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STEMI: Guidelines Udate 2009 and Clinical Practice

STEMI: Guidelines Udate 2009 and Clinical Practice. Yuejin Yang MD, PhD, FACC Cardiovascular Institute and Fu-wai Hospital, CAMS & PUMC 冰城国际心血管病会议， 哈尔滨 , China, 2010-09-04. 急性冠脉 综 合症（ ACS ）. 心源性猝死（ SCD ） ST 段抬高型急性心肌梗死（ STEMI ） 非 ST 段抬高型急性心肌梗死（ NSTEMI ） 不稳定型心绞痛（ UA ）. 是冠心病致死和致残的主要原因！.

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STEMI: Guidelines Udate 2009 and Clinical Practice

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  1. STEMI: Guidelines Udate 2009 and Clinical Practice Yuejin Yang MD, PhD, FACC Cardiovascular Institute and Fu-wai Hospital, CAMS & PUMC 冰城国际心血管病会议， 哈尔滨, China, 2010-09-04

  2. 急性冠脉综合症（ACS） • 心源性猝死（SCD） • ST段抬高型急性心肌梗死（STEMI） • 非ST段抬高型急性心肌梗死（NSTEMI） • 不稳定型心绞痛（UA） 是冠心病致死和致残的主要原因！

  3. Acute Coronary Syndromes (ACS) NSTEMI STEMI Van de Werf F. Throm Haemost. 1997;78(1):210-213.

  4. ST-elevation ACS UA NSTEMI STEMI UA NQWMI QwMI ACUTE CORONARY SYNDROMES Non–ST-elevation ACS CK-MB Tn

  5. Thrombus Formation and ACS Plaque Disruption/Fissure/Erosion Thrombus Formation Old Terminology: UA NQMI STE-MI New Terminology: Non-ST-Segment Elevation Acute Coronary Syndrome (ACS) ST-Segment Elevation Acute Coronary Syndrome (ACS)

  6. ACS PathophysiologyPlaque rupture, thrombosis and microembolization Inflammation, spasm endothelial dysfunction Plaquerupture Platelet-thrombin micro-emboli Thrombus TnT Curve Cutoff CK-MB Microvascular Obstruction CK-MB CK-MB 1st 2nd 3rd embolus embolus embolus

  7. 动脉粥样硬化病变进展和急性变化 粥样 斑块 泡沫 细胞 脂质 条纹 间质 损害 纤维化 斑块 多重损伤 /破裂 内皮功能障碍 从第一个10年 从第三个10年 从第四个10年 血栓形成, 血肿 平滑肌和胶原 进展主要由于：脂质聚集 Adapted from Stary HC et al. Circulation. 1995;92:1355-1374.

  8. 稳定型斑块（病变） 内膜平滑肌细胞 (修复型) 纤维帽 (平滑肌细胞和基质) 内皮细胞 脂质核 外膜 中层平滑肌细胞 (可伸缩型)

  9. 不稳定（易损）性斑块（病变） 发生在破裂/侵蚀口的血小板凝聚 脂质核 lipid core 外膜

  10. 血小板的粘附和激活 血小板粘附于损伤 的内皮表面并被激活 血小板聚集 形成血栓 血流中的正常血小板 血小板血栓 血小板粘附到内 皮下腔 血小板 内皮细胞 内皮下腔

  11. 斑块破裂处由GP IIb-IIIa 受体的作用使纤维蛋白原交联结合 通常为富含血小板的血栓 部分阻塞血管所引起 Unobstructedlumen GP IIb-IIIa 血小板 thrombus 纤维蛋白原 斑块破裂 血管壁 血小板（白色）血栓部分堵塞冠脉：UA/NSTEMI

  12. 纤维蛋白（红色）血栓堵死冠脉：STEMI 斑块破裂处:血小板血栓进一步 形成纤维蛋白血栓:急闭冠脉 通常是由冠状动脉内完全闭塞性血栓造成的 血小板 纤维蛋白网 GPIIb/IIIa 红细胞 RBC=红细胞 1. Adapted from Antman EM. In: Califf RM, ed. Atlas of Heart Diseases, VIII. Philadelphia, PA: Current Medicine, 1996. 仅限内部使用

  13. Onset of STEMI • Prehospital issues • Initial recognition and management • in the Emergency Department • Reperfusion • Hospital Management • Medications • Arrhythmias • Complications • Preparation for discharge Secondary Prevention/ Long-Term Management 1 2 3 4 5 6 Pathophysiology of STEMI Management Before STEMI Modified with permission from Libby Circulation.2001; 104: 365-372.

  14. 不稳定性心绞痛/非ST段抬高心肌梗死 ST抬高心肌梗死

  15. Evolution of Guidelines for ACS 1990 1992 1994 1996 1998 2000 2002 2004 2007 2009 1990ACC/AHAAMI R. Gunnar 1994AHCPR/NHLBIUA E. Braunwald 1996 1999Rev Upd ACC/AHA AMI T. Ryan 2000 2002 2007 Rev UpdRev ACC/AHA UA/NSTEMI E. Braunwald; J. Anderson 2004 2007 Rev Upd ACC/AHA STEMI E. Antman 2009 Upd ACC/AHA STEMI/PCI F. Kushner 17

  16. STEMI: Guidelines and Updates ACC/AHA 2004 STEMI GudelinesACC/AHA 2007 STEMI GUIDELINESNACB 2007guidelines for ACS ESC-ACCF-AHA-WHFUniversal Definition -2007 ACC/AHA2008 Care Metrics for AMIESC 2008STEMI guidelinesACC/AHA 2009STEMI/PCI Guidelines Focused Update

  17. STEMI Guidelines • 2004: Matured and evidence-based • 2007: Revised and supplement • 2009: Updated according to new further evidences (clinical trials)

  18. What is a Myocardial Infarction? • WHO Definition –1979 • ESC-ACC Redefinition –2000 • ESC-ACCF-AHA-WHF Universal Definition -2007

  19. WHO Definition –1979 The Criteria for the diagnosis of acute MI included 2 of the following 3: • History: Chest discomfort or equivalent • Diagnostic changes on ECG • Elevated cardiac enzymes (or markers)

  20. Myocardial Infarction: 2000 Redefined Why redefine myocardial infarction? • The arrival of the highly sensitive/specific troponin in routine clinical use. • Clinicians were defining MI differently even within the same hospital. • Hospitals were defining MI differently even within the same city. • Clinical trials defined MI differently. • Previous assays in definitions were confusing and inaccurate. JACC: 2000; 36: 959-969 and the EHJ: 2000; 21:1502-1513.

  21. Redefinition of MI ----------------------------REFERENCE LABORATORIES---------------------------- cTnI 0 - 0.08 12/04 0.13*# 1:03A (1) (1) >0.08 INDICATIVE OF MYOCARDIAL INJURY; NOTE NEW REFERENCE RANGE Press <Enter> to continue: or "P" to print screen : • Biomarker indicators of MI • Troponin is preferred biomarker for dx of MI • cTnT or cTnI > 99th %ile on any determination • CK-MB > 99th %ile on two successivemeasurements or > 2X ULN on any sample

  22. The new definition for MI is consistent with the pathological definition: The new definition seeks to identify the presence of myocardial necrosis in an appropriate clinical setting by measuring highly accurate blood levels of biomarkers of myocardial necrosis.

  23. What was lacking in the 2000 Redefinition of MI ? • Non-invasive imaging not considered diagnostic • No information for pts following CABG

  24. Microinfarction After Percutaneous Coronary Intervention AssociatedWith Mild Creatine Kinase-MB Elevation Ricciardi et al. Circulation 2001. 103:2780

  25. ESC-ACC Redefinition Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following: • Ischemic symptoms • Development of Q waves on the ECG • ECG changes indicative of ischemia • Coronary artery intervention • Biomarker rise further defined as above the 99% of normals with acceptable (<10%) precision

  26. Subsets of AMI(2007):Additional Classifications • Type 1: Spontaneous & Primary coronary event, CA sclerotic- & thrombotic-related • Type 2: Non-spontaneous & Secondary event, CA sclerotic but non-thrombotic- related, or non-CA sclerotic-related • Type 3: SCD • Type 4: PCI-related 4a: CA Embolic- & acute closure related 4b: Stent thrombosis related • Type 5: CABG-related

  27. Diagnosis of myocardial infarction Cardiac troponin is the preferred marker for the diagnosis of MI Creatine kinase MB (CK-MB) by mass assay is an acceptable alternative when cardiac troponin is not available Class I, Level of Evidence A

  28. Diagnosis of myocardial infarction Total CK, CK-MB activity, AST, and/or LDH should not be used as biomarkers for the diagnosis of MI Class III, Level of Evidence C

  29. Early Risk Stratification - cTn In patients with a clinical syndrome consistent with ACS, a maximal (peak) concentration exceeding the 99th percentile of values for a reference control group should be considered indicative of increased risk of death and recurrent ischemic events Class I, Level of Evidence A

  30. Diagnosis of myocardial infarction Use of total CK for diagnosis of MI is not recommended! However, in the absence of availability of data using a troponin or CK-MB assay (mass or activity), when only total CK values are available, the recommended decision-limit is 2 times the sex-specific upper reference limit. A rise and/or fall of CK-MB or total CK provides additional evidence supporting the diagnosis of acute MI.

  31. Myocardial Infarction:Definition? • WHO: Definition (1979) Basic definition (基础诊断标准) • ESC/ACC: Redefinition (2000) Unifying definition (统一诊断标准) • ESC/ACCF/AHA/WHF: Universal Definition (2007) Refined & improved definition (细化而完善的诊断标准)

  32. AMI的诊断依据 • 心肌坏死证据 特异性生物标志物(ESC/ACC,2000) TnT，TnI; CK-MB, T-CK; SGOT, LDH1, Hb et. 临床特征性表现(WHO, 1979) ECG特征性改变(WHO,1979) 影像学特征性改变(ESC/ACC/AHA,2007) ECHO，MRI，CT, SPECT, et. 造影下冠脉狭窄或堵塞

  33. ST抬高型急性心肌梗塞（STEMI）的诊断 • 国际诊断标准（WHO）：2/3条件 典型的临床表现 ECG动态演变 有任何2个均可确诊 心肌酶异常 • 临床表现: 持续胸痛>30 ’,伴出汗、恶心呕吐、面色苍白， 含NTG 1-2＃不缓解; • ECG: 前壁、下后壁导联ST或CLBBB,即可确诊。 • 酶学结果: 临床上最次要,诊断不及时. 只有症状或ECG不典型时，方有参考价值。

  34. AMI的特殊表现 • 以心衰肺水肿为首发表现－大缺血，小梗死 • 以晕厥为首发表现－ AVB伴大汗、面色苍白、HR30－40bpm,见于心肌梗死初起. • 以心源性休克为首发表现－BP 、面色苍白，皮肤湿冷， HR • 以上腹痛为首发表现－ 伴恶心、呕吐、大汗淋漓

  35. 主动脉夹层动脉瘤: 胸痛剧烈， 无ECG变化 心绞痛: 胸痛<30 ’ NIG可缓解 不伴恶心呕吐 急性肺栓塞 : ECG 　　　 酷似NSTEMI SI QIII TIII 气胸: CXR可鉴别 心包炎、心肌炎: ECG广泛ST上抬 急腹症: 有腹部体征 ECG无变化 应急性心肌病: 　　　　 应激发病 IRCA通畅 可逆性大室壁瘤 AMI的鉴别诊断

  36. Management of STEMI

  37. STEMI 的病理生理和治疗原则 • 病理生理： • 治疗原则：首选冠脉再通治疗（溶栓、PCI或 CABG）恢复心肌血流和再灌注 斑块破裂 血栓形成 冠脉急性闭塞 心肌坏死

  38. AMI的治疗原则 • 持续心电监测，及时发现和处理心律失常 • 维持血液动力学稳定 • 抗血小板抗凝 • 尽快给予再灌注治疗， • 使闭塞的IRCA迅速再通 • 降低心肌耗氧量，保护缺血心肌。 • 稳定易损斑块.

  39. AMI治疗:急救成效 • AMI的两大死因：心律失常（如Vf）和泵衰竭 （心衰和休克）； • 过去30年来，AMI治疗进展和巨大: CCU的建立: 除颤、心电和血液动力学监测, 药物: -B、硝酸酯、抗血小板制剂,ACEI和他丁类 再灌注治疗: 巨大突破,溶栓和PCI； • 30天病死率:CCU前期30％CCU期的15％  再灌注时期的5％。

  40. AMI的治疗流程 • 再灌注治疗: 首选溶栓（IV）-- r-tPA U.K r.S.K 急诊PCI • 一般治疗：心电血压监测、建立iv通道, 镇痛、吸氧, 溶栓或 PCI准备 • 药物治疗：硝酸酯、-B、ACEI、抗血小板、抗凝剂,他类； • 并发症治疗： 心律失常 低血压 心力衰竭 心源性休克 机械并发症 梗塞后心绞痛 再梗塞 • 恢复期（出院前）治疗 － 血运重建术（PCI、CABG）

  41. 药物治疗 • 硝酸酯 • -受体阻滞剂 无禁忌症者均必须使用 • ACEI、ARBS • 抗血小板、抗凝 • 镁制剂、钙拮抗剂：必要时使用 • G-I-K：可用可不用，最好不用 • 降脂药: 他丁类

  42. ACS的药物治疗及其作用机制 3.抗心肌缺血、减少坏死面积 (受体阻滞剂、硝酸盐类等) 纤维蛋白 凝块 2. 抗凝血酶 (肝素/低份子肝素) 人纤维蛋白原 凝血酶 IIb/IIIa受体 1.抗血小板粘附 / 激活作用 /聚集反应 (ASA, 抵克力得，氯吡格雷，IIb/IIIa 抑制剂) 血小板 4. 降胆固醇、稳定斑块 抗炎症 (hs-CRP)、感染 (他汀类)

  43. Therapeutic objective of STEMI (ESC 2008) • The present guidelines pertain to patients presenting with ischemic symptoms and persistent ST-segment elevation on the ECG (STEMI). The great majority of these patients will show a typical rise of biomarkers of myocardial necrosis and progress to Q-wave myocardial infarction. • Therapeutic objective is to achieve rapid, complete, and sustained reperfusion by primary angioplasty or fibrinolytic therapy

  44. 2004年ACC/AHA STEMI指南 • 再灌注治疗目标： 应在发病120’内完成 溶栓：应在30’内开始（door to-heedle tuise＜30’） PCI：应在90’内完成（door to-telloon time ＜90’） 主张：应将患者尽快转运到有条件医院行急诊PCI 强调：越快越好，争分夺秒，不得怠慢！ 时间就是心肌，就是生命，不得耽搁！ • 依据：大量循证医学证据（研究结果） Antman EM, et al.Circulation. 2004 Aug 3;110(5):588-636.

  45. Options for Transport of STEMI Patients and Initial Reperfusion Treatment Goals Hospital fibrinolysis: Door-to-Needle within 30 min. Not PCI capable Call fast • EMS on-scene • Encourage 12-lead ECGs. • Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min. Inter-Hospital Transfer Onset of symptoms of STEMI EMS Triage Plan EMS Dispatch PCI capable GOALS 5 min. 8 min. EMS Transport Patient EMS Prehospital fibrinolysis EMS-to-needle within 30 min. EMS transport EMS-to-balloon within 90 min. Patient self-transport Hospital door-to-balloon within 90 min. Dispatch 1 min. Golden Hour = first 60 min. Total ischemic time: within 120 min. Circulation. 2008;117:296-329. JACC. 2008;51:210-247.

  46. Options for Transport of Patients With STEMI and Initial Reperfusion Treatment Fibrinolysis Noninvasive Risk Stratification Late Hospital Care and Secondary Prevention Not PCI Capable Ischemia driven Rescue PCI Capable PCI or CABG Primary PCI • Patients receiving fibrinolysis should be risk-stratified to identify need for further revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG). • All patients should receive late hospital care and secondary prevention of STEMI.

  47. Laboratory Examinations Laboratory examinations should be performed as part of the management of STEMI patients, but should not delay the implementation of reperfusion therapy. • Serum biomarkers for cardiac damage • Complete blood count (CBC) with platelets • International normalized ratio (INR) • Activated partial thromboplastin time (aPTT) • Electrolytes and magnesium • Blood urea nitrogen (BUN) • Creatinine • Glucose • Complete lipid profile

  48. Biomarkers of Cardiac Damage Cardiac-specific troponins should be used as the optimum biomarkers for the evaluation of patients with STEMI who have coexistent skeletal muscle injury. For patients with ST elevation on the 12-lead ECG and symptoms of STEMI, reperfusion therapy should be initiated as soon as possible and is not contingent on a biomarker assay.

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