What is Coronary Stent Thrombosis? | Cardiology

Coronary Stent Thrombosis

Overview of coronary stent thrombosis

Coronary stent thrombosis is a thrombotic occlusion of a coronary stent. This is usually an acute process in contrast to restenosis, which is a gradual narrowing of the stent lumen due to neointimal proliferation. Stent thrombosis often results in acute coronary syndrome, while restenosis often results in anginal symptoms. Stent thrombosis is further defined according to the following characteristics:

  • Timing: early (within 1 month), late (from 1 to 12 months), and very late (more than 12 months). Timing is also sometimes categorized as acute (within 24 hours) or subacute (more than 24 hours).
  • Clinical scenario: stent thrombosis usually results in symptoms of the acute coronary syndrome; however, it can occasionally be clinically silent.
  • Underlying stent: bare-metal stent versus first-generation drug-eluting stent versus second-generation drug-eluting stent thrombosis.

Prevention of coronary stent

Stents caked with new cytotoxic drugs and polymers may have different properties in terms of affecting endothelialization, vascular inflammation, and induction of tissue factor activity.

  • Coating with NO donors can decrease platelet adhesion and aggregation.
  • CD34 antibody-coated stents can capture circulating endothelial progenitor cells and can prevent thrombosis by increasing and accelerating endothelial coverage.

Anti-thrombotic therapy is likely to be optimized with the development of newer anticoagulants and more efficient anti-platelet drugs with a lower risk of bleeding complications. Patients and health-care personnel should be informed of the risk associated with premature discontinuation of treatment.

The development of new tests capable of assessing platelet inhibition may identify patients with reduced benefit from aspirin or clopidogrel and may allow for greater individualization and optimization of anti-platelet therapy.

The risk of stent thrombosis has been a known complication after PCI for quite some time and could increase after DES implantation.

Though the indication is not conclusive, some studies indicate that the incidence of late and very late stent thrombosis increases after DES implantation.

As a consequence, large-scale clinical trials with long-term follow-up, as well as mechanistic studies, are highly justified. Currently, it is not known whether very late stent thrombosis is prevented with a prolonged course of dual antiplatelet therapy.

Predictors of coronary stent

Given the poor results despite early recognition and treatment, the most important step in ST management is prevention. This requires an understanding of common predictors and taking appropriate precautions to limit the factors that can be avoided. For early and late ST, there has been consistency in the identification of common risk factors after BMS or DES implantation. These factors have been classified as related to the patient, the injury, or the procedure.

The most important risk factor for early or late ST after first-generation SBA or DES implantation is premature discontinuation of DAPT. For BMS, this period seems to be 30 days, and for first-generation DES, it is at least 6 to 9 months. The minimum duration of DAPT for new-generation DES remains controversial, but Unplanned interruptions during the first 6 months appear to be associated with a significantly increased risk of ST. Interruptions related to serious bleeding complications appear to be associated with a particularly high risk.

Implantation of a BMS with 1 month DAPT may be a better option in patients who are at very high risk of bleeding, especially if the risk of restenosis is not high. On the other hand, there is a continuing benefit of reducing the risk of ST with DAPT continued well beyond 12 months in patients without bleeding complications during the first 12 months.

Another major avoidable risk factor is the under-expansion of the coronary stent. In an intravascular ultrasound analysis of ST after implantation of a sirolimus-eluting stent, stent sub expansion and residual stenosis were the most significant predictors. In all cases, routine post-dilation or intravascular ultrasound guidance should be considered to mitigate this risk.

Predictors of very late ST have been more difficult to define, but they share a common pathway of late healing, ongoing inflammatory changes, and the development of neoatherosclerosis. Much of the inflammatory environment and impaired healing have been overcome with an improved polymer and stent design, although in a recent autopsy study of pathologic correlates, neoatherosclerosis remained a common finding, even with next-generation.

To the extent that neoatherosclerosis may be an appearance of stent-related endothelial dysfunction, it will be of interest whether bioabsorbable scaffold skill can sufficiently limit this phenomenon or whether more complex bioengineering will be required.

What diagnostic tests should be done for a coronary stent?

The electrocardiogram is a first-line test in any patient with chest pain syndrome. Ischemia in the territory of a previous stent is thrombosis of the supporting stent. However, the patient may also have disease progression upstream or downstream of the stented segment, which is not due to stent thrombosis.

Conflicting diagnoses that may mimic stent thrombosis

Restenosis is the coronary stent that can be observed after percutaneous coronary intervention. This process was common with bare-metal stents and was significantly reduced with the advent of drug-eluting stents. In-stent restenosis typically presents as an insidious procedure in which patients have a gradual escalation of angina symptoms 6 to 12 months after their initial procedure. This is in contrast to stent thrombosis, which occurs suddenly and can occur at any time after the procedure.

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