Intraprocedural stent thrombosis: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* IPST can occur with [[bare metal stent]]s and [[DES]]. Several theories suggest possible explanation to IPST in [[DES]]. DES characteristics, such as drug-induced thrombogenicity, whether using [[sirolimus]] or [[paclitaxe]]l, and its in-vitro [[platelet]] aggregation effects<ref name="pmid9870481">{{cite journal| author=Babinska A, Markell MS, Salifu MO, Akoad M, Ehrlich YH, Kornecki E| title=Enhancement of human platelet aggregation and secretion induced by rapamycin. | journal=Nephrol Dial Transplant | year= 1998 | volume= 13 | issue= 12 | pages= 3153-9 | pmid=9870481 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9870481 }} </ref> along with its remarkable lipophilic bioavailability within the coronary milieu,<ref name="pmid14727933">{{cite journal| author=McKeage K, Murdoch D, Goa KL| title=The sirolimus-eluting stent: a review of its use in the treatment of coronary artery disease. | journal=Am J Cardiovasc Drugs | year= 2003 | volume= 3 | issue= 3 | pages= 211-30 | pmid=14727933 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14727933 }} </ref> stent platform effect,<ref name="pmid15029110">{{cite journal| author=Kereiakes DJ, Choo JK, Young JJ, Broderick TM| title=Thrombosis and drug-eluting stents: a critical appraisal. | journal=Rev Cardiovasc Med | year= 2004 | volume= 5 | issue= 1 | pages= 9-15 | pmid=15029110 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15029110 }} </ref> polymer coating material,<ref name="pmid15029110">{{cite journal| author=Kereiakes DJ, Choo JK, Young JJ, Broderick TM| title=Thrombosis and drug-eluting stents: a critical appraisal. | journal=Rev Cardiovasc Med | year= 2004 | volume= 5 | issue= 1 | pages= 9-15 | pmid=15029110 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15029110 }} </ref> and open-cell stent design all seem plausible hypotheses that nonetheless require further validation. Operator-dependent factors, such as adequate stent placement have also been postulated.<ref name="pmid15148281">{{cite journal| author=Chieffo A, Bonizzoni E, Orlic D, Stankovic G, Rogacka R, Airoldi F et al.| title=Intraprocedural stent thrombosis during implantation of sirolimus-eluting stents. | journal=Circulation | year= 2004 | volume= 109 | issue= 22 | pages= 2732-6 | pmid=15148281 | doi=10.1161/01.CIR.0000131890.83839.5B | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15148281 }} </ref> | * IPST can occur with [[bare metal stent]]s and [[DES]]. Several theories suggest possible explanation to IPST in [[DES]]. DES characteristics, such as drug-induced thrombogenicity, whether using [[sirolimus]] or [[paclitaxe]]l, and its in-vitro [[platelet]] aggregation effects<ref name="pmid9870481">{{cite journal| author=Babinska A, Markell MS, Salifu MO, Akoad M, Ehrlich YH, Kornecki E| title=Enhancement of human platelet aggregation and secretion induced by rapamycin. | journal=Nephrol Dial Transplant | year= 1998 | volume= 13 | issue= 12 | pages= 3153-9 | pmid=9870481 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9870481 }} </ref> along with its remarkable lipophilic bioavailability within the coronary milieu,<ref name="pmid14727933">{{cite journal| author=McKeage K, Murdoch D, Goa KL| title=The sirolimus-eluting stent: a review of its use in the treatment of coronary artery disease. | journal=Am J Cardiovasc Drugs | year= 2003 | volume= 3 | issue= 3 | pages= 211-30 | pmid=14727933 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14727933 }} </ref> stent platform effect,<ref name="pmid15029110">{{cite journal| author=Kereiakes DJ, Choo JK, Young JJ, Broderick TM| title=Thrombosis and drug-eluting stents: a critical appraisal. | journal=Rev Cardiovasc Med | year= 2004 | volume= 5 | issue= 1 | pages= 9-15 | pmid=15029110 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15029110 }} </ref> polymer coating material,<ref name="pmid15029110">{{cite journal| author=Kereiakes DJ, Choo JK, Young JJ, Broderick TM| title=Thrombosis and drug-eluting stents: a critical appraisal. | journal=Rev Cardiovasc Med | year= 2004 | volume= 5 | issue= 1 | pages= 9-15 | pmid=15029110 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15029110 }} </ref> and open-cell stent design all seem plausible hypotheses that nonetheless require further validation. Operator-dependent factors, such as adequate stent placement have also been postulated.<ref name="pmid15148281">{{cite journal| author=Chieffo A, Bonizzoni E, Orlic D, Stankovic G, Rogacka R, Airoldi F et al.| title=Intraprocedural stent thrombosis during implantation of sirolimus-eluting stents. | journal=Circulation | year= 2004 | volume= 109 | issue= 22 | pages= 2732-6 | pmid=15148281 | doi=10.1161/01.CIR.0000131890.83839.5B | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15148281 }} </ref> | ||
* AT-III is a naturally occurring thrombin inhibitor that suppresses tissue factor–factor VIIa complex, factor IXa, Xa and thrombin. Its irreversible combination with thrombin inhibits the effect of thrombin on fibrinogen and clot formation<ref name="pmid26188821">{{cite journal |vauthors=Jao YT, Fang CC |title=Intraprocedural stent thrombosis, antithrombin-III dependent heparin resistance and crush technique for bifurcation lesions: the "Devil's Triangle" |journal=Int. J. Cardiol. |volume=199 |issue= |pages=71–4 |date=November 2015 |pmid=26188821 |doi=10.1016/j.ijcard.2015.07.008 |url=}}</ref>. | * [[AT-III]] is a naturally occurring [[thrombin inhibitor]] that suppresses tissue factor–factor VIIa complex, factor IXa, Xa and [[thrombin]]. Its irreversible combination with [[thrombin]] inhibits the effect of [[thrombin]] on [[fibrinogen]] and [[clot]] formation<ref name="pmid26188821">{{cite journal |vauthors=Jao YT, Fang CC |title=Intraprocedural stent thrombosis, antithrombin-III dependent heparin resistance and crush technique for bifurcation lesions: the "Devil's Triangle" |journal=Int. J. Cardiol. |volume=199 |issue= |pages=71–4 |date=November 2015 |pmid=26188821 |doi=10.1016/j.ijcard.2015.07.008 |url=}}</ref>. | ||
* AT-III deficiency or decreased activity increase thrombin and fibrinogen activities, and thus clot formation. AT-III deficiency can be congenital or acquired. * The congenital form occurs in 1/3000 people, while the acquired form is seen in disseminated intravascular coagulation and nephrotic syndrome as a result of increased loss, or in malnutrition, liver cirrhosis or failure, as a result of decreased synthesis. | * AT-III deficiency or decreased activity increase thrombin and [[fibrinogen]] activities, and thus [[clot]] formation. [[AT-III deficiency]] can be [[congenital]] or acquired. * The [[congenital]] form occurs in 1/3000 people, while the acquired form is seen in [[disseminated intravascular coagulation]] and [[nephrotic syndrome]] as a result of increased loss, or in [[malnutrition]], [[liver cirrhosis]] or failure, as a result of decreased synthesis. | ||
* Heparin therapy is the most common iatrogenic cause as it decreases AT-III half-life, while other causes include nitroglycerin and oral estrogen. | * [[Heparin]] therapy is the most common[[ iatrogenic]] cause as it decreases AT-III half-life, while other causes include [[nitroglycerin]] and oral [[estrogen]]. | ||
* Heparin binds to AT-III and enhances the rate of AT-III and thrombin reaction. This interaction activates AT-III to start an anticoagulation cascade that inactivates thrombin, factor Xa and other clotting factors. | * [[Heparin]] binds to AT-III and enhances the rate of AT-III and [[thrombin]] reaction. This interaction activates AT-III to start an [[anticoagulation]] cascade that inactivates thrombin, [[factor Xa]] and other [[clotting factors]]. | ||
* Heparin has no anticoagulant effect in AT-III depleted plasma. | * [[Heparin]] has no anticoagulant effect in AT-III depleted [[plasma]]. | ||
* Heparin resistance is defined as the inability to raise Activating clotting time to expected levels despite adequate dose and plasma concentration. | * [[Heparin]] resistance is defined as the inability to raise Activating clotting time to expected levels despite adequate dose and plasma concentration. | ||
* In cardiothoracic surgery, Heparin resistance is ACT of b400–600 s after 300–600 U/kg of UFH has been given. | * In cardiothoracic surgery, Heparin resistance is ACT of b400–600 s after 300–600 U/kg of UFH has been given. | ||
* In patients with venous thromboembolism, HR is defined as needing N35,000 U of UFH in 24 h to achieve therapeutic levels. | * In patients with [[venous thromboembolism]], HR is defined as needing N35,000 U of UFH in 24 h to achieve therapeutic levels. | ||
* In interventional cardiology, an ACT of N250 s is needed to allow for a safe procedure. | * In [[interventional cardiology]], an ACT of N250 s is needed to allow for a safe procedure. | ||
* Heparin resistance can be AT-dependent or independent. In AT-dependent HR, the anticoagulant effect of heparin decreases when AT-III activity is b80%, and is completely ineffective at b70%. | * Heparin resistance can be AT-dependent or independent. In AT-dependent HR, the anticoagulant effect of heparin decreases when AT-III activity is b80%, and is completely ineffective at b70%. | ||
* AT independent mechanisms include heparin induced thrombocytopenia due to neutralization of heparin effect from binding to platelet factor 4; and increased levels and enhanced activity of factor VIII and fibrinogen<ref name="pmid24184169">{{cite journal |vauthors=Généreux P, Stone GW, Harrington RA, Gibson CM, Steg PG, Brener SJ, Angiolillo DJ, Price MJ, Prats J, LaSalle L, Liu T, Todd M, Skerjanec S, Hamm CW, Mahaffey KW, White HD, Bhatt DL |title=Impact of intraprocedural stent thrombosis during percutaneous coronary intervention: insights from the CHAMPION PHOENIX Trial (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention) |journal=J. Am. Coll. Cardiol. |volume=63 |issue=7 |pages=619–629 |date=February 2014 |pmid=24184169 |doi=10.1016/j.jacc.2013.10.022 |url=}}</ref>. | * AT independent mechanisms include heparin induced thrombocytopenia due to neutralization of heparin effect from binding to platelet factor 4; and increased levels and enhanced activity of factor VIII and fibrinogen<ref name="pmid24184169">{{cite journal |vauthors=Généreux P, Stone GW, Harrington RA, Gibson CM, Steg PG, Brener SJ, Angiolillo DJ, Price MJ, Prats J, LaSalle L, Liu T, Todd M, Skerjanec S, Hamm CW, Mahaffey KW, White HD, Bhatt DL |title=Impact of intraprocedural stent thrombosis during percutaneous coronary intervention: insights from the CHAMPION PHOENIX Trial (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention) |journal=J. Am. Coll. Cardiol. |volume=63 |issue=7 |pages=619–629 |date=February 2014 |pmid=24184169 |doi=10.1016/j.jacc.2013.10.022 |url=}}</ref>. | ||
Revision as of 15:22, 6 November 2019
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammed Salih
Synonyms and keywords: IPST
Overview
Intraprocedural stent thrombosis (IPST) is the formation of a new, increasing, or reappearing occlusive or non-occlusive thrombus of grade ≤2 that occurs before the completion of the Percutaneous Coronary Intervention (PCI) procedure, and is specifically located within the recently deployed stent or immediately adjacent to it.[1] It is considered a rare subset of Intraprocedural thrombotic events (IPTE). Although it rarely happens, it has been strongly associated with unfavorable periprocedural outcomes.[2] It is defined as an angiographically confirmed intraluminal filling defect within the stent that results in occlusive or non-occlusive thrombolysis in myocardial infarction (TIMI) grade-0 or 1 anterograde flow, secondary to the development of new or increasing thrombus within or adjacent to a recently implanted stent, occurring during the index procedure or before the percutaneous coronary intervention (PCI) is completed. It is also present when the baseline level of thrombus was decreasing or has resolved after balloon angioplasty or thrombus aspiration, but increased again any time after stent implantation, including stent postdilatation. In the large-scale CHAMPION PHOENIX trial, IPST was a relatively infrequent event, occurring in <1% of patients undergoing PCI, but was strongly associated with subsequent ischemic events, including out-of-laboratory ST, MI, and death. The reduction in IPST with cangrelor in CHAMPION PHOENIX contributed to this agent's effectiveness in reducing the rates of ARC-defined stent thrombosis and MI. These data provide strong evidence for a significant association between IPST and adverse short-term clinical outcomes after PCI and support the inclusion of IPST as an important endpoint in future pharmacological and device trials.
Pathophysiology
- IPST can occur with bare metal stents and DES. Several theories suggest possible explanation to IPST in DES. DES characteristics, such as drug-induced thrombogenicity, whether using sirolimus or paclitaxel, and its in-vitro platelet aggregation effects[3] along with its remarkable lipophilic bioavailability within the coronary milieu,[4] stent platform effect,[5] polymer coating material,[5] and open-cell stent design all seem plausible hypotheses that nonetheless require further validation. Operator-dependent factors, such as adequate stent placement have also been postulated.[6]
- AT-III is a naturally occurring thrombin inhibitor that suppresses tissue factor–factor VIIa complex, factor IXa, Xa and thrombin. Its irreversible combination with thrombin inhibits the effect of thrombin on fibrinogen and clot formation[7].
- AT-III deficiency or decreased activity increase thrombin and fibrinogen activities, and thus clot formation. AT-III deficiency can be congenital or acquired. * The congenital form occurs in 1/3000 people, while the acquired form is seen in disseminated intravascular coagulation and nephrotic syndrome as a result of increased loss, or in malnutrition, liver cirrhosis or failure, as a result of decreased synthesis.
- Heparin therapy is the most commoniatrogenic cause as it decreases AT-III half-life, while other causes include nitroglycerin and oral estrogen.
- Heparin binds to AT-III and enhances the rate of AT-III and thrombin reaction. This interaction activates AT-III to start an anticoagulation cascade that inactivates thrombin, factor Xa and other clotting factors.
- Heparin has no anticoagulant effect in AT-III depleted plasma.
- Heparin resistance is defined as the inability to raise Activating clotting time to expected levels despite adequate dose and plasma concentration.
- In cardiothoracic surgery, Heparin resistance is ACT of b400–600 s after 300–600 U/kg of UFH has been given.
- In patients with venous thromboembolism, HR is defined as needing N35,000 U of UFH in 24 h to achieve therapeutic levels.
- In interventional cardiology, an ACT of N250 s is needed to allow for a safe procedure.
- Heparin resistance can be AT-dependent or independent. In AT-dependent HR, the anticoagulant effect of heparin decreases when AT-III activity is b80%, and is completely ineffective at b70%.
- AT independent mechanisms include heparin induced thrombocytopenia due to neutralization of heparin effect from binding to platelet factor 4; and increased levels and enhanced activity of factor VIII and fibrinogen[8].
- In critically ill patients with coexisting severe inflammatory illnesses, where circulating acute phase reactants like platelet-derived factors, plasma proteins, and factor VIII levels are elevated, anti-Xa activity would be a more accurate measure of heparin activity. The reason is that these positively charged proteins readily bind to negatively charged heparin, thereby inhibiting and neutralizing its effect resulting in HR[7].
- Patients undergoing elective angiography and/or PCI are not usually screened for possible congenital or acquired deficiencies via natural anticoagulants prior to the procedure.
- Measuring anti-Xa activity instead of APTT or ACT is time consuming and not readily available in other facilities, especially in patients presenting with AMI, where door-to-balloon time is golden.
- Adventitial tissues and medial smooth muscle cells (SMC) are important sources of tissue factors that are responsible primarily for triggering the extrinsic clotting pathway.
- Thrombosis may occur when a large amount of tissue factor is released into the blood from the medial SMCs following medial tear secondary to excessive injury during stenting[9].
- Factors related to the procedures, including dissection of stent edge, remaining lesion stenosis, incomplete stent coverage, incomplete apposition, and incomplete expansion,can cause stent thrombosis[10].
Epidemiology and Demographics
- The frequency of occurrence currently ranges between 0.5 – 1.7% of all PCI procedures.
- IPST occurred in 0.7% of PCI when frame-by-frame analysis was done for 6591 patients enrolled in the ACUITY and HORIZONS-AMI (Harmonizing Outcomes With Revascularization And Stents In Acute Myocardial Infarction) trials.[2]
- Similarly, an IPST rate of 1.2% was document in another study in 2013 following enrollment of 1901 patients.[11]
- The incidence of IPST was 0.7% in two other studies, the first of which reviewed the frequency of IPST in 1320 patients less than 75 years old undergoing PCI with first generation DES and whereas the second study enrolled 670 patients undergoing elective DES.[6][9]
- Finally, 1.7% of 181 patients had IPST when evaluating DES implantation in bifurcation lesions using “crush technique” in 2005.[12]
Risk Factors
Interestingly, conventional risk factors and correlates of early and late postprocedural stent thrombosis do not seem to be the same as those for IPST.
Associated Factors
Although data in the literature is still conflicting, IPST has been variably correlated to several parameters:
- ST-segment elevation MI (STEMI) at presentation[13]
- High white blood cell count[13]
- Implantation of bare metal stents rather than drug-eluting stents (DES)[13]
- Increased total stent length: stent sizes are commonly lengthier in DES[6]
- Increased thrombus size: baseline thrombus was visible in 56.5% of cases with IPST vs. only 12.3% of cases with no IPST[1]
- Thrombotic lesions[13]
- Lesion location at bifurcations: increase of IPST risk from 0.5% to 1.3%[9]
- Increased diameter of stenosis: average degree of stenosis was 81.58% in patients with IPST vs. 70.23% in patients without IPST[1]
- “Crush” bifurcation stenting[14]
- Worse minimum pre-PCI TIMI flow: TIMI flow grade 0 or TIMI flow grade 1[1]
- Bivalirudin monotherapy: patients who receive treatment with elective glycoprotein IIb/IIIa inhibitors rather than bail-out use seem to be much less likely to experience IPST[6][13]
Natural History, Complications and Prognosis
IPST significantly reduces the overall success rate of PCI, as measured by frequency of achieving TIMI flow grade 3 at the end of index PCI. TIMI flow grade 3 is achieved in 90.9% of patients without IPST vs. 44.7% in patients with IPST. Given its significant and unique role in outcome, there is currently increasing advocacy to routinely report IPST in PCI and to add it as a distinctive entity in the Academic Research Consortium (ARC) definition of stent thrombosis.[2]
Intraprocedural and follow-up data on patients who experience IPST reveal the most common significant complications. The occurrence of IPST remarkably increases the risk of occurrence of IPTE-related complications. The following table summarizes intra-procedural complications of IPST.[2]
| Intraprocedural Complications | Patients with IPST | Patients without IPST |
| Slow or no reflow | 75.5% | 3.2% |
| Distal Embolization | 49% | 1.9% |
| Side branch closure | 14.3% | 0.6% |
Similar to IPTE in general, IPST is an important independent predictor of mortality and morbidity one year post-PCI. One year follow-up data shows a 41.1% rate of death, MI, or TVR in patients who had experienced IPST vs. only 14.5% in patients with no IPST.[2] Other adverse events were also increased in patients with IPST after one year post-PCI, such as postprocedural stent thrombosis, TVR, and non-CABG major bleeding.[11][2]
References
- ↑ 1.0 1.1 1.2 1.3 Xu Y, Qu X, Fang W, Chen H (2013). "Prevalence, correlation and clinical outcome of intra-procedural stent thrombosis in patients undergoing primary percutaneous coronary intervention for acute coronary syndrome". J Interv Cardiol. 26 (3): 215–20. doi:10.1111/joic.12029. PMID 23551235.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Brener, SJ.; Cristea, E.; Kirtane, AJ.; McEntegart, MB.; Xu, K.; Mehran, R.; Stone, GW. (2013). "Intra-procedural stent thrombosis: a new risk factor for adverse outcomes in patients undergoing percutaneous coronary intervention for acute coronary syndromes". JACC Cardiovasc Interv. 6 (1): 36–43. doi:10.1016/j.jcin.2012.08.018. PMID 23266233. Unknown parameter
|month=ignored (help) - ↑ Babinska A, Markell MS, Salifu MO, Akoad M, Ehrlich YH, Kornecki E (1998). "Enhancement of human platelet aggregation and secretion induced by rapamycin". Nephrol Dial Transplant. 13 (12): 3153–9. PMID 9870481.
- ↑ McKeage K, Murdoch D, Goa KL (2003). "The sirolimus-eluting stent: a review of its use in the treatment of coronary artery disease". Am J Cardiovasc Drugs. 3 (3): 211–30. PMID 14727933.
- ↑ 5.0 5.1 Kereiakes DJ, Choo JK, Young JJ, Broderick TM (2004). "Thrombosis and drug-eluting stents: a critical appraisal". Rev Cardiovasc Med. 5 (1): 9–15. PMID 15029110.
- ↑ 6.0 6.1 6.2 6.3 Chieffo A, Bonizzoni E, Orlic D, Stankovic G, Rogacka R, Airoldi F; et al. (2004). "Intraprocedural stent thrombosis during implantation of sirolimus-eluting stents". Circulation. 109 (22): 2732–6. doi:10.1161/01.CIR.0000131890.83839.5B. PMID 15148281.
- ↑ 7.0 7.1 Jao YT, Fang CC (November 2015). "Intraprocedural stent thrombosis, antithrombin-III dependent heparin resistance and crush technique for bifurcation lesions: the "Devil's Triangle"". Int. J. Cardiol. 199: 71–4. doi:10.1016/j.ijcard.2015.07.008. PMID 26188821.
- ↑ Généreux P, Stone GW, Harrington RA, Gibson CM, Steg PG, Brener SJ, Angiolillo DJ, Price MJ, Prats J, LaSalle L, Liu T, Todd M, Skerjanec S, Hamm CW, Mahaffey KW, White HD, Bhatt DL (February 2014). "Impact of intraprocedural stent thrombosis during percutaneous coronary intervention: insights from the CHAMPION PHOENIX Trial (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention)". J. Am. Coll. Cardiol. 63 (7): 619–629. doi:10.1016/j.jacc.2013.10.022. PMID 24184169.
- ↑ 9.0 9.1 9.2 Biondi-Zoccai GG, Sangiorgi GM, Chieffo A, Vittori G, Falchetti E, Margheri M, Barbagallo R, Tamburino C, Remigi E, Briguori C, Iakovou I, Agostoni P, Tsagalou E, Melzi G, Michev I, Airoldi F, Montorfano M, Carlino M, Colombo A (June 2005). "Validation of predictors of intraprocedural stent thrombosis in the drug-eluting stent era". Am. J. Cardiol. 95 (12): 1466–8. doi:10.1016/j.amjcard.2005.01.099. PMID 15950573.
- ↑ Inoguchi Y, Kaku B, Kitagawa N, Katsuda S (May 2019). "Novel use of a stent graft for uncontrollable intraprocedural stent thrombosis in a patient with acute myocardial infarction". Catheter Cardiovasc Interv. doi:10.1002/ccd.28346. PMID 31141303.
- ↑ 11.0 11.1 Xu, Y.; Qu, X.; Fang, W.; Chen, H. (2013). "Prevalence, correlation and clinical outcome of intra-procedural stent thrombosis in patients undergoing primary percutaneous coronary intervention for acute coronary syndrome". J Interv Cardiol. 26 (3): 215–20. doi:10.1111/joic.12029. PMID 23551235. Unknown parameter
|month=ignored (help) - ↑ Ge L, Airoldi F, Iakovou I, Cosgrave J, Michev I, Sangiorgi GM; et al. (2005). "Clinical and angiographic outcome after implantation of drug-eluting stents in bifurcation lesions with the crush stent technique: importance of final kissing balloon post-dilation". J Am Coll Cardiol. 46 (4): 613–20. doi:10.1016/j.jacc.2005.05.032. PMID 16098424.
- ↑ 13.0 13.1 13.2 13.3 13.4 Brener SJ, Cristea E, Kirtane AJ, McEntegart MB, Xu K, Mehran R; et al. (2013). "Intra-procedural stent thrombosis: a new risk factor for adverse outcomes in patients undergoing percutaneous coronary intervention for acute coronary syndromes". JACC Cardiovasc Interv. 6 (1): 36–43. doi:10.1016/j.jcin.2012.08.018. PMID 23266233.
- ↑ Hoye A, Iakovou I, Ge L, van Mieghem CA, Ong AT, Cosgrave J; et al. (2006). "Long-term outcomes after stenting of bifurcation lesions with the "crush" technique: predictors of an adverse outcome". J Am Coll Cardiol. 47 (10): 1949–58. doi:10.1016/j.jacc.2005.11.083. PMID 16697310.