INTRODUCTION — Coronary artery stents, particularly drug-eluting stents, are used in the majority of patients who undergo percutaneous coronary intervention (PCI) to improve symptoms in patients with obstructive coronary artery disease. They function both to prevent abrupt closure of the stented artery soon after the procedure as well as to lower the need for repeat revascularization compared to balloon angioplasty alone (formerly referred to as percutaneous transluminal coronary angioplasty).
Stent thrombosis is an uncommon but serious complication of PCI with stenting. Most patients present with an acute coronary syndrome, usually with ST-segment elevation on the electrocardiogram. Its cause is total or subtotal thrombotic occlusion of a coronary artery by thrombus that originates in or close to an intracoronary stent. This finding is seen at the time of coronary angiography, which is necessary in most cases to secure the diagnosis. Death and myocardial infarction are not infrequent complications of stent thrombosis.
This topic will discuss the presentation and management of and outcomes after acute coronary artery stent thrombosis. Issues related to its incidence, timing, risk factors, and prevention are discussed elsewhere. (See "Coronary artery stent thrombosis: Incidence and risk factors" and "Long-term antiplatelet therapy after coronary artery stenting in stable patients".)
DEFINITIONS — Although earlier clinical trials posed a problem for comparing stent thrombosis rates due to non-standardized definition, since 2007, most trials have adopted the criteria and classification proposed by the Academic Research Consortium (ARC) .
●Definite – Angiographic confirmation of a thrombus that originates in the stent or in the segment 5 mm proximal or distal to the stent, with or without vessel occlusion, which is associated with acute onset of ischemic symptoms at rest or electrocardiographic (ECG) signs of acute ischemia or typical rise and fall in cardiac biomarkers within 48 hours of angiography or pathologic confirmation of stent thrombosis determined at autopsy or from tissue obtained following thrombectomy.
●Probable – Unexplained death occurring within 30 days after the index procedure, or a myocardial infarction occurring at any time after the index procedure that was documented by ECG or imaging to occur in an area supplied by the stented vessel in the absence of angiographic confirmation of stent thrombosis or other culprit lesion.
●Possible – Unexplained death occurring more than 30 days after the index procedure. Of note, the possible category was dropped in an update of the definitions due to lack of specificity with longer-term follow-up.
In the discussion that follows, studies using definitions other than ARC will be noted.
CLINICAL PRESENTATION — Patients with stent thrombosis usually present with an acute coronary syndrome (ACS; unstable angina, non-ST elevation myocardial infarction [NSTEMI], or ST-elevation MI [STEMI]). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".)
In most cases, patients present with criteria for the diagnosis of acute STEMI . (See "Diagnosis of acute myocardial infarction".) In a report from the United States CathPCI Registry, among almost 7100 cases of stent thrombosis identified during a 16-month period, approximately 60 percent presented with STEMI, 23 percent with NSTEMI, and 17 percent with unstable angina . Patients with early stent thrombosis (<1 month after stent placement) are somewhat more likely to develop cardiogenic shock than those with late (1 to 12 months) or very late (>12 months) stent thrombosis . (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Clinical presentation'.)
At the time of coronary angiography, most patients have complete thrombotic occlusion (TIMI flow grade 0) of the involved vessel (table 1) . The culprit lesion is more common in the left anterior descending artery (48 percent) in patients with early and late stent thrombosis, whereas the right coronary artery (38 percent) is more commonly involved in cases of very late stent thrombosis .
In the CathPCI Registry, 1.8 percent of all PCI for ACS were attributable to stent thrombosis . In a 2012 report from two hospitals in Minneapolis, Minnesota, USA, nearly 11 percent of all STEMI was attributable to definite stent thrombosis according to the Academic Research Consortium (ARC) criteria . These data have not been updated, but our experts believe this frequency is likely lower with contemporary DES.
While the possibility of stent thrombosis should be considered in any patient who presents with ACS after stent placement, particularly within one year, there is no information from the history, physical examination, or electrocardiogram (ECG) that can be used to clearly discriminate between stent thrombosis and ACS due to ischemia from a lesion(s) not related to prior stent placement. In the presence of ST-elevation or other changes suggestive of target (stented) vessel ischemia, the suspicion for stent thrombosis should be higher. Such an event would be classified as probable stent thrombosis by the ARC criteria unless angiography confirms another culprit. (See 'Definitions' above.)
DIAGNOSIS — The definition of definite stent thrombosis is as follows: angiographic or tissue (from thrombectomy at the time of angiography) confirmation of a thrombus that originates in the stent or in the segment 5 mm proximal or distal to the stent, with or without vessel occlusion, which is associated with acute onset of ischemic symptoms at rest or ECG signs of acute ischemia or typical rise and fall of cardiac biomarkers within 48 hours of angiography. Definite stent thrombosis may also be determined by pathologic confirmation of stent thrombosis at the time of an autopsy. (See "Long-term antiplatelet therapy after coronary artery stenting in stable patients", section on 'Duration and Type of Antiplatelet Treatment'.)
While the (incidental) finding of thrombus within a stent in a patient without clinical findings is possible, this is likely infrequent. Most of these individuals will have an ACS or have an elevated troponin value.
MANAGEMENT — Patients with ST-elevation myocardial infarction (STEMI) due to stent thrombosis should be managed with primary percutaneous coronary intervention, although restoration of blood flow with intracoronary fibrinolysis has been used . (See "Primary percutaneous coronary intervention in acute ST-elevation myocardial infarction: Periprocedural management".)
Since stents are often placed in proximal segments of major coronary arteries, acute thrombotic occlusion presents as severe ischemia or MI, often STEMI [5-7]. The approach to the management of patients with unstable angina or acute MI is discussed elsewhere. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)
The management of patients with stent thrombosis is similar to that for other patients with an acute coronary syndrome (ACS). However, as outcomes in these patients appear to be worse than in individuals with ACS due to plaque rupture in a native coronary artery, it is critically important that the time to reperfusion be as short as possible. (See 'Compared with de novo coronary thrombosis' below.) While a non-urgent invasive or a conservative strategy may be reasonable for some patients with unstable angina or non-ST elevation MI who have not had prior stenting, urgent coronary angiography should be considered for most patients in whom the diagnosis of stent thrombosis has been considered.
Periprocedural considerations — Recanalization of the occluded artery is possible in over 95 percent of cases. Manual thrombus aspiration can be used in this setting  and, in one study, was associated with greater epicardial and microvascular myocardial perfusion . Similar to patients with STEMI due to de novo thrombosis, we do not perform thrombectomy routinely in cases of stent thrombosis, but given potential for larger thrombus burden, it may have a role in some cases. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'Thrombectomy'.)
In some cases, contributing factors such as suboptimal stent apposition or prior placement of an undersized stent are present. We perform intravascular ultrasound in all cases of stent thrombosis when possible and use this information for subsequent stent sizing and to confirm complete stent apposition. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Risk factors'.)
Some experts feel that new stent implantation should be avoided unless there is a clear indication such as a flow-limiting dissection. However, in many cases, we repeat stent placement unless thrombus aspiration and balloon angioplasty yield an optimal result. As in patients with de novo stenting, we prefer drug-eluting over bare-metal stents in almost all patients. Given the risk for recurrence, compliance with the recommended duration of dual antiplatelet therapy (DAPT) is critical after repeat stenting. (See "Long-term antiplatelet therapy after coronary artery stenting in stable patients", section on 'Summary and recommendations'.)
The periprocedural antithrombotic approach, including the use of parenteral antiplatelet and anticoagulant therapies, does not differ from that recommended for patients with acute STEMI. (See "Acute ST-elevation myocardial infarction: Management of anticoagulation" and "Acute ST-elevation myocardial infarction: Antiplatelet therapy".)
Long-term antiplatelet therapy — Poor compliance with the recommendation for DAPT is a common cause of stent thrombosis within one year and especially within 30 days. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Risk factors'.)
In addition, resistance to clopidogrel may be an important contributing factor in some cases. The optimal approach to antiplatelet therapy after stent thrombosis in patients who demonstrate clopidogrel nonresponse on platelet testing, or a genetic predisposition to it, is not known. (See "Clopidogrel resistance and clopidogrel treatment failure", section on 'Definitions'.)
In patients who present with stent thrombosis while on clopidogrel, it is likely the risk of recurrent stent thrombosis is increased. While no trials of alternate antiplatelet regimens, such as switching to prasugrel or ticagrelor or higher-dose clopidogrel, have been performed in these patients, we believe that the benefit from the use of more potent antiplatelet therapy outweighs the increase in risk of bleeding in most patients. Therefore, we suggest discharging the patient on prasugrel 10 mg daily or ticagrelor 90 mg twice daily, in addition to aspirin. The minimum duration of DAPT should be one year, with longer courses for patients who are tolerating such therapy.
Similarly, for patients who present with stent thrombosis after completing the recommended duration of treatment with clopidogrel, the optimal preventative antiplatelet strategy is unknown. We suggest initiating prasugrel 10 mg daily or ticagrelor 90 mg twice daily after an appropriate loading dose rather than restarting clopidogrel and continuing DAPT for a minimum of one year or longer in patients tolerating this regimen. However, in patients who will not receive either prasugrel or ticagrelor, clopidogrel 75 mg daily after a 600 mg loading dose (in addition to aspirin) should be restarted.
In patients who have sustained stent thrombosis, the optimal duration of DAPT is unknown. While we suggest continuing DAPT for more than one year in all patients with stent thrombosis, continual monitoring of the relative benefits and risks (primarily the risk of bleeding) is necessary. Many operators prefer indefinite DAPT after stent thrombosis unless a remediable factor is identified or higher bleeding risk is a concern.
MI and death — The following studies highlight high rates of myocardial infarction (MI) and death after acute stent thrombosis:
●Among patients with an acute coronary syndrome and angiographically-confirmed (definite) stent thrombosis in a pooled analysis, the 30-day rate of MI was 60 percent .
●The 30-day mortality rates after stent thrombosis are 7 percent for angiographically confirmed and 19 percent for clinically identified stent thrombosis for bare metal stents (BMS) based upon pooled clinical trial data  and 15 percent with drug-eluting stents (DES) based upon a large real-world registry . One study of 7315 stent thrombotic events found that in-hospital mortality was higher in patients with early stent thrombosis (up to 30 days after stent placement) compared with late (30 days to one year) and very late stent (after one year) thrombosis (7.9 versus 3.8 and 3.6 percent; p <0.01) .
●Six-month mortality is between 20 and 25 percent among survivors of stent thrombosis . Some studies have reported higher six-month mortality rates after stent thrombosis with DES compared to BMS (17 to 45 percent [11-14] and 9 to 21 percent [5,6], respectively). However, other studies have shown equivalent mortality . Predictors of six-month mortality include very late stent thrombosis, implantation of a stent during percutaneous coronary intervention (PCI) for stent thrombosis, and failure to achieve optimal angiographic reperfusion .
●Mortality at one year after definite DES thrombosis is between 10 and 20 percent [10,15-17].
●Longer-term mortality (450 days) after definite stent thrombosis was 22 percent in the TRITON-TIMI 38 trial of acute coronary syndrome patients who were randomly assigned to either clopidogrel or prasugrel and then underwent PCI with stenting .
●The overall rates of death and MI at four years were 31 and 83 percent, respectively, after definite or possible stent thrombosis (Academic Research Consortium definition) in a pooled analysis of eight randomized trials comparing DES to BMS . The outcomes with DES and BMS stent thrombosis were combined.
Recurrent stent thrombosis — Although not well studied, the incidence of recurrent stent thrombosis is relatively high. In a review of 95 patients with BMS thrombosis, 11 patients (12 percent) had recurrent stent thrombosis at six months . In a registry of DES, recurrence was 4.6 percent at one year . In a report of 431 patients in the Dutch stent thrombosis registry, the cumulative incidence of definite or probable recurrent stent thrombosis was 20.1 percent at three years .
Angiographic predictors of recurrent stent thrombosis include a larger post-procedural vessel diameter and a larger residual thrombus burden .
Compared with de novo coronary thrombosis — ST-elevation MI (STEMI) is characterized by intraluminal thrombus irrespective of whether the initial event is de novo (in association with plaque rupture) or stent related. However, clinical outcomes appear worse with the latter [6,10]. (See "Long-term antiplatelet therapy after coronary artery stenting in stable patients", section on 'Duration and Type of Antiplatelet Treatment'.)
In an attempt to understand this difference, clinical and angiographic outcomes in patients with STEMI due to stent thrombosis (n = 92) and de novo coronary thrombosis (n = 98) were compared in a retrospective study of patients who underwent primary PCI for STEMI . The following findings were noted in patients with stent thrombosis compared to those with de novo coronary thrombosis:
●In-hospital major adverse cardiovascular and cerebrovascular events were significantly higher (22.6 versus 9.2 percent), including a significantly higher in-hospital death rate (17.4 versus 7.1 percent). However, there were no differences at six-month follow-up.
●Successful reperfusion using angiographic criteria was significantly lower (80.4 versus 96.9 percent)
In another study of approximately 3300 patients with STEMI between 2002 and 2010, mortality was similar between those with STEMI due to stent thrombosis compared to those with de novo coronary thrombosis . However, the rate of reinfarction was higher in those with stent thrombosis.
In a cohort of 2464 individuals with STEMI treated with primary PCI, the mid-term outcomes of those with angiographically proven stent thrombosis (3 percent) were compared to those with a primary coronary artery event (97 percent) . At six months, those with stent thrombosis were shown to have significantly higher rates of non-fatal MI and restenosis/reocclusion (54 versus 17 and 10 versus 1 percent), while the rate of death was not significantly different (12 versus 8 percent).
INTRAPROCEDURAL STENT THROMBOSIS — The importance of intraprocedural stent thrombosis (IPST) as a risk factor for subsequent mortality and recurrent thrombosis has been highlighted [22,23]. IPST was defined as the development of occlusive or non-occlusive new or increasing thrombus in or adjacent to a recently implanted stent before the percutaneous coronary intervention (PCI) procedure is completed. IPST is not included in the Academic Research Consortium (ARC) definitions and thus its presentation and management are not evaluated uniformly in studies of stent thrombosis [22,23]. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Definitions' and "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Intraprocedural stent thrombosis'.)
In a study of over 10,000 individuals who underwent PCI with stenting, patients with IPST had a higher rate of composite ischemia (death, MI, ischemia-driven revascularization, or new-onset out-of-laboratory stent thrombosis) at 48 hours and 30 days compared to those without IPST (29.2 versus 4.5 and 31.5 versus 5.7 percent, respectively) . The finding of a significantly higher rate of ARC definite or probable stent thrombosis at 30 days has been noted in other studies . Most cases were in the setting of non-ST elevation acute coronary syndrome or ST elevation myocardial infarction. The impact of thrombus burden and the no-reflow phenomenon may be important contributors. While clearly distinguished from classic stent thrombosis after a successful procedure, the known adverse consequences of procedural complications remain important and ongoing studies are needed to assess methods for improved procedural success in these high-risk patients.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Percutaneous coronary intervention".)
SUMMARY AND RECOMMENDATIONS
●Background and clinical presentation – Stent thrombosis is an uncommon but serious complication of percutaneous coronary intervention with stenting from a total or subtotal thrombotic occlusion of a coronary artery by thrombus that originates in or close to an intracoronary stent. Most patients with stent thrombosis present with an acute coronary syndrome (ACS), usually with ST-segment elevation on the electrocardiogram. (See 'Clinical presentation' above.)
●Diagnosis – Stent thrombosis is seen at the time of coronary angiography; this test is necessary in most cases to secure the diagnosis. (See 'Clinical presentation' above.)
•Procedural – In general, the acute management of patients with stent thrombosis is similar to that for other patients with an ACS. Important points include considering the diagnosis in any patient ACS with prior stent placement and a rapid attempt to restore vessel patency. (See 'Management' above.)
•Antiplatelet therapy – For patients diagnosed with stent thrombosis while on clopidogrel, we suggest switching the patient to prasugrel 10 mg daily or ticagrelor 90 mg twice daily (Grade 2C). (See 'Long-term antiplatelet therapy' above.)
For patients diagnosed with stent thrombosis who have completed the minimum recommended course of clopidogrel, we suggest starting prasugrel 10 mg daily or ticagrelor 90 mg twice daily (after appropriate loading doses), rather than restarting clopidogrel 75 mg daily given the ACS setting (Grade 2C). (See 'Long-term antiplatelet therapy' above.)
In patients with stent thrombosis, irrespective of whether they were or were not on dual antiplatelet therapy (DAPT) at the time of the event, we suggest DAPT for a minimum of one year after the event, rather than shorter periods of time (Grade 2C). The ultimate duration of DAPT will require continual assessment of the benefits and risks (in particular, bleeding risk).
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