to it. It is considered a rare subset of Intraprocedural thrombotic events (IPTE). Although it rarely happens, it has been strongly associated with unfavorable periprocedural outcomes. It is defined as an angiographically confirmed intraluminal filling defect within the stent that results in occlusive or non-occlusive thrombolysis in myocardial infarction (TIMI) grade-0 or 1 anterograde flow, secondary to the development of new or increasing thrombus within or adjacent to a recently implanted stent, occurring during the index procedure or before the percutaneous coronary intervention (PCI) is completed. It is also present when the baseline level of thrombus was decreasing or has resolved after balloon angioplasty or thrombus aspiration, but increased again any time after stent implantation, including stent postdilatation. In the large-scale CHAMPION PHOENIX trial, IPST was a relatively infrequent event, occurring in <1% of patients undergoing PCI, but was strongly associated with subsequent ischemic events, including out-of-laboratory ST, MI, and death. The reduction in IPST with cangrelor in CHAMPION PHOENIX contributed to this agent's effectiveness in reducing the rates of ARC-defined stent thrombosis and MI. These data provide strong evidence for a significant association between IPST and adverse short-term clinical outcomes after PCI and support the inclusion of IPST as an important endpoint in future pharmacological and device trials.

Pathophysiology

  • IPST can occur with bare metal stents and DES.[1] Several theories suggest possible explanation to IPST in DES. DES characteristics, such as drug-induced thrombogenicity, whether using sirolimus or paclitaxel, and its in-vitro platelet aggregation effects[2] along with its remarkable lipophilic bioavailability within the coronary milieu,[3] stent platform effect,[4] polymer coating material,[4] and open-cell stent design all seem plausible hypotheses that nonetheless require further validation. Operator-dependent factors, such as adequate stent placement have also been postulated.[5][6]
  • AT-III is a naturally occurring thrombin inhibitor that suppresses tissue factor–factor VIIa complex, factor IXa, Xa and thrombin. Its irreversible combination with thrombin inhibits the effect of thrombin on fibrinogen and clot formation[7].
  • AT-III deficiency or decreased activity increase thrombin and fibrinogen activities, and thus clot formation. AT-III deficiency can be congenital or acquired. * The congenital form occurs in 1/3000 people, while the acquired form is seen in disseminated intravascular coagulation and nephrotic syndrome as a result of increased loss, or in malnutrition, liver cirrhosis or failure, as a result of decreased synthesis.
  • Heparin therapy is the most commoniatrogenic cause as it decreases AT-III half-life, while other causes include nitroglycerin and oral estrogen.
  • Heparin binds to AT-III and enhances the rate of AT-III and thrombin reaction. This interaction activates AT-III to start an anticoagulation cascade that inactivates thrombin, factor Xa and other clotting factors.
  • Heparin has no anticoagulant effect in AT-III depleted plasma.
  • Heparin resistance is defined as the unexpected steady levels of activating clotting time while the patient is receiving adequate dose of heparin and having an adequate plasma concentration.
  • In cardiothoracic surgery, heparin resistance is ACT of b400–600 s after 300–600 U/kg of UFH has been given.
  • In patients with venous thromboembolism, HR is defined as needing N35,000 U of UFH in 24 h to achieve therapeutic levels.
  • In interventional cardiology, an ACT of N250 s is needed to allow for a safe procedure.
  • Heparin resistance can be AT-dependent or independent. In AT-dependent HR, the anticoagulant effect of heparin decreases when AT-III activity is b80%, and is completely ineffective at b70%.
  • AT independent mechanisms include heparin induced thrombocytopenia due to neutralization of heparin effect from binding to platelet factor 4; and increased levels and enhanced activity of factor VIII and fibrinogen[8].
  • In critically ill patients with coexisting severe inflammatory illnesses, where circulating acute phase reactants like platelet-derived factors, plasma proteins, and factor VIII levels are elevated, anti-Xa activity would be a more accurate measure of heparin activity. The reason is that these positively charged proteins readily bind to negatively charged heparin, thereby inhibiting and neutralizing its effect resulting in HR[7].
  • Patients undergoing elective angiography and/or PCI are not usually screened for possible congenital or acquired deficiencies via natural anticoagulants prior to the procedure.
  • Measuring anti-Xa activity instead of APTT or ACT is time consuming and not readily available in other facilities, especially in patients presenting with AMI, where door-to-balloon time is golden.
  • Adventitial tissues and medial smooth muscle cells (SMC) are important sources of tissue factors that are responsible primarily for triggering the extrinsic clotting pathway.
  • Thrombosis may occur when a large amount of tissue factor is released into the blood from the medial SMCs following medial tear secondary to excessive injury during stenting[9].
  • Factors related to the procedures, including dissection of stent edge, remaining lesion stenosis, incomplete stent coverage, incomplete apposition, and incomplete expansion,can cause stent thrombosis[10].

Epidemiology and Demographics

  • The frequency of occurrence currently ranges between 0.5 – 1.7% of all PCI procedures.
  • IPST occurred in 0.7% of PCI when frame-by-frame analysis was done for 6591 patients enrolled in the ACUITY and HORIZONS-AMI (Harmonizing Outcomes With Revascularization And Stents In Acute Myocardial Infarction) trials.[1]
  • Similarly, an IPST rate of 1.2% was document in another study in 2013 following enrollment of 1901 patients.[11]
  • The incidence of IPST was 0.7% in two other studies, the first of which reviewed the frequency of IPST in 1320 patients less than 75 years old undergoing PCI with first generation DES and whereas the second study enrolled 670 patients undergoing elective DES.[5][9]
  • Finally, 1.7% of 181 patients had IPST when evaluating DES implantation in bifurcation lesions using “crush technique” in 2005.[12]

Risk Factors

Interestingly, conventional risk factors and correlates of early and late postprocedural stent thrombosis do not seem to be the same as those for IPST. Each risk factor is likely to predispose the patient to stent thrombosis, which is characterized by platelet activation and aggregation, by one or more of the following mechanisms:[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]

  • Incomplete stent expansion.
  • Greater stent length.
  • Small vessel caliber.
  • Inflow or outflow obstruction.
  • Nonionic contrast media.
  • Emergent stent placement.
  • Post-procedure TIMI flow grade <3.
  • No aspirin at the time of the procedure.
  • CAD ≥50 percent proximal of culprit lesion.
  • Treatment of bifurcation lesions.
  • High on treatment (oral antiplatelet therapy) platelet reactivity[35], including polymorphisms in the genes controlling hepatic enzymes involved in the metabolism of clopidogrel.
  • Stent location does not increase the risk of stent thrombosis occurrence but the stent location in the left main or proximal left anterior descending artery poses increased risk of an adverse outcome if stent thrombosis occurs and may be regarded as an indication for more aggressive prevention strategies.

Associated Factors

Although data in the literature is still conflicting, IPST has been variably correlated to several parameters:

Natural History, Complications and Prognosis

  • IPST significantly reduces the overall success rate of PCI, as measured by frequency of achieving TIMI flow grade 3 at the end of index PCI.
  • TIMI flow grade 3 is achieved in 90.9% of patients without IPST vs. 44.7% in patients with IPST.
  • Given its significant and unique role in outcome, there is currently increasing advocacy to routinely report IPST in PCI and to add it as a distinctive entity in the Academic Research Consortium (ARC) definition of stent thrombosis.[1]
  • Intraprocedural and follow-up data on patients who experience IPST reveal the most common significant complications.
  • The occurrence of IPST remarkably increases the risk of occurrence of IPTE-related complications.
  • The following table summarizes intra-procedural complications of IPST.[1]
Intraprocedural Complications Patients with IPST Patients without IPST
Slow or no reflow 75.5% 3.2%
Distal Embolization 49% 1.9%
Side branch closure 14.3% 0.6%


  • Similar to IPTE in general, IPST is an important independent predictor of mortality and morbidity one year post-PCI.
  • One year follow-up data shows a 41.1% rate of death, MI, or TVR in patients who had experienced IPST vs. only 14.5% in patients with no IPST.[1] Other adverse events were also increased in patients with IPST after one year post-PCI, such as postprocedural stent thrombosis, TVR, and non-CABG major bleeding.[11][1]
  • The reduction in IPST with cangrelor in CHAMPION PHOENIX contributed to this agent's effectiveness in reducing the rates of ARC-defined stent thrombosis and MI.
  • These data provide strong evidence for a significant association between IPST and adverse short-term clinical outcomes after PCI and support the inclusion of IPST as an important endpoint in future pharmacological and device trials[8].

References

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