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Simultaneous multivessel acute drug-eluting stent thrombosis
International Journal of Cardiology 113 (2006) e11 – e15 www.elsevier.com/locate/ijcard
Letter to the Editor
Simultaneous multivessel acute drug-eluting stent thrombosis Joel A. Garcia, Adam Hansgen, Ivan P. Casserly ⁎ Division of Cardiology, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262, United States Denver VA Medical Center, Department of Cardiology, 1055 Clermont Street, Denver, CO 80220, United States Received 17 December 2005; accepted 28 January 2006
Abstract Stent thrombosis (ST) in the era of bare metal stents (BMS) using high-pressure stent deployment and combined anti-platelet therapy is an uncommon but feared complication. There is concern for an elevated risk of stent thrombosis (ST) with drug-eluting stents (DES). We describe a case of simultaneous multivessel drug-eluting stent thrombosis 8 h after deployment of paclitaxel-eluting stents in the right coronary (RCA) and left anterior descending (LAD) arteries. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Stent thrombosis (ST); Drug-eluting stents (DES); Percutaneous coronary intervention (PCI); Acute coronary syndrome (ACS)
1. Introduction Stent thrombosis (ST) is a feared complication of percutaneous coronary interventions (PCI). Data from the bare metal stent (BMS) era shows an ST frequency of 1–2%. There is a concern for an increased risk of ST in the drugeluting stent (DES) era, although convincing data is lacking. We report an unusual case of acute ST in separate coronary arteries following multivessel stent placement. We discuss the potential mechanism of ST in this patient and highlight the need for extra vigilance with respect to anti-platelet therapy in the DES era. 2. Case report A 58-year-old male was referred for cardiac catheterization following presentation with a 2-week history of unstable angina and an electrocardiogram that demonstrated anterolateral ST wave depression (Fig. 1). There was no evidence of myonecrosis. His past medical history was significant for coronary artery disease (CAD) with multiple myocardial
⁎ Corresponding author. Tel.: +1 303 393 2826; fax: +1 303 393 5054. E-mail address: [email protected] (I.P. Casserly). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.01.073
infarctions (MI), two prior percutaneous coronary interventions (PCI), diabetes mellitus (DM), hypertension (HTN), and hyperlipidemia. The patient was on chronic aspirin (ASA) therapy and was pre-loaded with clopidogrel (300 mg) the day before the initial procedure. Coronary angiography showed that the left anterior descending artery (LAD) had a focal area of severe in-stent restenosis (80%) at the distal margin of a previously placed BMS (Fig. 2A). The circumflex artery had no significant disease. The right coronary artery (RCA) was dominant and had a 90% stenosis in its mid segment (Fig. 2B). Based on the angiographic findings, the patient underwent LAD and RCA stenting. The periprocedural antithrombotic regimen consisted of a 3500 unit bolus of unfractionated heparin (UFH) to a target ACT of 250–300 s. A 6 Fr AR2 guiding catheter (Vistabrite, Cordis, Miami, FL) was used to engage the RCA. An Asahi soft 0.014″ × 300 cm guidewire (Abbott Vascular Laboratories, Abbott Park, IL, USA) was used to cross the lesion. The lesion was predilated with a 2.5 × 12 mm Maverick balloon (Boston Scientific, MA, USA) at 8 ATM and stented with a 3.5 × 28 mm Taxus Express Stent (Boston Scientific, MA, USA) which was deployed at 14 ATM. Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 2C).
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Fig. 1. Baseline electrocardiogram (ECG) showing lateral ischemia with ST depression in the precordial leads V5–V6 (see arrows).
A 6 Fr 3.75 EBU guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the LCA. An Asahi soft 0.014″ × 300 cm guidewire (Abbott Vascular Laboratories, Abbott Park, IL, USA) was used to cross the LAD lesion. Direct stenting was performed with a 3.0 × 24 mm Taxus Express Stent (Boston Scientific, MA, USA) which was deployed at 14 ATM. Post-dilation was performed with a 3.5 × 15 mm Quantum Maverick balloon (Boston Scientific, MA, USA). Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 2D). Final ACT was 270 s. Post intervention, the patient was admitted to the ICU for observation. After 8 h he developed acute sub-sternal chest pain and a subsequent electrocardiogram (ECG) showed anterior and inferior ST segment elevations (Fig. 3). At this point it was unclear if this represented ST of the wrap-around LAD and/or the RCA. Abciximab was started (bolus and infusion) and the patient was taken emergently to the cardiac catheterization laboratory. He was hemodynamically stable during this period. Angiography of the LAD showed ST with TIMI 3 flow (Fig. 4A). Angiography of the RCA demonstrated a proximal thrombotic occlusion (Fig. 4B), with faint left-toright collaterals to the PDA on injection of the LCA. A 7 Fr AR2 guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the RCA. A Whisper 0.014″ × 300 cm guidewire (Guidant Corporation, St Paul, MN, USA) was used to cross the RCA lesion. A 3.5 × 12 mm Stormer (Medtronic, Minneapolis, MN, USA) NC (noncompliant) balloon was used to dilate the lesion. Cineangiography demonstrated TIMI III flow, but there was persistent evidence of significant thrombus at the distal and proximal margins of the previously placed stent. A 3.5 × 16 mm Taxus Express Stent (Boston Scientific, MA, USA) was deployed at 14 ATM at the distal margin of the stent. A 3.5 × 12 mm Taxus Express Stent (Boston Scientific, MA, USA) was deployed at 14 ATM at the proximal margin of the initial
stent. The overlap areas were dilated with a 3.75 × 21 mm Stormer (Medtronic, Minneapolis, MN, USA) NC (noncompliant) balloon. Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 4C). A 7 Fr 3.75 EBU guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the LCA. A 0.014″ × 300 cm Patriot guidewire (Boston Scientific, MA, USA) was used to cross the LAD lesion. An Atlantis SR Plus 40 MHz intra-vascular ultrasound (IVUS) catheter interrogation of the LAD revealed no dissection, good stent apposition, and the presence of an intraluminal filling defect consistent with thrombus. A 2.75 × 15 mm Sprinter balloon (Medtronic, Minneapolis, MN, USA) was used to dilate the lesion. Following angioplasty, there was evidence of a dissection at the distal edge of the previously placed stent, which was treated with a 3.0 × 12 mm Taxus Express Stent (Boston Scientific, MA, USA). The overlap area between these stents was dilated with a 3.25 × 21 NC Stormer (Medtronic, Minneapolis, MN, USA) NC (non-compliant) balloon. Cineangiography demonstrated 0% residual stenosis, no dissection, no thrombus, and TIMI III flow (Fig. 4D). The patient was hemodynamically stable. There were no vascular complications and the patient was discharged 72 h later on aspirin and clopidogrel 75 mg twice a day for 3 months, and then once a day for a further 9 months. 3. Discussion Simultaneous multivessel ST is a rare, and to our knowledge, a previously unreported phenomenon. The angiographic result at the time of the index intervention showing no residual stenosis or dissection, and the presence of adequate stent apposition in the LAD by IVUS at the time of repeat intervention, clearly argue against mechanical factors as being responsible for this event. During the stent thrombosis event, the patient was hemodynamically stable, arguing against secondary thrombosis of one stent due to hypotension
J.A. Garcia et al. / International Journal of Cardiology 113 (2006) e11–e15
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Fig. 2. (A) Severe in-stent restenosis (80%) at the distal margin of the previous stent within the LAD (see arrows). (B) Mid RCA severe stenosis (see arrow). (C) LAD angiography demonstrating 0% residual stenosis, TIMI III flow, and no dissection. (D) RCA angiography demonstrating 0% residual stenosis, TIMI III flow, and no dissection.
Fig. 3. Follow up electrocardiogram (ECG) showing anterior and inferior ST elevation (see arrows).
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Fig. 4. (A) LAD with acute stent thrombosis (see arrows). (B) RCA with acute stent thrombus and no flow (see arrow). (C) Post procedure angiography of the LAD demonstrating 0% residual stenosis, TIMI III flow, and no dissection. (D) Post procedure angiography of the RCA demonstrating 0% residual stenosis, TIMI III flow, and no dissection.
from an initial single stent thrombosis. A lack of adequate anti-platelet effect in the peri-procedural period seems a more reasonable explanation, given the simultaneous thrombosis of stents in two different coronary territories. An important question raised by this case is whether our current practices of peri-procedural anti-platelet therapy are valid in the era of DES. Since the availability of DES, there has been a definite trend toward a lower rate of utilization of glycoprotein (GP) IIb/IIIa inhibitors in PCI. This has been partially driven by the monetary cost of procedures, and additionally by several studies demonstrating that pre-treatment with clopidogrel may obviate the need for periprocedural GP IIb/IIIa inhibition. For example, the ISAR-REACT (Intracoronary Stenting and Anti-thrombotic Regimen-Rapid Early Action for Coronary Treatment) and ISAR-SWEET studies (Intra-
coronary Stenting and Antithrombotic Regimen: Is Abciximab a Superior Way to Eliminate Elevated Thrombotic Risk in Diabetics) demonstrated no difference in ischemic complications between patients treated with pre-procedural clopidogrel, and those treated with GP IIb/IIIa inhibitors and routine clopidogrel treatment at the time of the procedure [1,2]. Although it should be accepted that the patient populations studied in these trials were low-risk, post-hoc analyses of higher-risk patient subsets with acute coronary syndromes have demonstrated that the benefit for GPIIb/IIIa inhibitors is largely confined to those with evidence of myonecrosis (i.e., Troponin positive) [3–7]. Based on this data, it was felt that in the absence of elevation of cardiac biomarkers, that pretreatment with clopidogrel and aspirin represented adequate peri-procedural anti-platelet therapy in our patient. The clinical outcome in this case argues that it was inadequate. It is
J.A. Garcia et al. / International Journal of Cardiology 113 (2006) e11–e15
unclear if this reflects an element of resistance to anti-platelet medication in this individual patient, or if the use of a DES was a major contributor, or both. This case has certainly lowered our threshold for the use of GP IIb/IIIa inhibitors in troponin negative acute coronary syndrome patients treated with DES, and may serve as a cautionary tale for other interventional cardiologists. It needs to be highlighted that much of our data with respect to clopidogrel pre-treatment and GP IIb/IIIa inhibition were performed in the era of BMS. Therefore, it may be prudent to pursue a more conservative (i.e., use of more aggressive anti-platelet regimens) approach to anti-platelet therapy in higher risk clinical situations (clinical and anatomic) until the paradigms for periprocedural anti-platelet therapy can be re-established in the era of DES.
[3]
[4]
[5]
[6]
References [1] Kandzari DE, Berger PB, et al, for the ISAR-REACT Study investigators. Influence of treatment duration with a 600-mg dose of clopidogrel before percutaneous coronary revascularization. J Am Coll Cardiol 2004;44: 2133–6. [2] Mehilli J, Kastrati A, Schulen H, et al, for the Intracoronary Stenting and Antithrombotic Regimen: Is abciximab a Superior Way to Eliminate
[7]
e15
Elevated Thrombotic Risk in Diabetics (ISAR-SWEET) Study Investigators. Randomized clinical trial of abciximab in diabetic patients undergoing elective percutaneous coronary interventions after treatment with a high loading dose of clopidogrel. Circulation 2004;110:3627–35. Yusuf S, Zhao F, Mehta SR, et al, for the Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. Effects of Clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345: 494–502. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: The PCI-CURE study. Lancet 2001;358:527–33. Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. C7E3 Fab antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) Study Investigators. N Engl J Med 1999;340:1623–9. Lenderinnk T, Boersma E, Heeschen C, et al. Elevated troponin T and C-reactive protein predict impaired outcome for 4 years in patients with refractory unstable angina, an troponin T predicts benefit of treatment with abciximab in combination with PTCA. Eur Heart J 2003;24: 136–7. Heeschen C, Hamm CW, Goldmann B, et al. Troponin concentration for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of Tirofiban. PRISM Study Investigators. Platelet Receptor Inhibition in Ischemic Syndrome Management. Lancet 1999;354:1757–62.
Letter to the Editor
Simultaneous multivessel acute drug-eluting stent thrombosis Joel A. Garcia, Adam Hansgen, Ivan P. Casserly ⁎ Division of Cardiology, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262, United States Denver VA Medical Center, Department of Cardiology, 1055 Clermont Street, Denver, CO 80220, United States Received 17 December 2005; accepted 28 January 2006
Abstract Stent thrombosis (ST) in the era of bare metal stents (BMS) using high-pressure stent deployment and combined anti-platelet therapy is an uncommon but feared complication. There is concern for an elevated risk of stent thrombosis (ST) with drug-eluting stents (DES). We describe a case of simultaneous multivessel drug-eluting stent thrombosis 8 h after deployment of paclitaxel-eluting stents in the right coronary (RCA) and left anterior descending (LAD) arteries. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Stent thrombosis (ST); Drug-eluting stents (DES); Percutaneous coronary intervention (PCI); Acute coronary syndrome (ACS)
1. Introduction Stent thrombosis (ST) is a feared complication of percutaneous coronary interventions (PCI). Data from the bare metal stent (BMS) era shows an ST frequency of 1–2%. There is a concern for an increased risk of ST in the drugeluting stent (DES) era, although convincing data is lacking. We report an unusual case of acute ST in separate coronary arteries following multivessel stent placement. We discuss the potential mechanism of ST in this patient and highlight the need for extra vigilance with respect to anti-platelet therapy in the DES era. 2. Case report A 58-year-old male was referred for cardiac catheterization following presentation with a 2-week history of unstable angina and an electrocardiogram that demonstrated anterolateral ST wave depression (Fig. 1). There was no evidence of myonecrosis. His past medical history was significant for coronary artery disease (CAD) with multiple myocardial
⁎ Corresponding author. Tel.: +1 303 393 2826; fax: +1 303 393 5054. E-mail address: [email protected] (I.P. Casserly). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.01.073
infarctions (MI), two prior percutaneous coronary interventions (PCI), diabetes mellitus (DM), hypertension (HTN), and hyperlipidemia. The patient was on chronic aspirin (ASA) therapy and was pre-loaded with clopidogrel (300 mg) the day before the initial procedure. Coronary angiography showed that the left anterior descending artery (LAD) had a focal area of severe in-stent restenosis (80%) at the distal margin of a previously placed BMS (Fig. 2A). The circumflex artery had no significant disease. The right coronary artery (RCA) was dominant and had a 90% stenosis in its mid segment (Fig. 2B). Based on the angiographic findings, the patient underwent LAD and RCA stenting. The periprocedural antithrombotic regimen consisted of a 3500 unit bolus of unfractionated heparin (UFH) to a target ACT of 250–300 s. A 6 Fr AR2 guiding catheter (Vistabrite, Cordis, Miami, FL) was used to engage the RCA. An Asahi soft 0.014″ × 300 cm guidewire (Abbott Vascular Laboratories, Abbott Park, IL, USA) was used to cross the lesion. The lesion was predilated with a 2.5 × 12 mm Maverick balloon (Boston Scientific, MA, USA) at 8 ATM and stented with a 3.5 × 28 mm Taxus Express Stent (Boston Scientific, MA, USA) which was deployed at 14 ATM. Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 2C).
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Fig. 1. Baseline electrocardiogram (ECG) showing lateral ischemia with ST depression in the precordial leads V5–V6 (see arrows).
A 6 Fr 3.75 EBU guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the LCA. An Asahi soft 0.014″ × 300 cm guidewire (Abbott Vascular Laboratories, Abbott Park, IL, USA) was used to cross the LAD lesion. Direct stenting was performed with a 3.0 × 24 mm Taxus Express Stent (Boston Scientific, MA, USA) which was deployed at 14 ATM. Post-dilation was performed with a 3.5 × 15 mm Quantum Maverick balloon (Boston Scientific, MA, USA). Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 2D). Final ACT was 270 s. Post intervention, the patient was admitted to the ICU for observation. After 8 h he developed acute sub-sternal chest pain and a subsequent electrocardiogram (ECG) showed anterior and inferior ST segment elevations (Fig. 3). At this point it was unclear if this represented ST of the wrap-around LAD and/or the RCA. Abciximab was started (bolus and infusion) and the patient was taken emergently to the cardiac catheterization laboratory. He was hemodynamically stable during this period. Angiography of the LAD showed ST with TIMI 3 flow (Fig. 4A). Angiography of the RCA demonstrated a proximal thrombotic occlusion (Fig. 4B), with faint left-toright collaterals to the PDA on injection of the LCA. A 7 Fr AR2 guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the RCA. A Whisper 0.014″ × 300 cm guidewire (Guidant Corporation, St Paul, MN, USA) was used to cross the RCA lesion. A 3.5 × 12 mm Stormer (Medtronic, Minneapolis, MN, USA) NC (noncompliant) balloon was used to dilate the lesion. Cineangiography demonstrated TIMI III flow, but there was persistent evidence of significant thrombus at the distal and proximal margins of the previously placed stent. A 3.5 × 16 mm Taxus Express Stent (Boston Scientific, MA, USA) was deployed at 14 ATM at the distal margin of the stent. A 3.5 × 12 mm Taxus Express Stent (Boston Scientific, MA, USA) was deployed at 14 ATM at the proximal margin of the initial
stent. The overlap areas were dilated with a 3.75 × 21 mm Stormer (Medtronic, Minneapolis, MN, USA) NC (noncompliant) balloon. Angiography demonstrated 0% residual stenosis, TIMI III flow, and no dissection (Fig. 4C). A 7 Fr 3.75 EBU guiding catheter (Medtronic, Minneapolis, MN, USA) was used to engage the LCA. A 0.014″ × 300 cm Patriot guidewire (Boston Scientific, MA, USA) was used to cross the LAD lesion. An Atlantis SR Plus 40 MHz intra-vascular ultrasound (IVUS) catheter interrogation of the LAD revealed no dissection, good stent apposition, and the presence of an intraluminal filling defect consistent with thrombus. A 2.75 × 15 mm Sprinter balloon (Medtronic, Minneapolis, MN, USA) was used to dilate the lesion. Following angioplasty, there was evidence of a dissection at the distal edge of the previously placed stent, which was treated with a 3.0 × 12 mm Taxus Express Stent (Boston Scientific, MA, USA). The overlap area between these stents was dilated with a 3.25 × 21 NC Stormer (Medtronic, Minneapolis, MN, USA) NC (non-compliant) balloon. Cineangiography demonstrated 0% residual stenosis, no dissection, no thrombus, and TIMI III flow (Fig. 4D). The patient was hemodynamically stable. There were no vascular complications and the patient was discharged 72 h later on aspirin and clopidogrel 75 mg twice a day for 3 months, and then once a day for a further 9 months. 3. Discussion Simultaneous multivessel ST is a rare, and to our knowledge, a previously unreported phenomenon. The angiographic result at the time of the index intervention showing no residual stenosis or dissection, and the presence of adequate stent apposition in the LAD by IVUS at the time of repeat intervention, clearly argue against mechanical factors as being responsible for this event. During the stent thrombosis event, the patient was hemodynamically stable, arguing against secondary thrombosis of one stent due to hypotension
J.A. Garcia et al. / International Journal of Cardiology 113 (2006) e11–e15
e13
Fig. 2. (A) Severe in-stent restenosis (80%) at the distal margin of the previous stent within the LAD (see arrows). (B) Mid RCA severe stenosis (see arrow). (C) LAD angiography demonstrating 0% residual stenosis, TIMI III flow, and no dissection. (D) RCA angiography demonstrating 0% residual stenosis, TIMI III flow, and no dissection.
Fig. 3. Follow up electrocardiogram (ECG) showing anterior and inferior ST elevation (see arrows).
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J.A. Garcia et al. / International Journal of Cardiology 113 (2006) e11–e15
Fig. 4. (A) LAD with acute stent thrombosis (see arrows). (B) RCA with acute stent thrombus and no flow (see arrow). (C) Post procedure angiography of the LAD demonstrating 0% residual stenosis, TIMI III flow, and no dissection. (D) Post procedure angiography of the RCA demonstrating 0% residual stenosis, TIMI III flow, and no dissection.
from an initial single stent thrombosis. A lack of adequate anti-platelet effect in the peri-procedural period seems a more reasonable explanation, given the simultaneous thrombosis of stents in two different coronary territories. An important question raised by this case is whether our current practices of peri-procedural anti-platelet therapy are valid in the era of DES. Since the availability of DES, there has been a definite trend toward a lower rate of utilization of glycoprotein (GP) IIb/IIIa inhibitors in PCI. This has been partially driven by the monetary cost of procedures, and additionally by several studies demonstrating that pre-treatment with clopidogrel may obviate the need for periprocedural GP IIb/IIIa inhibition. For example, the ISAR-REACT (Intracoronary Stenting and Anti-thrombotic Regimen-Rapid Early Action for Coronary Treatment) and ISAR-SWEET studies (Intra-
coronary Stenting and Antithrombotic Regimen: Is Abciximab a Superior Way to Eliminate Elevated Thrombotic Risk in Diabetics) demonstrated no difference in ischemic complications between patients treated with pre-procedural clopidogrel, and those treated with GP IIb/IIIa inhibitors and routine clopidogrel treatment at the time of the procedure [1,2]. Although it should be accepted that the patient populations studied in these trials were low-risk, post-hoc analyses of higher-risk patient subsets with acute coronary syndromes have demonstrated that the benefit for GPIIb/IIIa inhibitors is largely confined to those with evidence of myonecrosis (i.e., Troponin positive) [3–7]. Based on this data, it was felt that in the absence of elevation of cardiac biomarkers, that pretreatment with clopidogrel and aspirin represented adequate peri-procedural anti-platelet therapy in our patient. The clinical outcome in this case argues that it was inadequate. It is
J.A. Garcia et al. / International Journal of Cardiology 113 (2006) e11–e15
unclear if this reflects an element of resistance to anti-platelet medication in this individual patient, or if the use of a DES was a major contributor, or both. This case has certainly lowered our threshold for the use of GP IIb/IIIa inhibitors in troponin negative acute coronary syndrome patients treated with DES, and may serve as a cautionary tale for other interventional cardiologists. It needs to be highlighted that much of our data with respect to clopidogrel pre-treatment and GP IIb/IIIa inhibition were performed in the era of BMS. Therefore, it may be prudent to pursue a more conservative (i.e., use of more aggressive anti-platelet regimens) approach to anti-platelet therapy in higher risk clinical situations (clinical and anatomic) until the paradigms for periprocedural anti-platelet therapy can be re-established in the era of DES.
[3]
[4]
[5]
[6]
References [1] Kandzari DE, Berger PB, et al, for the ISAR-REACT Study investigators. Influence of treatment duration with a 600-mg dose of clopidogrel before percutaneous coronary revascularization. J Am Coll Cardiol 2004;44: 2133–6. [2] Mehilli J, Kastrati A, Schulen H, et al, for the Intracoronary Stenting and Antithrombotic Regimen: Is abciximab a Superior Way to Eliminate
[7]
e15
Elevated Thrombotic Risk in Diabetics (ISAR-SWEET) Study Investigators. Randomized clinical trial of abciximab in diabetic patients undergoing elective percutaneous coronary interventions after treatment with a high loading dose of clopidogrel. Circulation 2004;110:3627–35. Yusuf S, Zhao F, Mehta SR, et al, for the Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. Effects of Clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345: 494–502. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: The PCI-CURE study. Lancet 2001;358:527–33. Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. C7E3 Fab antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) Study Investigators. N Engl J Med 1999;340:1623–9. Lenderinnk T, Boersma E, Heeschen C, et al. Elevated troponin T and C-reactive protein predict impaired outcome for 4 years in patients with refractory unstable angina, an troponin T predicts benefit of treatment with abciximab in combination with PTCA. Eur Heart J 2003;24: 136–7. Heeschen C, Hamm CW, Goldmann B, et al. Troponin concentration for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of Tirofiban. PRISM Study Investigators. Platelet Receptor Inhibition in Ischemic Syndrome Management. Lancet 1999;354:1757–62.