Тромбоз коронарного стента — причины, симптомы, диагностика и лечение

How to Minimize Stent Thrombosis

From the Columbia University Medical Center/New York-Presbyterian Hospital and the Cardiovascular Research Foundation, New York, NY.

From the Columbia University Medical Center/New York-Presbyterian Hospital and the Cardiovascular Research Foundation, New York, NY.

Case Presentation—A 58-year-old diabetic woman with stable angina pectoris (class II symptoms despite medical therapy) presented for elective cardiac catheterization after undergoing a stress test that demonstrated anterior wall ischemia at a low-moderate workload. Coronary angiography demonstrated single-vessel disease with a 90% lesion in the left anterior descending (LAD) coronary artery (Figure, A). Treatment with percutaneous coronary intervention (PCI) was selected as a revascularization strategy, and a drug-eluting stent (DES) was deployed in the LAD without complications (Figure, B). Before discharge, a treating physician concerned about the risk for stent thrombosis assessed the patient’s platelet reactivity using point-of-care testing, which demonstrated minimal platelet response to clopidogrel. This clinician update will discuss strategies for the prevention of stent thrombosis.

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Figure. A, Diagnostic angiogram demonstrating severe stenosis of mid LAD (arrow). B, Postintervention angiogram demonstrating successful PCI of the LAD with a drug-eluting stent (arrow).

Stent Thrombosis Background

The most feared complication related to coronary stent placement is stent thrombosis, which, although fortunately rare (occurring in ≈0.5% to 1% of patients within 1 year), most commonly presents as an acute myocardial infarction (MI). 1 Treatment for stent thrombosis almost always requires emergent repeat PCI, although optimal reperfusion is only achieved in two thirds of patients. 2 As a result, stent thrombosis has been associated with 30-day mortality rates of 10% to 25%. Moreover, ≈20% of patients with a first stent thrombosis experience a recurrent stent thrombosis episode within 2 years.

The mechanisms underlying stent thrombosis are multifactorial (Table 1) and include patient-related factors, procedural factors (including stent choice), and postprocedural factors (including type and duration of antiplatelet therapy). Numerous strategies may be employed to reduce the occurrence of stent thrombosis (Table 2).

Table 1. Potential Mechanisms of Stent Thrombosis

PCI indicates percutaneous coronary intervention.

Table 2. Strategies to Minimize the Occurrence of Stent Thrombosis

BMS indicates bare metal stents; DES, drug-eluting stents.

Role of Patient Selection

Stent thrombosis occurs more frequently in complex patients and lesions, especially in those with acute coronary syndromes, diabetes mellitus, chronic kidney disease and diffuse disease, small vessels, and bifurcation lesions requiring multiple stents. 1,3 Additionally, premature discontinuation of dual-antiplatelet therapy within 6 months has been strongly associated with stent thrombosis, especially in the setting of trauma or performance of surgical procedures. 4 These patient-related factors can be critical in clinical decision making relative to the overall revascularization strategy (whether to implant a bare metal stent [BMS] or DES, or to instead consider coronary artery bypass grafting). Understanding the risk of stent thrombosis according to these patient-related factors facilitates use of procedural strategies to minimize the risk of stent thrombosis, especially in high-risk patients (see Procedural Factors).

Procedural Factors

Procedural factors associated with stent thrombosis include the stent type selected (whether BMS or DES, and even the specific DES used), as well as whether the stent is adequately expanded and apposed to the vessel wall and is placed in a vessel with sufficient runoff to support adequate flow through the stent.

High-Pressure Stent Deployment and Adequate Expansion

Early in the stent experience, Colombo and colleagues demonstrated with intravascular ultrasound that stent underexpansion and/or malapposition occurred not infrequently after stent deployment and was associated with stent thrombosis. 5 On the basis of these and other observations, adequate stent sizing and high-pressure (>14 atmospheres) stent deployment and postdilation to ensure expansion are considered essential to minimize stent thrombosis. Although the use of adjunctive intravascular ultrasound to ensure appropriate sizing and expansion has not been proven in randomized trials to be essential, intravascular ultrasound can be useful to confirm stent apposition and expansion, which in observational studies has been linked to lower stent thrombosis at both 30 days and 1 year. 6

Bare Metal Stent Versus Drug-Eluting Stent and Stent-Related Factors

Stent thrombosis after BMS typically occurs within the first 30 days after implantation, although rarely can occur later. In contrast, stent thrombosis after DES can occur years afterward, with an annual incidence of 0.2% to 0.3% in patients with noncomplex coronary artery disease 7 and 0.4% to 0.6% after unrestricted use. 8 Thus, stent thrombosis rates arising from within the original stent are higher with DES than BMS, with the differences emerging predominantly beyond the first year after implantation. 9 A variety of potential causes of late stent thrombosis occurring with DES have been implicated, including delayed or absent endothelialization of the stent struts, hypersensitivity/inflammatory and/or thrombotic reactions to the DES polymer, strut fractures, late malapposition, and the development of neoatherosclerosis within stents with new plaque rupture.

Despite concerns about late stent thrombosis with DES, long-term follow-up of randomized DES versus BMS studies has demonstrated that after taking into account stent thrombotic events after procedures for restenosis (so called “secondary” stent thrombosis events, which occur more commonly after BMS than DES), the overall incidence of stent thrombosis (primary plus secondary) does not seem to be increased with DES compared to BMS, 10 and the overall late rates of death and MI are similar with DES and BMS. 11 Moreover, the benefits of DES in reducing restenosis and subsequent adverse events offset the small excess risk of very late primary stent thrombosis with DES, 12 albeit by a slim margin.

Potential stent modifications to reduce stent thrombosis have included improving the biocompatibility of the stent and polymer, using bioabsorbable polymers, eliminating the polymer entirely, and/or using stent surface modifications to stimulate vascular endothelialization. Many of these designs are currently undergoing clinical evaluation. At present, data with second-generation DES including the Xience V/Promus everolimus-eluting stent and the Endeavor zotarolimus-eluting stent have demonstrated favorable rates of stent thrombosis compared to first-generation DES. 13,14

Antiplatelet Regimens

Choice of Antiplatelet Therapy

Dual antiplatelet therapy with aspirin and a thienopyridine is currently recommended for PCI patients in whom stents are implanted on the basis of randomized trials showing reduced rates of stent thrombosis with aspirin plus ticlopidine compared to aspirin alone or aspirin plus warfarin. 15 Clopidogrel compared to ticlopidine has comparable efficacy with an enhanced safety profile. 16 Therefore, poststent therapy with aspirin and clopidogrel is currently the standard of care for the majority of patients undergoing PCI with either BMS or DES worldwide. In patients with acute coronary syndromes, the rates of stent thrombosis have also been reduced by replacing clopidogrel with more potent antiplatelet agents such as prasugrel and ticagrelor, although this benefit is achieved at the cost of increased bleeding. 17,18 Additionally, although some interventionalists have adopted a practice of routinely administering double-dose clopidogrel for either a week or longer after stent implantation in order to prevent stent thrombosis, this practice is largely empirically based rather than supported by clinical data, particularly among the elective PCI population.

Clopidogrel is a prodrug that requires the CYP2C19 enzyme to be converted into its active metabolite. The US Food and Drug Administration recently added a boxed warning to the label of clopidogrel about its reduced effectiveness in patients who are poor metabolizers of this drug. 19 However, although polymorphisms in the gene encoding the CYP2C19 allele as well as high on-clopidogrel platelet reactivity have been associated with adverse clinical events in patients undergoing PCI, 20,21 genetic testing is not widespread, its utility has not been prospectively validated, and what to do if a poor metabolizer is identified is uncertain. At present, no prospective randomized studies have demonstrated benefits of using a more potent alternative antiplatelet regimen (such as higher-dose clopidogrel, prasugrel, or ticagrelor) for stable PCI patients identified at increased risk for events on clopidogrel by either a polymorphism in CYP2C19 or high on-treatment residual platelet reactivity. In fact, the first such randomized trial to examine this hypothesis, Gauging Responsiveness With a VerifyNow Assay: Impact on Thrombosis and Safety (GRAVITAS) recently reported no benefit of a strategy of doubling the standard daily dose of clopidogrel (from 75 to 150 mg per day) after PCI in patients with high on-treatment platelet reactivity. 22 Importantly, after successful DES implantation in this study cohort, the 6-month composite rate of cardiovascular death, MI, or stent thrombosis was low in both groups (2.3% at 6 months) despite higher on-treatment platelet reactivity with standard-dose clopidogrel.

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Duration of Antiplatelet Therapy

Observational studies have uniformly documented that premature thienopyridine discontinuation within 6 months after DES placement is strongly associated with stent thrombosis. 4 Whether prolonged dual antiplatelet therapy beyond this time will enhance freedom from stent thrombosis and/or death and MI is unknown, with some studies in support of this hypothesis and others against. Only 1 randomized trial addressing the issue of prolonged dual antiplatelet therapy for the prevention of stent thrombosis has been completed, with no significant differences in the primary composite end point of cardiac death/MI (or stent thrombosis) observed in patients treated with an additional 2 years of clopidogrel along with aspirin compared to aspirin alone. 23 Several additional randomized trials are ongoing to address the relative safety and efficacy of prolonged dual antiplatelet therapy. 24 In the absence of prospective randomized data on extended-duration dual antiplatelet therapy, current recommendations are for 12 months of dual antiplatelet therapy in most patients after DES and BMS. 25 Among DES-treated patients who are at higher risk for bleeding, shorter durations of dual antiplatelet therapy (generally, minimum 6 months) can be considered on the basis of the early clinical trial experiences with predominantly first-generation DES; ongoing trials assessing earlier discontinuation regimens should shed further light on this issue. For BMS-treated patients, a minimum of 2 to 4 weeks of dual-antiplatelet therapy is currently recommended, but 12 months is still considered to be ideal, especially among patients with acute coronary syndromes.

Summary

Stent thrombosis is a devastating complication of stent implantation, and strict attention to patient risk factors and ability to adhere to prescribed medical regimens is necessary before proceeding with stent implantation. Assiduous care to technical detail is necessary to optimize stent implantation and deployment, particularly in complex disease, and novel stents are emerging with the potential to inherently lower the risk of stent thrombosis. Elective surgery within the first year after DES placement should be avoided or performed without discontinuation of either aspirin or clopidogrel if possible. Finally, data on the use of antiplatelet agents more potent than clopidogrel for high-risk patients are limited to those with acute coronary syndromes, for whom prasugrel and ticagrelor can be beneficial, albeit at a potentially greater risk of bleeding complications. It is thus essential to carefully consider the individual patient’s risk of stent thrombosis (and MI) compared to bleeding before using these agents.

Case Resolution

Despite the patient’s high on-treatment platelet reactivity with clopidogrel, given the excellent stent result achieved and absent randomized trial data demonstrating a favorable risk–benefit ratio of double-dose clopidogrel or prasugrel/ticagrelor in elective PCI for stable angina, the patient was discharged uneventfully from the hospital on aspirin plus standard-dose clopidogrel to continue for 1 year, with plans for routine clinical follow-up with her referring cardiologist. One year later, the patient was doing well, without stent thrombosis or recurrent symptoms, and clopidogrel was discontinued. The patient remains free of symptoms or events at 2 years. In the interim, the patient’s treating physicians have stopped routinely testing platelet reactivity for elective PCI patients while awaiting prospective clinical data demonstrating the benefit of treatment modifications based on these results.

Disclosures

Dr Stone has served on an advisory board for and received honoraria from Abbott Vascular and Boston Scientific . He has consulted for Volcano, Medtronic, BMS-Sanofi, Merck, AstraZeneca, and Eli Lilly. Dr Kirtane reports no conflicts.

Stent Thrombosis

I. Stent Thrombosis: What Every Physician Needs to Know

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 an 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 an 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.

II. Diagnostic Confirmation: Are You Sure Your Patient Has Stent Thrombosis?

Consensus Definition of Stent Thrombosis—Academic Research Consortium

Definite stent thrombosis: a patient with clinical signs or symptoms of an acute coronary syndrome and angiographic or autopsy evidence of a thrombus 5 mm proximal or distal to the stent.

Probable stent thrombosis: an unexplained death within 30 days of stent implant or any myocardial infarction with ischemia in the same territory of the stent, but angiography was not performed.

Possible stent thrombosis: any unexplained death beyond 30 days of stent implant.

A. History Part I: Pattern Recognition

Any patient with prior percutaneous coronary intervention who presents with signs/symptoms consistent with an acute coronary syndrome, especially when there is ischemia in the territory of the prior stent, should be considered for stent thrombosis. A consideration which raises the likelihood of stent thrombosis is recent termination of an adenosine diphosphate(ADP) receptor antagonist (i.e., clopidogrel, prasugrel, or ticagrelor) and/or aspirin.

B. History Part 2: Prevalence

While stent thrombosis can be a devastating event, fortunately it is a rare problem after percutaneous coronary intervention (PCI). With bare-metal stents, most stent thromboses occur within the first month of implant at a frequency 10% among all-comers) and was significantly reduced with the advent of drug-eluting stents. In-stent restenosis usually presents as an insidious process in which patients have a gradual escalation of anginal symptoms 6 to 12 months after their index procedure. This is in contrast to stent thrombosis, which presents suddenly and can occur at any time after the procedure.

D. Physical Examination Findings

Since stent thrombosis patients present with an acute coronary syndrome, they may have signs/symptoms of heart failure or cardiogenic shock.

E. What Diagnostic Tests Should Be Performed?

The electrocardiogram is a first-line test in any patient with a chest pain syndrome. Ischemia in the territory of a prior stent is supportive stent thrombosis; however, the patient may also have progression of disease upstream or downstream of the stented segment, which would not be due to stent thrombosis per se. A silent electrocardiogram in a patient with chest pain and prior stent does not rule-out an acute coronary syndrome, since a myocardial infarction in the circumflex territory may not result in ischemic changes.

1. What Laboratory Studies (if any) Should Be Ordered to Help Establish the Diagnosis? How Should the Results Be Interpreted?

Laboratory studies are not necessary to establish the diagnosis of stent thrombosis. Suspected stent thrombosis is an emergent condition which needs to be handled like any acute myocardial infarction. Laboratory studies (i.e., CBC, chemistry, cardiac enzymes) can be obtained at the time of patient presentation, but they should not slow referral to the catheterization laboratory.

2. What Imaging Studies (if any) Should Be Ordered to Help Establish the Diagnosis? How Should the Results Be Interpreted?

Similar to laboratory studies, imaging studies (i.e., chest x-ray) are not necessary to establish the diagnosis of stent thrombosis. A chest x-ray can be obtained at the time of patient presentation, but it should not slow referral to the catheterization laboratory.

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III. Management

The management of stent thrombosis is the same as the management of an acute coronary syndrome.

A. Immediate Management

The immediate management of stent thrombosis is the same as the management of an acute coronary syndrome. Patients who present with a non-ST-elevation acute coronary syndrome are usually managed invasively accordingly to local practice patterns. For example, these patients would usually undergo urgent catheterization. Medical management consists of antiplatelet therapy (i.e., aspirin, and an ADP receptor antagonist), antithrombin therapy (i.e., heparin or direct thrombin inhibitor), statin, beta-blocker, and nitroglycerin. Patients who present with an ST-elevation acute coronary syndrome should undergo emergent reperfusion therapy according to local practice patterns (i.e., normally by primary PCI). Successful reperfusion of an acute myocardial infarction from stent thrombosis is less likely than for acute myocardial infarction due to native artery/plaque rupture. Supportive medical therapy is the same as for non-ST-elevation acute coronary syndrome.

The intravenous ADP receptor antagonist cangrelor has been shown to reduce intra-procedural stent thrombosis versus clopidogrel. This is important because intra-procedural stent thrombosis can increase subsequent rates of cardiovascular ischemic events, including death.

B. Physical Examination Tips to Guide Management

The physical examination is nonspecific with stent thrombosis; however, there may be findings of heart failure (i.e., rales, elevated jugular venous distention, hypotension, etc.).

C. Laboratory Tests to Monitor Response to, and Adjustments in, Management

Tests that assay for platelet reactivity are sometimes used in stent thrombosis; however, clinical studies have been unable to document an improvement in clinical outcomes by testing for platelet reactivity. If the patient had a stent thrombosis event on single antiplatelet therapy, use of indefinite dual antiplatelet therapy would be reasonable. If the patient had a stent thrombosis event on dual antiplatelet therapy (i.e., aspirin and clopidogrel), replacing clopidogrel with a more potent ADP receptor antagonist would be reasonable.

D. Long-Term Management

The perioperative period can pose unique risks to patients with coronary stents. The following recommendations are taken from the American College of Cardiology/American Heart Association:

Bare-metal stents. Delay elective surgery for 4 to 6 weeks after stenting at which time clopidogrel can be stopped. An important caveat is that patients who received a bare-metal stent for treatment of an acute coronary syndrome should receive up to 3 to 12 months of therapy, and elective surgery should be delayed depending on how elective it is.

Aspirin must be maintained during the perioperative period, other than very delicate surgery, such as brain surgery. For emergent/urgent surgeries, it is recommended that patients proceed to the operating room on dual antiplatelet therapy.

Drug-eluting stents. Delay elective surgery for 12 months at which time clopidogrel can be stopped. Aspirin must be maintained during the perioperative period.

For emergent/urgent surgeries, it is recommended that patients proceed to the operating room on dual antiplatelet therapy. The question of using a glycoprotein IIb/IIIa inhibitor as a bridge often comes up as a mechanism to perform surgery sooner than 12 months.

Since most stent thromboses occur in the perioperative or postoperative period rather than the preoperative period, a preoperative glycoprotein IIb/IIIa inhibitor bridge is likely ineffective at preventing thrombotic events. Therefore, there are no guideline recommendations endorsing the use of a glycoprotein IIb/IIIa inhibitor bridge. An unfractionated heparin (or low-molecular weight heparin) bridge would not be expected to prevent stent thrombosis since these thrombotic events are prevented by antiplatelet (not antithrombin) therapy.

With either type of stent, aspirin therapy should be maintained; however, this may be problematic with certain types of surgical procedures (i.e., intracranial, spinal canal, and posterior chamber of the eye). Studies have shown that when stent thrombosis occurs in the setting of complete termination of antiplatelet therapy, the median time that antiplatelet agents were held was 7 days. Therefore, antiplatelet agents should be held for the shortest possible duration (i.e., not longer than 7 days).

E. Common Pitfalls and Side-Effects of Management

When stent thrombosis occurs, it is imperative to determine the cause for the event; however, the suspected cause of stent thrombosis is often not reported. Likely in the majority of cases, this is due to lack of antiplatelet therapy. This is especially a concern in the perioperative period. Other reasons for stent thrombosis can lie with the stent itself, such as stent underexpansion or malapposition (acute or delayed). This would only be discerned by intravascular ultrasound or optical coherence tomography, which should be considered in all cases of stent thrombosis.

IV. Management with Co-Morbidities

Patient noncompliance is an important comorbidity thatmay have resulted in the stent thrombosis. For example, such a patient may not have taken the recommended aspirin/ADP receptor antagonist. This history might influence if an additional stent is used during PCI for the stent thrombosis and if an additional stent is used, a bare-metal stent might be a better choice.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission

Patient education is critically important to prevent stent thrombosis. It is mandatory that patients who receive a stent are educated about the importance of dual antiplatelet therapy and the recommended duration of therapy. Any deviation from this recommendation (i.e., for a surgical procedure) should be under the direction of a cardiologist.

Prognosis and Scope of the Problem

Patients who suffer from stent thrombosis have a poor prognosis. Up to two thirds of patients who have stent thrombosis will die or have a large myocardial infarction.

Predictors of Early Stent Thrombosis

Early stent thrombosis is often due to a technical aspect related to the procedure. This includes issues such as stent underexpansion, stent asymmetry, incomplete apposition, tissue prolapse through stent struts, residual dissection, thrombus, persistent slow flow, or untreated upstream or downstream lesions.

Lack of adequate antiplatelet therapy during this early period increases the risk of stent thrombosis. Examples of inadequate antiplatelet therapy would be aspirin without a periprocedural glycoprotein IIb/IIIa inhibitor or an adenosine diphosphate (ADP) receptor antagonist (i.e., clopidogrel, prasugrel, or ticagrelor).

After bare-metal stent PCI, aspirin is recommended for life and an ADP receptor antagonist for a minimum of 4 to 6 weeks and ideally up to 12 months. Early drug-eluting stent thrombosis shares the same predictors of early bare-metal stent thrombosis.

Predictors of Late Stent Thrombosis

Late and very late stent thrombosis is usually due to the type of stent (i.e., first generation drug-eluting) and antiplatelet therapy (i.e., premature termination of ADP receptor antagonist within 6 months or complete termination of antiplatelet agents at any time). As mentioned previously, late stent thrombosis of a bare-metal stent is exceedingly rare and based on available data, stent thrombosis of a second generation drug-eluting stent also appears quite rare.

While restenosis usually presents with gradually worsening anginal symptoms, the culminating event of this process is sometimes an acute coronary syndrome (up to one third of the time). For example, during PCI, restoration of flow through a thrombotic occlusion may sometimes reveal severe underlying restenosis. This could be the mechanism of very late stent thrombosis of a bare-metal stent.

For completeness, the following other characteristics have been associated with late stent thrombosis: acquired incomplete stent apposition, diabetes, small vessels/small stents, long stent length/multiple stents, stent underexpansion, renal failure, acute coronary syndrome at the index procedure, bifurcation lesion, left ventricular dysfunction, residual disease in the culprit vessel, left main or left anterior descending artery stent, malignancy, calcified vessel, chronic total occlusion, in-stent restenosis, younger age, peripheral artery disease, current smoking, and prior stroke.

Management of antiplatelet therapy in the perioperative period is especially problematic and will be discussed below.

Risk of Stent Thrombosis with Second Generation Drug-Eluting Stents

The risk of stent thrombosis with second generation drug-eluting stents appears to be quite low. Meta-analyses have documented lower rates of stent thrombosis with everolimus-eluting stents than first generation drug-eluting stents.

Although it is recommended that patients who receive a second generation drug-eluting stent receive 12 months of uninterrupted antiplatelet therapy, some lines of evidence suggest that durations as short as 6 months may be safe; however, other data support a longer duration of therapy. Further research is needed and ongoing to clarify what the optimal duration of dual antiplatelet therapy should be with these newer devices.

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What’s the evidence?

Iakovou, I. “Incidence, predictors, and outcome of thrombosis after successful implantation of drug-eluting stents”. JAMA. vol. 293. 2005. pp. 2126-31. (Observation study that describes the incidence, predictors, and outcome of drug-eluting stent thrombosis.)

Bavry, AA. “Late thrombosis of drug-eluting stents: a meta-analysis of randomized clinical trials”. Am J Med. vol. 119. 2006. pp. 1056-61. (Meta-analysis of randomized clinical trials that documented a 5-fold increased risk of very late stent thrombosis with drug-eluting stents versus bare-metal stents.)

Stone, GW. “Safety and efficacy of sirolimus- and paclitaxel-eluting coronary stents”. N Engl J Med. vol. 356. 2007. pp. 998-1008. (Pooled analysis of randomized clinical trials that documented an increased rate of very late stent thrombosis with drug-eluting stents versus bare-metal stents.)

Daemen. “Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: Data from a large two-institutional cohort study”. Lancet. vol. 369. 2007. pp. 667-78. (Large observational study which documented an increasing cumulative incidence of drug-eluting stent thrombosis during the follow-up period.)

“ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery”. Circulation. vol. 116. 2007. pp. 1971-96. (Guideline document that defines the minimum duration of dual antiplatelet therapy for bare-metal and drug-eluting stents.)

Genereux, P. “Impact of Intraprocedural stent thrombosis during percutaneous coronary intervention”. J Am Coll Cardiol. vol. 63. 2014. pp. 619-29. (Observational study from CHAMPION PHOENIX trial, which documented a reduction in intra-procedural stent thrombosis with cangrelor.)

Palmerini, T. “Long-term safety of drug-eluting and bare-metal stents: evidence from a comprehensive network meta-analysis”. J Am Coll Cardiol. vol. 65. 2015. pp. 2496-507. (Comprehensive network meta-analysis, which documented very low rates of stent thrombosis with second generation drug-eluting stents.)

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Stent thrombosis

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A stent, like any foreign body that comes into contact with blood, can cause thrombosis at the site of implantation. The surface of the stent has the ability to «attract» platelets, but after a short time the metal surface is covered with precipitating proteins, which somewhat reduces the risk for stent thrombosis. In 2-4 weeks. After implantation of HTIC and a few months after implantation of SLP, coating of the protein film with an unintentional coating takes place, which sharply reduces the risk of stent thrombosis.

Temporary stent thrombosis characteristics

Type of thrombosis

Time of development

24 hours — 30 days

After 1 year or more

[1], [2]

Causes of stent thrombosis

The risk factors for acute stent thrombosis are stenting in acute myocardial infarction, intervention on venous shunts, lack of ASA, clopidogrel on the eve of the procedure, as well as inadequate coagulation during PCI, preservation of residual dissection. The main risk factors for subacute stent thrombosis are: retention of residual dissection, thrombus, protrusion of tissue through the stent cells into the lumen of the vessel, stenting of large and complicated lesions, as well as under-opening of the stent, and stopping the use of antiplatelet agents.

The risk of stent thrombosis in patients with ACS and type 2 diabetes is increased. In patients with ACS, the most important risk factors for stent thrombosis are severity of coronary artery disease, low hemoglobin level, small diameter of implantable stent, and lack of reception of thienopyridipes before the procedure.

Among all stent thromboses, the most common are subacute (41%) and acute TC (32%), late and very late stent thromboses account for about 26% of all cases. In contrast to late thrombosis, the frequency of development of acute and subacute stent thrombosis is the same with NPS and SLP. In at least one study, the use of stents coated with heparin reduced the incidence of acute carotid artery disease compared to conventional NPCs.

In early studies in which post-stenting was recommended, the use of ASA, dipyridamole and warfarin, the incidence of stent thrombosis reached 20%, and bleeding often developed. Later it was shown that in most cases acute TC occurs when the stent is underopen, which led to routine use of high pressure during stenting. In addition, the efficacy of a 4-week course of dual antiplatelet therapy (ASA + ticlopidine) after stenting was proven. All these measures have made it possible to reduce the incidence of acute and subacute stent thrombosis to less than 1%. The average time of onset of subacute TS decreased from 6 to 1-2 days. At the same time, the exclusion of warfarin from the obligatory TS prophylaxis regimen reduced the frequency of hemorrhagic complications. In the following, ticlopidine was almost universally replaced with clopidogrel, since at the same efficacy it is characterized by a lower incidence of adverse events.

Despite the reduction in frequency, stent thrombosis remains one of the most dangerous complications of stenting. As a rule, it manifests itself as a severe anginal infection, accompanied by ST segment elevation. In the STRESS study, mortality in subacute stent thrombosis was 20%, and in the remaining 80% of cases, Q-IM silt developed and emergency CABG was needed. In the last registers, the total 30-day mortality and MI frequency remain high — at the level of 15 and 78%, respectively. In the OPTIMIST study, mortality, even with PCI, for stent thrombosis was 12% at 30 days pi 17% at 6 months. The type of stent at which thrombosis developed does not affect short-term and long-term mortality. Adverse factors that worsen the 6-month prognosis in such patients are the absence of recovery of optimal blood flow, the implantation of the second stent for barely stent thrombosis, the three-vessel lesion, and the presence of 2 or more overlapping stents.

[3], [4], [5], [6], [7], [8], [9], [10], [11]

Treatment of stent thrombosis

Stent thrombosis is an emergency life-threatening situation. The procedure of choice is primary angioplasty, the task of which is the mechanical recanalization of the thrombosed stent. Restoration of antegrade blood flow can be achieved on average in 90% of cases, but the optimal result is observed only in 64% of cases. The optimal result was rarely achieved with PNA involvement, development of CLS, multivessel lesions, and also with distal embolization by thrombotic masses. During the procedure, the use of IIb / IIIa receptor blockers is recommended, especially in high-risk patients: hypercoagulability, thrombocytosis, long stent implantation, bifurcation lesion, small vessel diameter, residual dissection, no-reflow phenomenon. In most cases, balloon angioplasty is sufficient, possibly with the use of devices for thrombus aspiration. Reinstallation of the stent should be performed only in the case of pronounced residual dissection. According to the OPTIMIST register, stent implantation is required on average 45% of the time. If it is impossible to perform PCI, TLT is used.

The total frequency of repeated vehicle in the next 6 months. A high of about 16.2% (while according to the ARC classification, the frequency of proven, probable and possible TS is 6.7, 5.7 and 3.8% respectively). The average time to the occurrence of a repeated TC is 45 days (from 2 to 175 days). The type of stent does not affect the frequency of the repeated vehicle. In the case of repeated implantation of the stent in emergency PCI, the risk of repeated TS is increased 4-fold. Treatment of re-stent thrombosis is identical to the primary one. If there is insufficient platelet aggregation when taking standard double antiplatelet therapy (

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