Perspective:

The following are 10 points to remember about this state-of-the-art review on stent thrombosis (ST) from a clinical perspective:

1. At this time, >1 million coronary stent implantations are performed each year in the United States. But together with the growing use of stents, ST, the most feared complication after stent implantation, has emerged as an important entity to understand and prevent.

2. The typical clinical presentation of ST consists of chest pain and ischemic electrocardiographic changes in the target vessel territory. However, ST can also present as sudden death, or it can be asymptomatic in the setting of collateral vessels.

3. A multitude of mechanisms lead to the occurrence of ST. Many patient-related, lesion-related, procedural, and post-procedural factors are associated with ST. These predispose to ST by one of the following pathophysiological mechanisms: 1) exposure of blood before re-endothelialization to prothrombotic subendothelial constituents, stent struts, and/or polymer material leading to activation of the extrinsic pathway of the coagulation cascade; 2) persistent slow coronary blood flow and low shear stress leading to activation of the intrinsic pathway; 3) inadequate pharmacological suppression of platelet activation (e.g., after premature discontinuation of dual antiplatelet therapy [DAPT]); and 4) the presence of a systemic prothrombotic state (e.g., due to acute coronary syndrome or malignancy).

4. Early ST occurs within 30 days after stent implantation, when technical and procedural factors are important. A suboptimal procedural result (e.g., slow flow, inadequate post-procedural lumen dimensions, residual dissection, and tissue prolapse) is associated with the incidence of early ST.

5. Delayed endothelial coverage, persistent fibrin deposition, and ongoing vessel inflammation are associated with ST >30 days after stent implantation. Re-endothelialization after stent implantation is significantly delayed in drug-eluting stents (DES) compared with bare-metal stents, and is likely responsible for the higher rates of very late ST with first-generation DES.

6. Compliance with DAPT is paramount to minimize the risk of ST, particularly if it occurs within 30 days of implantation. Unclear communication of treatment plans, low levels of patient education, and other social factors have been shown to influence DAPT compliance and should routinely be taken into account.

7. Stent underexpansion is a common mechanism underlying ST. A rigid arterial segment has severely restricted the expansion of the initially implanted stent, or an undersized stent may have been selected initially. If confirmed by intravascular ultrasound (IVUS)/optical coherence tomography (OCT), high-pressure balloon angioplasty with noncompliant balloons sized according to the normal adjacent reference segment should be attempted.

8. Stent malapposition can be verified by the existence of a space filled with blood between the stent struts and the vessel wall. The extent of this low-flow area has been associated with ST. Angioplasty with an appropriately sized balloon, as determined by the IVUS/OCT-derived measurement of the arterial wall diameter at the culprit cross-sections, typically suffices to ameliorate this problem.

9. The preferred treatment for ST is emergency percutaneous coronary intervention, including the possibility of thrombus aspiration restoring antegrade blood flow. Additional stent implantation is not absolutely necessary and is advised for treatment of significant residual dissections.

10. Finally, an optimal procedural result is important to minimize the risk of ST. Proper stent expansion and apposition over the full length of the stent should be ascertained, and residual dissections should be avoided. Adequate patient, lesion, and stent selection; a good technical result; and effective DAPT are critical in minimizing the risk of ST.