Stent Thrombosis

Article Author:
Kalgi Modi
Article Author (Archived):
Michael Soos
Article Editor:
Kunal Mahajan
7/4/2019 6:22:33 PM
PubMed Link:
Stent Thrombosis


Stent thrombosis is one of the fatal complications of the percutaneous coronary intervention if it occurs acutely. It is also known as intraprocedural abrupt vessel closure and acute stent thrombosis. [1][2][3]Academic Research Consortium is an academic collaboration between the United States and Europe to universally define stent thrombosis based on the timing of the stent thrombosis and the level of certainty of the event.

Definition  based on the timing of stent thrombosis is as follows:

The acute stent thrombosis occurs between zero to 24 hours after coronary stent implantation. The subacute stent thrombosis occurs between 24 hours to 30 days after coronary stent implantation. Late stent thrombosis occurs between 30 days to one year after coronary stent implantation. Finally,  very late stent thrombosis occurs 1 year after coronary stent implantation.[4]

The definition of stent thrombosis based on the certainty of the event is as follows:

Definite stent thrombosis is confirmed when there is angiographic confirmation of stent thrombosis.

The presence of a thrombus that originates in the stent or the segment 5 mm proximal or distal to the stent, and the presence of at least one of the following criteria within a 48-hour period:

  • Acute onset of ischemic symptoms at rest
  • New ischemic ECG changes 
  • Typical rise and fall in cardiac biomarkers
  • Nonocclusive thrombus
  • Intracoronary thrombus
  • Occlusive thrombus
  • TIMI 0 or TIMI 1 flow intrastent or proximal to a stent up to the most adjacent proximal side branch or main branch.

Definite stent thrombosis is confirmed when there is a pathological confirmation of stent thrombosis.

Evidence of recent thrombus within the stent at autopsy or by examination of tissue retrieved following thrombectomy.

Probable stent thrombosis is considered to have occurred after intracoronary stenting in the following cases:

  • Any unexplained death within the first 30 days
  • Irrespective of the time after the index stenting, any myocardial infarction due to acute ischemia in the distribution of the implanted stent without angiographic evidence of stent thrombosis and the absence of any other obvious cause.

Possible cause of stent thrombosis is considered to have occurred with any unexplained death from 30 days after intracoronary stenting until the end of follow-up.


Large randomized trials and registry have identified patient/lesion, procedural, or stent factors related to stent thrombosis. [5][6]Champion-phoenix trial identified Non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) at presentation, angiographic thrombus burden, and total stent length as independent predictors of acute stent thrombosis.  An acuity trial revealed diabetes, renal insufficiency, Duke jeopardy score, final stent minimal luminal diameter, preprocedural thienopyridine administration, baseline hemoglobin, and extent of coronary artery disease as independent factors associated with early stent thrombosis. In an intravascular ultrasound (IVUS) substudy of the Horizon AMI trial, the small cross-sectional area of less than 5 mm, malposition of stent struts, plaque prolapse or protrusion, edge dissection, and residual stenosis played significant roles in predicting early stent thrombosis. Also, bifurcation stenting contributed to stent thrombosis. The Triton TIMI 38 trial showed that patients with STEMI are at higher risk of stent thrombosis regardless of stent type and that more potent antiplatelet therapy such as Prasugrel reduced that risk by 50%.


Stent thrombosis has been recognized from the early era of stent deployment with an incidence as high as 16% in older studies. Fifteen to 30% of the patients with stent thrombosis die within 30 days of the event. Acetylsalicylic acid (ASA), dipyridamole, coumadin, and dextran were tried in early stenting era to prevent the event. With the current practice of dual antiplatelet therapy and high-pressure inflation has significantly decreased incidence to 0.7% in one year and about 0.2% to 0.6% the year after that. The rate is lower for elective percutaneous intervention (PCI) (0.3% to 0.5%) but as high as 3.4% for acute coronary syndrome. There has been overall no significant difference between the rate of stent thrombosis between bare-metal stents and eluting drug stents. Only the timing of event varies. The bare metal stent tends to have an early event with a peak around 30 days compared to drug-eluting stents around three months to even later depending on the drug-coated. [7][8]


Virchow’s triad explains the major factors that lead to stent thrombosis. First, stasis and turbulence caused by an under-expanded stent, a stent in a small vessel, or a long lesion. Second, injury or endothelial disruption caused by edge dissection or delayed healing with eluting drug stents. Finally, hypercoagulability caused by congenital or acquired or nonresponder.

History and Physical

A thorough history, medication compliance review, laboratory testing for P2Y12 resistance, a 12 lead EKG, echocardiogram looking for a new wall motion abnormality, and laboratory testing of cardiac enzymes is recommended for initial evaluation of a patient with recent percutaneous coronary intervention presenting with angina. Universally, 60% of the patients with stent thrombosis present with STEMI and 40% with NSTEMI or unstable angina. Patients with STEMI, in the context of stent thrombosis, have greater rates of in-hospital mortality  (17.4%). Patients with early stent thrombosis are more likely to develop cardiogenic shock than to develop late or very late stent thrombosis. It is very unlikely that patient with nonacute coronary syndrome presentation would have evidence of stent thrombosis on subsequent coronary angiogram performed.


High clinical suspicion is the most important evaluation for a patient presenting with angina and recent history of coronary stenting. The patient is usually evaluated with a history, physical, ECG, echocardiogram, and cardiac enzymes. Almost all patients with STEMI undergo urgent coronary angiography.

Treatment / Management

During angiography, a prompt aspiration thrombectomy or angioplasty should be performed to restore patency of the thrombosed vessel. Compliance and drug resistance should be evaluated. More potent antiplatelet therapy should be considered, for example, prasugrel or ticagrelor. [9][10][11]The current recommendation is to continue the dual antiplatelet drug therapy for one year after drug-eluting stent placement and at least one month following bare metal stent. The stent should be assessed with either IVUS or optical coherence tomography (OCT) to determine stent apposition, expansion, and the presence of edge dissections. Optimization of stent deployment with appropriate postulation and treatment of edge dissections with additional stents are imperative to prevent repeat stent thrombosis. Additional stent implantation should be avoided if possible because each millimeter of the stent increases the probability of stent thrombosis.

Enhancing Healthcare Team Outcomes

When patients with stents present with chest pain to the primary care provider, internist, and nurse practitioner, one should always consider stent thrombosis. These patients should be immediately referred to the cardiologist for further investigation and treatment. Stent thrombosis when it occurs acutely can be fatal if not treated right away. The triage nurse should be aware of this condition and immediately admit the patient and consult with the emergency department physician. The prognosis depends on many factors including patient age, duration of thrombosis, number of stents involved and response to medical treatment. In some cases, an urgent coronary bypass is required.[12][13] [14](Level II)


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