Résumé
Le syndrome coronarien ou coronaire aigu (SCA) est constitué des manifestations cliniques, électrocardiographiques et biologiques liées à la rupture d’une plaque « vulnérable » d’athérome ayant induit la formation d’un thrombus limitant le flux sanguin dans le réseau artériel coronaire [1,2] Merci de replacer ces appels de référence dans le texte. Les SCA sont classés en SCA avec élévation (ou sus-décalage) du segment ST (SCA ST+) et en SCA sans élévation du segment ST (SCA non ST+). Dans les SCA ST +, le thrombus est constitué principalement de fibrine entraînant une occlusion coronaire aiguë totale responsable d’une nécrose complète du tissu myocardique dans les six heures, tandis que dans les SCA non ST+, il est plutôt de type plaquettaire n’obstruant pas complètement la lumière artérielle [3] Merci de replacer cet appel de référence dans le texte. La douleur thoracique est le signe d’appel le plus courant. Le facteur temps est l’élément clé dans la prise en charge des SCA. Le rôle des Samu-Smur-Centre 15 est essentiel, permettant une prise en charge rapide. Quel que soit le type de SCA, le traitement comporte la prise d’aspirine, de clopidogrel ou de prasugrel, d’anticoagulant, une anxiolyse (si besoin) et un traitement antalgique. Dans les SCA non ST +, l’évaluation des marqueurs biologiques de souffrance myocardique (troponine) peut permettre une orientation diagnostique et thérapeutique dès la phase préhospitalière. L’apport récent de nouvelles et puissantes molécules antiagrégantes plaquettaires et anticoagulantes a modifié les stratégies décisionnelles et de prise en charge des SCA en préhospitalier afin de garantir une reperfusion optimale et dans les meilleurs délais.
Abstract
Acute coronary syndrome (ACS) is defined a spectrum of clinical, electrical and biological manifestations due to the rupture of an unstable atheromatous plaque causing the development of a thrombus, which limits blood flow in the coronary circulation [1,2]. ACS is classified as ST-segment elevation ACS (STEMI) and non-ST-segment elevation ACS (NSTEMI). In STEMI, the thrombus is made of fibrin, which causes complete obstruction of the artery associated with total necrosis of myocardial tissue within 6 hours [3]. In NSTEMI, the thrombus is made of platelets, which causes incomplete obstruction of the artery. The commonest symptom is thoracic pain. Time is the major limiting factor in ACS management. The prehospital emergency department (SAMU) plays a fundamental role in ACS management in France. Whatever is the type of ACS, the treatment is based on aspirin, clopidogrel or prasugrel, anticoagulant, anxiolysis (if necessary) and analgesia. In NSTEMI, the level of risk for death and severe infarction is based, at least in part, on the measurement of troponin serum concentration in MICU AU: Please expand.. New antiplatelets and anticoagulant molecules have been recently developed to improve the prehospital management of ACS and to optimize and reduce time to artery reperfusion.
Références
Libby P (2001) Current concepts of the pathogenesis of acute coronary syndromes. Circulation 104:365–372
Maseri A, Fuster V (2003) Is there a vulnerable plaque? Ciruclation 107:2068–2071
Virmani R, Kolodgie FD, Burke AP, et al (2000) Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions arterioscle. Thromb Vasc Biol 20:1262–1275
Fox KAA, Cokkinos DV, Deckers J, et al (2000) On the behalf of the ENACT (European Network for Acute Coronary Treatment) Investigators. The ENACT study: a pan-European survey of acute coronary syndromes. Eur Heart J 21:1440–1449
Collinson PO, Premachandram S, Hashemi K (2000) Prospective audit of incidence of prognostically important myocardial damage in patients discharged from emergency department. BMJ 320:1702–1705
Silvain J, Collet JP, Nagaswami C, et al (2011) Composition of coronary thrombus in acute myocardial infarction. J Am Coll Cardiol 57:1359–1367
Bax JJ, Bonow RO, Tschope D, et al (2006) Global dialogue group for the evaluation of cardiovascular risk in patients with diabetes. The potential of myocardial perfusion scintigraphy for risk stratification of asymptomatic patients with type 2 diabetes. J Am Coll Cardiol 48:754–760
Diderholm E, Andren B, Frostfeldt G, et al (2002) The fast revascularization during instability in coronary artery D. ST depression in ECG at entry indicates severe coronary lesions and large benefits of an early invasive treatment strategy in unstable coronary artery disease. The FRISC II ECG substudy. Eur Heart J 23:41–49
Ramsay M, Podogrodzka C, McClure, et al (2007) Risk prediction in patients presenting with suspected cardiac pain: the GRACE and TIMI scores versus clinical evaluation. QJM 100:11–18
Bassand JP, Hamm CW, Ardissino D, et al (2007) The Task Force for the diagnosis and treatment of non-ST segment elevation acute coronary syndromes of the European Society of Cardiology guidelines for the diagnosis and treatment of non-ST segment elevation acute coronary syndromes. Eur Heart J 28:1598–1660
Silver S, Albertsson P, Aviles FF, et al (2005) Guidelines for percutaneous coronary interventions. Eur Heart J 26:804–847
Bertrand ME, Simoons ML, Fox KA, et al (2002) Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 23:189–140
Omland T, de Lemos JA, Sabatine MS, et al (2009) A sensitive cardiac troponin T assay in stable coronary artery disease. N Engl J Med 361:2538–2547
Keller T, Tzikas S, Zeller T, et al (2010) Copeptin improves early diagnosis of acute myocardial infarction. J Am Coll Cardiol 55:2096–2106
Mehta SR, Tanguay JF, Eikelboom JW, et al (2010). Double-dose versus standard-dose clopidogrel and high-dose versus low-dose aspirin in indivuduals undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. Lancet 376:1233–1243
Van de Werf F, Bax J, Betriu A, et al (2008) Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation. The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J 29:2909–2945
Danchin N, Coste P, Ferrieres J, et al (2008) Comparison of thrombolysis followed by broad use of percutaneous coronary intervention with primary percutaneous coronary intervention for ST-segment elevation acute myocardial infarction: data from the French registry on acute ST-elevation myocardial infarction (FAST-MI). Circulation 118:268–276
Chen ZM, Jiang LX, Chen YP, et al (2005) Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet 366:1607–1621
Gurbel PA, Bliden KP, Hiatt BL, et al (2003) Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity. Circulation 107:2908–2913
Nguyen TA, Diodati JG, Pharand C (2005) Resistance to clopidogrel: a review of the evidence. J Am Coll Cardiol 45:1157–1164
Hochholtzer W, Trenk D, Frundi D, et al (2005) Time dependance of platelet inhibition after 600 mg loading dose of clopidogrel in a large unselected cohort of candidates for percutaneous coronary intervention. Circulation 111:2560–2564
Von Beckerath, Taubert D, Pogatsa-Murray G, et al (2005) Absorption, metabolization, and antiplatelet effects of 300, 600 and 900 mg loading doses of clopidogrel: results of the ISARCHOICE (intracoronary stenting and antithrombotic regimen: choose between 3 high oral doses for immediate clopidogrel effect) trial. Circulation 112:2946–2950
Widimsky P, Motovska Z, Simek S, et al (2008) Clopidogrel pretreatment in stable angina: for all patients superior to six hours before elective coronary angiography or only for angiographically selected patients a few minutes before PCI? A randomized multicentre trial PRAGUE-8 trial. Eur Heart J 29:1495–1503
Collet JP, Hulot JS, G Anzaha G, et al (2011) High dosesof clopidogrel to overcome genetic resistance: the randomized crossover CLOVIS-2 (clopidogrel and response variability investigation Study 2). J Am Coll Cardiol Intv 4:392–402
Wiviott SD, Brunwald E, McCabe CH, et al (2007) Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 357:2001–2015
Wallentin L, Becker RC, Budaj A, et al (2009) Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 361:1045–1057
Topol EJ (2001) Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V randomised trial. Lancet 357:1905–1914
Bosch X, Marrugat J, Sanchis J (2010) Platelet glycoprotein IIb/IIIa blockers during percutaneous coronary intervention and as the initial medical treatment of non-ST segment elevation acute coronary syndromes. Cochrane Database Syst Rev 9:CD002130
Ellis SG, Tendera M, de Belder MA, et al (2008) Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med 358:2205–2217
Van’t Hof AW, Ten Berg J, Heestermans T, et al (2008) Prehospital initiation of tirofiban in patients with ST-elevation myocardial infarction undergoing primary angioplasty (On-Time 2): a multicentre, double-bind, randomised controlled study. Lancet 372:537–546
Anderson JL, Adams CD, Antman EM, et al (2007) ACC/AHA 2007 Guidelines for the management of patients with unstable angina/non-ST elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/non-ST elevation myocardial infarction) developed in collaboration with the American College of Emergency Physicians, the Society of Cardiovascular Angiography and interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol 50:e1–e157
Antman EM, Cohen M, Radley D, et al (1999) Assessment of the treatment effect of enoxaparin for unstable angina/non-Q-wave myocardial infarction. TIMI11B-ESSENCE meta-analysis. Circulation 100:1602–1608
Cohen M, Mahaffey KW, Pieper K, et al (2006) A subgroup analysis of the impact of prerandomization antithrombin therapy on outcomes in the SYNERGY trial: enoxaparin versus unfractionated heparin in non-ST-segment elevation acute coronary syndromes. J Am Coll Cardiol 48:1346–1354
Montalescot G, Collet JP, Lison L, et al (2000) Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina. J Am Coll Cardiol 36:110–114
Ferguson JJ, Califf RM, Antman EM, et al (2004) Enoxaparin vs unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndromes managed with an intended early invasive strategy: primary results of the SYNERGY randomized trial. JAMA 292:45–54
Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-3 Investigators (2001) Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction. Lancet 358:605–613
Wallentin L, Dellborg DM, Lindhal B, et al (2001) The lowmolecular-weight heparin dalteparin as adjuvant therapy in acute myocardial infarction. The ASSENT PLUS study. Clin Cardiol 24:112–114
Antman EM, Morrow DA, McCabe CH, et al (2006) Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction. New Engl 354:1477–1488
Montalescot G, Zeymer U, Silvain J, et al (2011) Intravenous enoxaparin or unfractionated heparin inprimary percutaneous coronary intervention for ST-elevation myocardial infarction: the international randomised open-label ATOLL trial. Lancet 378:693–703
Wijns W, Kolh P, Danchin N, et al (2010) Guidelines on myocardial revascularization: the Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 31: 2501–2505
Stone GW, McLaurin BT, Cox DA, et al (2006) Bivalarudin for patients with acute coronary syndromes. N Engl J Med 355:2203–2216
Stone GW, Witzenbichler B, Guagliumi G, et al (2008) Bivalarudin during primacy PCI in acute myocardial infarction. N Engl J Med 358:2218–2230
Mehran R, Lansky AJ, Witzenbichler B, et al (2009) Bivalirudin in patients undergoing primary angioplasty for acute myocardial infarction (HORIZON-AMI): 1-year results of a randomized controlled trial. Lancet 374:1149–1159
Yusuf S, Mehta SR, Chrolavicius S, et al (2006) Comparison of fondaparinux and enoxaparin in acute coronary syndromes. N Engl J Med 354:1464–1476
Yusuf S, Mehta SR, Chloravicius S, et al (2006) Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA 295: 1519–1530
Goldstein P (2010) Une nouvelle génération de thiénopyridine, quel bénéfice clinique pour l’urgentiste ? JEUR 23:S17–S21
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Assez, N., Wiel, E., Lemanski-Brulin, C. et al. Syndromes coronariens aigus : prise en charge thérapeutique en urgence. Ann. Fr. Med. Urgence 1 (2011). https://doi.org/10.1007/s13341-011-0116-2
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DOI: https://doi.org/10.1007/s13341-011-0116-2