Stent thrombosis is a rare but serious complication following the placement of a coronary stent, a small mesh tube used to keep a blocked heart artery open. The condition occurs when a blood clot suddenly forms inside the stent, rapidly blocking blood flow to the heart muscle. This acute blockage almost always results in a heart attack (myocardial infarction) and carries a high risk of death or major complications. Despite the low overall incidence due to advances in technology and medication, understanding its causes and management is important for individuals with coronary stents.
The Mechanism of Clot Formation
The process of clot formation begins because the stent is a foreign object placed within the blood vessel. The body’s defense system recognizes the metallic struts and attempts to seal off the exposure, triggering the activation of platelets. Platelets are small blood cells that become sticky upon activation, causing them to aggregate at the site of the foreign material.
The initial adhesion of platelets leads to the rapid formation of a blood clot (thrombus). Ideally, a healing process called endothelialization occurs, where native endothelial cells grow over the stent struts. This creates a smooth, non-thrombogenic lining, effectively hiding the foreign material from the bloodstream. If this process is incomplete or delayed, the exposed surface continues to promote platelet activation, sustaining the risk of clot formation.
In drug-eluting stents (DES), medications embedded in the polymer prevent excessive cell growth that could narrow the artery again (restenosis). Unfortunately, these anti-proliferative drugs can also hinder the beneficial growth of protective endothelial cells, leaving the stent struts exposed longer. This delayed endothelialization is a primary reason why DES carry a persistent, small risk of thrombosis that extends years after the initial procedure.
Classifying Stent Thrombosis by Timing
Stent thrombosis is classified based on the time elapsed since implantation, as timing often suggests the underlying cause. Acute stent thrombosis occurs within the first 24 hours and is typically linked to procedural issues, such as incomplete stent expansion or artery dissection.
Subacute stent thrombosis occurs between 24 hours and 30 days after the procedure. Events happening between 30 days and one year are categorized as late stent thrombosis. Beyond the first year, any occurrence is termed very late stent thrombosis. The shift from acute to very late events reflects a change in contributing factors, moving from procedural issues to biological healing failure or patient behavior.
Key Factors Contributing to Risk
A patient’s susceptibility to stent thrombosis is influenced by their health, the technical aspects of the procedure, and post-procedure compliance. Patient factors that increase baseline risk include pre-existing conditions like diabetes mellitus and chronic kidney disease. Patients who presented with an acute coronary syndrome, such as a heart attack, also face a higher risk compared to those stented for stable symptoms.
Procedural factors involve the quality of stent placement and the complexity of the treated lesion. Suboptimal deployment, such as an underexpanded stent or one not fully pressed against the artery wall (malapposition), creates turbulent blood flow that encourages clot formation. Treating complex lesions, such as those at artery bifurcations or requiring multiple overlapping stents, also increases mechanical risk.
The greatest modifiable risk factor, particularly for later events, is medication non-adherence. Patients are prescribed Dual Antiplatelet Therapy (DAPT) to prevent clot formation. Stopping this medication prematurely dramatically increases the risk of thrombosis, especially in the early post-procedure period.
Immediate Treatment and Long-Term Prevention
Stent thrombosis is a medical emergency requiring immediate intervention to restore blood flow to the heart. The standard immediate treatment is typically a repeat percutaneous coronary intervention (PCI). This often involves thrombectomy, a procedure to physically remove the fresh blood clot, aiming to quickly open the blocked artery and minimize damage to the heart muscle.
The cornerstone of long-term prevention is strict adherence to Dual Antiplatelet Therapy (DAPT), which combines two types of medication to keep platelets from aggregating. This regimen includes aspirin and a P2Y12 inhibitor, such as clopidogrel, prasugrel, or ticagrelor. The P2Y12 inhibitor targets a receptor on the platelet surface, blocking a pathway necessary for platelet activation.
The duration of DAPT is determined by balancing the patient’s risk of clot formation against the risk of bleeding complications. Patients are typically prescribed DAPT for a minimum period, often 6 to 12 months, and sometimes longer. Patients should never stop their DAPT regimen without consulting their cardiologist, as discontinuing the medication significantly raises the chance of a life-threatening thrombotic event.