Pci in stemi. state of the art. Petr widimsky
- 1. PCI in STEMI State of the art Petr Widimsky Cardiocenter, Third Faculty of Medicine, Charles University Prague, CZ.
- 2. Thrombolysis (50% success rates 7% reocclusion risk) Primary PCI (90% success rates 3% reocclusion risk) Modern therapy of AMI: Thrombus removal, Flow restoration
- 3. Reperfusion methods in STEMI: Primary PCI: 90% success rate 8% death /re-MI /stroke 3% reinfarctions 1% strokes 3-7% mortality in trials 5-9% mortality in registries Thrombolysis: 50% success rate 14% death /re-MI /stroke 7% reinfarctions 2% strokes 6-9% mortality in trials 10-17% mortality in registries
- 4. Otto Klein, Praha 1930: World first DIAGNOSTIC cardiac catheterization.
- 7. University Hospital Prague - change of AMI treatment strategy on October 5, 1995: thrombolysis declared non-lege artis 0 2 4 6 8 10 12 STEMI mortality 1994 1996
- 8. CZ 1995: STEMI mortality in the real life according to the hospital type 29 17 17 8 0 5 10 15 20 25 30 In-hospital mortality Small hospitals Medium size hospitals Tertiary hospitals without PCI Tertiary hospitals with PCI
- 9. The „PRAGUE“ Study PRimary Angioplasty in AMI pts. from General community hospitals transported to PTCA Units with / without Emergency thrombolysis (June 2, 1997 - March 23, 1999) Hot Line Session ESC Barcelona 1999 Eur Heart J 2000; 21: 823-31
- 10. Treatment arms (P-1) Group A (TL) Group B (TL+ facil.PCI) Group C (P-PCI) Aspegic 0.5 g SK 1.5 mil. U Aspegic 0.5 g SK 1.5 mil. U Aspegic 0.5 g Heparin 10000 U Treatment in the community hospital SK infusion during the transport to PTCA center Transport to PTCA center
- 11. PRAGUE-1: Combined end- point at 30 days 23% 15% 8% 0 5 10 15 20 25 A B C +/reMI/stroke
- 12. PRAGUE-1: Mortality at 30 days 0 2 4 6 8 10 12 14 A B C Mortality %
- 13. Treatment arms (P-2) Group TL Group P-PCI Aspegic 0.5 g SK 1.5 mil. U Aspegic 0.5 g Heparin 10000 U Treatment in the community hospital Transport to PTCA center
- 14. PRAGUE-2: 30 day outcomes Eur Heart J. 2003 Jan;24(1):94-104 10 6,80 15,2 8,4 0 2 4 6 8 10 12 14 16 Mortality +/re-MI/stroke TL PCI P = 0,12 P < 0,003
- 17. VINO Study: primary PCI for non-STEMI Eur Heart J. 2002 Feb;23(3):230-8. 30days 6months Invasive Conserv 7.5% 13.4% 1.6% 3.1% p<0.05
- 18. P-PCI (after transport) improves outcomes of pts. presenting to small local hospitals.….. 5,7%
- 19. ….to the same extent as P-PCI in pts. presenting directly to PCI centers ! 5,6%
- 20. Metaanalysis of 23 studies TL vs. PCI (Keeley et al., Lancet 2003; 361: 13-20) 9 7 7 3 2 1 14 8 0 2 4 6 8 10 12 14 Mortality Re-MI Stroke Comb.end- point TL PCI % n=7739
- 21. CZECH GUIDELINES FOR STEMI PCIPCIPCIPain-ECG 3-12 hours TLPCIPCIPain-ECG < 3 hours ECG-PCI > 90 min. ECG-PCI 30-90 min. ECG-PCI < 30 min. STEMI (Cor et Vasa 2002; 44: K123-143)
- 22. The Czech Soc.of Cardiology guidelines: the world first guidelines proposing primary PCI as the default treatment strategy 2002 Czech Society of Cardiology 2003 European Society of Cardiology 2004 American College of Cardiology / American Heart Association
- 23. Transport distances to PCI centers (all 22 operating non-stop) in the Czech Republic.
- 24. Czech STEMI registries 1998 vs 2005: The nationwide implementation of P-PCI strategy increased the use of ANY reperfusion therapy from 45% to 93% 7% 55% 38% TL P-PCI No reperfusion therapy 1% 7% 92% P-PCI TL No reperfusion therapy
- 25. Czech STEMI registries 1999 vs 2005: The nationwide implementation of P-PCI strategy completely abolished mortality differences between smaller hospitals and tertiary PCI centers 8 18 0 5 10 15 20 In-hospital mortality Tertiary PCI centers Hospitals without cath-lab 6,8 6,9 0 5 10 15 20 In-hospital mortality Tertiary PCI centers Hospitals without cath-lab
- 26. Recommendations Class LOE • PPCI for STEMI (within 2 hours) •Rescue PCI for failed fibrinolysis (within 12 hours) • PCI for STEMI with shock and contraindications to fibrinolytic therapy irrespective of time delay • Angiography and PCI after successful fibrinolysis (within 24 hours) • Urgent PCI for hemodynamically unstable NSTE- ACS (within 2 hours) • Early PCI for high-risk NSTE-ACS (within 72 hours) I IIa I IIa I I A A B A C A ESC Guidelines for STEMI (2003 2008): PCI for acute CAD
- 27. ESC guidelines: antithrombotic treatment in STEMI
- 28. Acute STEMI is the most thrombogenic situation in atherosclerosis Ruptured / exulcerated coronary plaque Endothelial dysfunction / coronary spasm Platelet activation Coagulation activation Decreased coronary flow / transstenotic gradient LV dysfunction / cardiac output / hypotension
- 29. ESC Guidelines: Antithrombotic treatment options in STEMI treated by PCI
- 30. Initial treatment after diagnostic ECG - aspirin - ADP-receptor blocker - parenteral anticoagulant as early as possible before angiography. The preferred ADP-receptor blockers are prasugrel (60-mg p.o. loading dose, 10-mg maintenance dose) or ticagrelor (180-mg p.o. loading dose, 90-mg maintenance dose b.i.d).
- 31. Anticoagulants in acute STEMI - Heparin (UFH) bolus 70–100 U/kg (no GP IIb/IIIa inhibitor planned) or 50–60 U/kg (GP IIb/IIIa inhibitors expected) - Enoxaparin - Bivalirudin No placebo-controlled trials evaluating UFH in primary PCI but there is a large body of experience with this agent. There are no solid data to recommend the use of activated clotting time to dose or monitor heparin, and if activated clotting time is used, it should not delay recanalization of the infarct-related artery.
- 32. Enoxaparin in STEMI Enoxaparin (0.5 mg/kg i.v. followed by s.c. treatment) was suggested by several nonrandomized studies to provide benefit over UFH in primary PCI. Silvain J et al. BMJ 2012; 344:e553. Montalescot G et al. JACC Cardiovasc Interv 2010; 3(2):203-212. Navarese EP et al. J Thromb Haemost 2011; 9(10):1902-1915. ATOLL trial compared Enox vs. UFN. Primary endpoint (30-day death/ MI complication/ procedural failure / major bleeding) reduced 17% (NS, p = 0.063). Reductions in the composite secondary endpoints (death, re-MI or urgent TVR) and death or MI complication. No indication of increased bleeding from use of enoxaparin over heparin. Montalescot G et al. Lancet 2011; 378(9792):693-703.
- 33. Bivalirudin in STEMI HORIZONS–AMI trial: superiority of bivalirudin over UFH + GP IIb/IIIa inhibitor. Benefit driven by a marked reduction in bleeding (associated with an initial increase in stent thrombosis, which disappeared after 30 days). A large fraction of patients received prerandomization UFH and approximately 10% bailout GP IIb/IIIa blockers. The interpretation of the trial result is slightly confounded by an interaction between prerandomization use of UFH, use of a 600-mg loading dose of clopidogrel. Mehran R et al. Lancet 2009; 374(9696):1149-1159. Stone GW et al. N Engl J Med 2008; 358(21):2218-2230. Dangas GD et al. Circulation 2011; 123(16):1745-1756.
- 34. Anticoagulant therapy after primary PCI ? Routine post-procedural anticoagulant therapy is not indicated after primary PCI. Exception: separate indication for either full-dose anticoagulation (atrial fibrillation, mechanical valves, LV thrombus, pulmonary embolism) or for prophylactic doses (to prevent DVT/PE) in patients requiring prolonged bed rest.
- 35. ESC Guidelines: Antiplatelet therapy in STEMI DAPT: ASA (150–300 mg p.o. or 250 –500 mg i.v. LD, 75–100 mg MD) & prasugrel (60 mg LD, 10 mg MD) or ticagrelor (180 mg LD, 2x90 mg MD). Clopidogrel (600 mg LD, 75 mg MD) if the more effective ADP receptor blockers are contraindicated or unavailable.
- 36. Ticagrelor or prasugrel vs. clopidogrel: 12-month outcomes (G Biondi-Zoccai, International Journal of Cardiology, online Sep 7, 2010) Outcome OR (95% CI) p Death/MI/stroke 0.83 (0.77-0.89) <0.001 Death 0.83 (0.74-0.93) 0.001 Nonfatal MI 0.79 (0.73-0.86) 0.001 Nonfatal stroke 1.12 (0.91-1.38) 0.28 Stent thrombosis 0.61 (0.51-0.74) <0.001 Major bleeding 1.09 (0.99-1.21) 0.08 Drug discontinuation 1.12 (1.05-1.19) <0.001
- 37. Upfront use of GP IIb/IIIa inhibitors Most studies of GPIIb–IIIa inhibitors in STEMI have evaluated abciximab. Findings are mixed regarding the effectiveness of facilitation (early administration) with GPIIb–IIIa inhibitors before catheterization. The controversial literature data, the negative outcome of the only prospective RCT and the beneficial effects of faster acting and more efficacious ADPreceptor blockers in primary PCI do not support pre-hospital or pre- catheterization use of GPIIb–IIIa inhibitors.
- 38. STEMI treated by p-PCI with other (e.g. AF) indication for chronic anticoagulation: ESC guidelines ‘Triple therapy’ (ASA + ADP receptor antagonist + oral anticoagulant) is recommended to reduce the burden of thromboembolic complications and minimize the risk of stent thrombosis. Camm AJ et al. ESC guidelines for the management of atrial fibrillation. Eur Heart J 2010; 31: 2369-2429. Wijns W et al. ESC guidelines on myocardial revascularization. Eur Heart J 2010; 31: 2501-2555.
- 39. This is an area of controversy with missing evidence. Triple therapy increases bleeding complications. Should be used for the shortest possible duration. STEMI pts with an indication for anticoagulation should receive BMS (rather than DES) to minimize the duration of triple therapy to minimize the risk of bleeding. These benefits should be weighed against the benefits of DES in preventing restenosis. Hansen ML et al. Arch Intern Med 2010; 170:1433-1441. Lip GY et al. Eur Heart J 2010; 31(11):1311-1318. Faxon DP et al. Circ Cardiovasc Interv 2011; 4(5):522-534. Rubboli A et al. Ann Med 2008; 40(6):428-436. STEMI treated by p-PCI with other (e.g. AF) indication for chronic anticoagulation: Warnings
- 40. The key question in STEMI therapy 2013: What antithrombotic medication should be used…… …. prior to primary PCI Acute phase pre-PCI antithrombotics ASA P2Y12inhibitor Anticoagulant iv. (+ selective – after CAG - GPIIb/IIIa inhibitors ?) When ≥4 agents are used, no additional benefit, but high bleeding risk …. after primary PCI secondary prevention antithrombotics ASA P2Y12inhibitor (Anticoagulant ???) When ≥3 agents are used, no additional benefit, but high bleeding risk Petr R et al., ESC 2009
- 41. Primary PCI - SUMMARY: The introduction of primary PCI as a default treatment strategy for AMI: 1. Dramatically increased the availability of reperfusion therapy as such 2. Decreased in-hospital and post-discharge mortality 3. Offered similar survival chance to patients from small vilages as to patients from large cities
- 42. Primary PCI – real life cases
- 43. A 39-years old heavy smoker: two infarctions simultaneously due to double stent thrombosis!
- 45. A 73-years old patient with recurrent pain during last 48 hours, inferior Q-waves on admission
- 46. 52-years, man, first STEMI, Killip I. RCA 100%, LAD 90%, OM 80%.
- 47. 68-years, woman, diabetes, second STEMI, Killip III. LAD 95% (culprit, ISR), RCA 100% (CTO), LCX 50%.
- 48. 75-years, man, co-morbidities, inferior STEMI, Killip IV, EF 15% LM 70%, LCX 99% (culprit), RCA 100% (CTO)
- 49. How to treat multivessel disease in STEMI patients Petr Widimsky Cardiocenter „Royal Vineyards“ Charles University Prague Czech Republic
- 50. „Primary PCI strategy“ is not just PCI ! Diagnostic part: Extent of coronary disease Infarct artery + culprit lesion Hemodynamic information, LV function Other diagnosis (AMI excluded) in 2-5% Therapeutic part: Reperfusion Revascularization
- 51. Relative proportion of single-VD vs. three most frequently used PCI strategies for multi-VD Corpus et al. Am Heart J 2004, 148: 493-500.
- 52. In-hospital mortality after multi-vessel vs. single-vessel PCI in STEMI from the US National Cardiovascular Data Registry (Chen LY et al. Am J Cardiol 2005, 95: 349-354).
- 53. Aggressive approach: acute multi-vessel PCI during STEMI Advantages Complete revascularization Treat ischaemia at a distance Treat secondary unstable lesions (plaque instability may not be limited to the culprit lesion) Patient preference/comfort Disadvantages Contrast nephropathy Radiation exposure Complications may be fatal Instable situation for PCI of stable lesions Risk of stent thrombosis Prothrombotic and inflammatory milieu in the acute phase of STEMI Coronary spasm = overestimation of stenosis severity in non-infarct arteries
- 54. Conservative approach: acute PCI of IRA + medical therapy (unless recurrent ischaemia occurs) Advantages Treat only culprit lesion Avoid complications associated with treating other lesions Indication for non-infarct artery PCI can be supported by the objective evidence for ischaemia Ability to discuss with patients and their families the relative risks and benefits of treating the non-infarct related lesion vs. continued medical therapy or surgical options Disadvantages May leave behind significant ischaemia-producing lesions May not treat other unstable lesions May not prevent recurrent Ischaemia Patients have to return to cath-lab
- 55. Intermediate approach: acute PCI of the infarct- related artery followed by staged PCI of secondary lesions Advantages Optimize potential for complete revascularization PCI of a stable stenosis might be intervened more safely at a later phase, after stabilization Disadvantages Economics May treat asymptomatic lesions Complications of treating secondary lesions early after index event Timing uncertain
- 56. Real life: extreme variation of different clinical and angiographic scenarios! Angiographic: Number of diseased vessels Lesion severity, location and type Chronic total occlusions TIMI flow Collaterals CABG candidate (angiographically) Clinical / echo / lab: Killip class Immediate post-PCI haemodynamic situation LV function (wall motion in the infarct / contralateral territory) Renal function Diabetes CABG candidate (clinically)
- 57. It is unlikely that any randomized clinical trial in the future can be able to fully address this complexity and thus, experienced, wise clinical judgement will probably remain the most important factor in this difficult situation.
- 58. Kornowski R, HORIZONS-AMI Trial Investigators. Staged vs "one-time" multivessel PCI in AMI: analysis from the HORIZONS-AMI trial. J Am Coll Cardiol 2011; 58: 704-11 CONCLUSION: A deferred PCI strategy of nonculprit lesions should remain the standard approach in STEMI, as multivessel PCI may be associated with a greater hazard for mortality and stent thrombosis. 0 2 4 6 8 10 12 14 16 18 20 Mortality Stent thrombosis MACE Acute MV-PCI (n=275) Staged PCI (n=393) HR: 4.1 95% CI 1.93-8.86 p < 0.0001 HR: 2.49 95% CI 1.09-5.70 p = 0.02 HR: 1.42 95% CI: 0.96-2.1 p = 0.08
- 59. What do the ESC guidelines recommend? In multi-vessel disease, p-PCI should be directed only at the infarct- related coronary artery. Decisions about PCI of non-culprit lesions should be done later and guided by objective evidence of residual ischaemia. Only in the setting of cardiogenic shock is there a consensus for attempting multi-vessel PCI in selected patients with multiple critical lesions.
- 60. Recommendations for reperfusion strategies in STEMI patients
- 61. Recommendations for treatment of patients with AHF in the setting of acute MI
- 62. Conclusions Multi-vessel disease in STEMI is not a single entity and thus the treatment approach should be individualized. However, the general rules can be proposed till future large randomized trials prove otherwise: Single-vessel (IRA) acute PCI should be the default strategy. Acute multi-vessel PCI might be justified only in haemodynamically unstable patients with multiple truly critical (>90%) lesions. Significant lesions of the non-culprit arteries should be treated either medically or by staged revascularization procedures— both options are currently acceptable.
- 64. Currently running „PRAGUE“ trials • P-14: perioperative bleeding / ischemia in cardiac patients undergoing non-cardiac surgery • P-15: renal denervation • P-16: catheter-based thrombectomy in acute ischemic stroke • P-18: ticagrelor vs. prasugrel in STEMI • P-19: bioresorbable stents in STEMI
- 68. 45-years mother from 3 children 11:30 sudden loss of consciousness, hemiplegia 12:30 CT scan 13:00 transfemoral angiography 13:30 thrombus retrieval (Solitaire stent) 13:45 conscious, speaking 16:00 moving (photo) Next morning willing to go home
- 69. Reperfusion therapy for acute myocardial infarction and acute stroke: similarities and differences Petr Widimsky Cardiocenter Vinohrady, Third Faculty of Medicine, Charles University Prague Czech Republic
- 70. Combined „hard“ end-points Death / re-MI / stroke in STEMI patients Death / severe disability (mRS >2) in stroke patients
- 71. Intravenous thrombolysis versus conservative treatment. 0 10 20 30 40 50 60 70 80 STEMI AIS IV. TL Placebo *Death / re-MI / stroke *Death / severe disability (mRS >2) OR 0.81 (95% CI 0.73 - 0.90) N Engl J Med 1995 Dec 14;333(24):1581-7. Cochrane Database Syst Rev 2009 Oct 7; (4): CD000213. Lancet 1988 2(8607):349-60 P < 0,001
- 72. Intraarterial versus intravenous thrombolysis. 0 10 20 30 40 50 60 70 80 STEMI AIS IV. TL IA. TL *Death / re-MI / stroke Mazighi M et al., Stroke 2012 OR 2,20 (CI 1,12 – 4,33) *Death / severe disability (mRS >2) n.s. No large randomized study available. Data extrapolated from non-randomized comparisons
- 73. TL-facilitated intervention versus intravenous thrombolysis alone. 0 10 20 30 40 50 60 70 STEMI AIS IV. TL alone TL+intervention *Death / re-MI / stroke *Death / severe disability (mRS >2) Abs.dif. 1,5% (CI -6,1% to +9,1%) Broderick JP et al., NEJM 2013 Vermeer F. Heart 1999 Widimsky P. Eur Heart J 2000 n.s.
- 74. TL-facilitated intervention versus mechanical intervention alone. 0 2 4 6 8 10 12 14 16 STEMI AIS Catheter alone TL+intervention No data available. *Death / re-MI / stroke *Death / severe disability (mRS >2) Vermeer F. Heart 1999 Widimsky P. Eur Heart J 2000
- 75. Intravenous thrombolysis alone versus mechanical intervention alone. 0 2 4 6 8 10 12 14 16 STEMI AIS Catheter alone IV TL alone No data available. *Death / re-MI / stroke *Death / severe disability (mRS >2) Keeley EC. Lancet 2003 P < 0,0001
- 77. Intravenous thrombolysis versus conservative treatment. 0 5 10 15 20 25 STEMI AIS IV. TL Placebo P = 0,30 N Engl J Med 1995 Dec 14;333(24):1581-7. Cochrane Database Syst Rev 2009 Oct 7; (4): CD000213. OR 42% (95% CI 34-50%) Lancet 1988 2(8607):349-60
- 78. Intraarterial versus intravenous thrombolysis. 0 5 10 15 20 25 STEMI AIS IV. TL IA. TL Mazighi M et al., Stroke 2012 OR 0,77 (CI 0,45 – 1,33) No large randomized study available. Data extrapolated from non-randomized comparisons
- 79. TL-facilitated intervention versus intravenous thrombolysis alone. 0 5 10 15 20 25 STEMI AIS IV. TL alone TL+intervention P = 0,52 Broderick JP et al., NEJM 2013 Vermeer F. Heart 1999 Widimsky P. Eur Heart J 2000
- 81. Intravenous thrombolysis versus conservative treatment. 0 1 2 3 4 5 6 7 STEMI AIS IV. TL Placebo P < 0,001 N Engl J Med 1995 Dec 14;333(24):1581-7. Cochrane Database Syst Rev 2009 Oct 7; (4): CD000213. Lancet 1988 2(8607):349-60
- 82. Intraarterial versus intravenous thrombolysis. 0 1 2 3 4 5 6 7 8 9 STEMI AIS IV. TL IA. TL Mazighi M et al., Stroke 2012 OR 1,26 (CI 0,74 – 2,14) No large randomized study available. Data extrapolated from non-randomized comparisons
- 83. TL-facilitated intervention versus intravenous thrombolysis alone. 0 1 2 3 4 5 6 7 STEMI AIS IV. TL alone TL+intervention P = 0,83 Broderick JP et al., NEJM 2013 n.s. Vermeer F. Heart 1999 Widimsky P. Eur Heart J 2000
- 84. EuroPCR 2013: Hot Line session Wednesday May 22 PRAGUE-19 First-in-man results