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Síndrome Coronariana Aguda

Síndrome Coronariana Aguda. IAM – COM SUPRA-ST. SCA - Tipos. Angina Instável Angina de Prinzmetal IAM sem Supra ST (Subendocárdico) IAM com Supra ST (transmural). Importancia. Maior causa de morte no mundo -IAM ST : 3 mi -IAM sem ST: 4mi Fatores genéticos e estilo de vida envolvidos

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Síndrome Coronariana Aguda

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  1. Síndrome Coronariana Aguda IAM – COM SUPRA-ST

  2. SCA - Tipos • Angina Instável • Angina de Prinzmetal • IAM sem Supra ST (Subendocárdico) • IAM com Supra ST (transmural)

  3. Importancia • Maior causa de morte no mundo -IAM ST : 3 mi -IAM sem ST: 4mi • Fatores genéticos e estilo de vida envolvidos • Redução na Mortalidade -Década 60 : Unidades Coronarianas -1986: Trombo líticos

  4. Fisiopatologia Ruptura da placa ateromatosa (CATE + CRVM) Trombo Oclusivo/Suboclusivo + Embolização (Fibrinolíticos + antiplaquetários)

  5. Fisiopatologia • Outros: - Vasoespasmo - Êmbolos - Dissecção de Aorta - Anemia/Arritmia/Hipotensão

  6. Classificação – Lancet 2008 • Type 1: Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaquef issuring, erosion or rupture, or dissection • Type 2: Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supplies—eg, coronary artery spasm, coronary embolism (thrombus, vegetations, or atrial myxoma), anaemia, arrhythmias, hypertension, or hypotension Type 3: Sudden unexpected cardiac death with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new left bundle branch block, but dying before blood samples could be obtained, or in the lag phase of cardiac biomarkers in the blood • Type 4 A: Myocardial infarction associated with PCI Type 4 B: Stent thrombosis • Type 5: Myocardial infarction associated with coronary artery bypass grafting

  7. Fatores Determinantes - IAM • Capacidade de Redes Colaterais • Demanda metabólica Miocárdica • Reperfusão Precoce

  8. Diagnóstico • História Clinica - Fatores de Risco - Características da Dor - Exame Físico • ECG • Marcadores de Necrose Miocárdica

  9. IAM – Apresentação • Início súbito de dor torácica, intensa, em repouso • Localização subesternal ou precordial – pode ou não irradiar-se • Caráter constrictivo: em peso ou aperto • Duração > 30min • Não melhora com Nitrato sublingual • 40-60% - Fator desencadeante • Circadiana – 6-12h • 1/3 – pródromos (24h precedentes) – desconforto (angina instável) • DM e Idosos: Equivalentes Anginosos (Dor atípica, AIT/AVE, Choque cardiogênico/EAP, Morte súbita)

  10. Exame Físico • Ansiedade, diaforese, náuseas/vomitos, iminencia de morte • Bradicardia/Taquicardia sinusal • B4 • Sinais de IVE – Killip/Kimbal

  11. Killip (1967) • I – Sem dispnéia, B3 ou estertores – mortalidade 6% • II – Dispnéia e estertores nos 1/3 inferiores ou B3 – mortalidade 17% • III – EAP – mortalidade 38% • Choque cardiogênico (Pas < 80mmhg – sem resposta a volume) – mortalidade 81%

  12. Diagnóstico Diferencial - Clínico • Dor Torácica Aguda: Angina Instável, Dissecção de Aorta, pericardite, pneumotórax, embolia pulmonar, trauma torácico • Dispnéia Aguda: Embolia pulmonar, EAP hipertensivo, asma, ICC descompensada • Choque Agudo: Choque hipovolemico, embolia, choque séptico, tamponamento cardíaco, pneumotórax hipertensivo. • Morte Súbita: Isquemia miocárdica, FV relacionada a cardiopatia, FV idiopática.

  13. ECG • Supra – ST > ou = 1mm, 2 ou > derivacoes consecutivas ou novo BRE • Características do ECG - Fase hiperaguda – supra ST - Fase Subaguda – supra ST (convexo) + onda Q (>40ms e > 0,2mm) - Fase crônica: desaparece o desnivel de ST; onda Q patológica; pode permanecer alterações de T

  14. Causas de Supra ST • IAM • Angina de Prinzmetal • Repolarizacao Precoce • Pericardite • Hipertrofia ventricular • “Constitucional” • Hipercalemia • Sindrome de Brugada • Aneurisma de VE • BRE

  15. Marcadores de Necrose Miocárdica • Mioglobina – exclusão • CPK – MB • Troponinas

  16. Panel 2: Causes of elevated troponin values in clinical • settings other than acute myocardial infarction • Cardiac • • Tachyarrhythmia, bradyarrhythmia, heart block • • Hypertension, hypotension • • Congestive heart failure • • Aortic dissection • • Aortic stenosis or regurgitation • • Hypertrophic cardiomyopathy • • Rhabdomyolysis with cardiac myocyte necrosis • • Apical ballooning syndrome (Takotsubo cardiomyopathy) • • Transplant vasculopathy • • Myopericarditis • • Rheumatic fever • • Rheumatoid arthritis • • Systemic vasculitis • • Post-viral • Infi ltrative diseases of the myocardium • • Amyloidosis • • Sarcoidosis • • Haemochromatosis • • Scleroderma • Traumatic • • Atrioventricular ablation • • Defi brillation • • Chest wall trauma • • Cardiac surgery • Miscellaneous • • Renal failure • • Transient ischaemic attack, stroke, or subarachnoid • haemorrhage • • Drug toxicity (eg, adriamycin, 5-fl uorouracil, • daunorubicin, herceptin, etc) • • Hypothyroidism • • Pulmonary embolism • • Severe asthma • • Pulmonary hypertension • • Sepsis (including sepsis occurring with shock) • • Critically ill patients • • Phaeochromocytoma • • Severe burns • • Kawasaki disease • • Extreme exertion • • Snake venom

  17. Panel 1: Universal criteria for acute myocardial infarction • Detection of rise and or fall of troponins with at least one value above the 99th percentile of the upper reference limit together with evidence of myocardial ischaemia with at least one of: • Symptoms of ischaemia • ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block) • Development of pathological Q waves • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality • Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myocardial ischaemia, and accompanied by presumably new ST elevation, new left bundle branch block, evidence of fresh thrombus by coronary angiography or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of troponins in the blood • For PCI, increases of biomarkers greater than 3×99th percentile upper reference limit. A subtype is related to a stent thrombosis • For coronary artery bypass grafting increases of biomarkers greater than 5×99th percentile upper reference limit plus either new Q waves or new left bundle branch block, or documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium • Pathological findings of acute myocardial infarction at post mortem

  18. Revisão – 2007 – ACC/AHA Tratamento

  19. Objetivos - TTO • Tratamento das condições que ameaçam a vida • Alívio da dor • Reperfusão miocárdica • Terapia antitrombótica para evitar retrombose ou estenose subtotal do sítio da ruptura da placa • Terapia Pós – IAM (secundária)

  20. Analgesia • Morfina • Nitrato • Beta-bloqueador • Bloqueador de Cálcio • Anti-inflamatórios

  21. Morfina e Anti-inflamatórios • Class I - Morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals) is the analgesic of choice for management of pain associated with STEMI. (Level of Evidence: C) - Patients routinely taking NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, before STEMI should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use. (Level of Evidence: C)

  22. Nitratos • Nitroglicerina Sublingual – 0,4mg – 3 doses • Brasil – Isordil – 5mg • Nitroglicerina venosa em caso de não esoluçãao da dor • Contra-indicações: Pas <90mmhg/IAM VD/uso de inibidores da fosfodiasterase/FC <50 ou >100.

  23. Oxigênio • O2 3L/min • Congestão Pulmonar ou SatO2 < 90% • Aplicação rotineira nas primeiras 6h • Efeito Adverso: Vasoconstrição sistêmica -> aumenta RVP e PA -> redução débito cardíaco.

  24. AAS • 160 – 325mg – mastigar • Todos, exceto com contra-indicações: intolerância, sangramentos • Efeito antiagregante plaquetário • ISIS 2 – Redução de 20% na mortalidade, isoladamente

  25. B-Bloqueador • Reduz consumo miocárdico e arritmias • Reduz mortalidade • Terapia oral iniciada nas primeiras 24hs (IB), em pac. Sem contra-indicações: -ICC - História de broncoespasmo - PR >0,24 - Bloqueio Ramo – 2 ou 3 graus - Fatores de risco para choque cardiogênico (idade >70ª, PA <120mmhg, FC <60 ou > 110, tempo prolongado dos sintomas) - C

  26. Terapia de Reperfusão Miocárdica • Fibrinolíticos • PCI + STENT • CRVM

  27. Fibrinolíticos • Fibrino-inespecíficos (Estreptoquinase) - Não usar anti-trombóticos • Fibrino-específicos (alteplase) • Efeitos adversos: AVE hemorrágico (0,75%), hipersensibilidade, hipotensão, arritmias de reperfusão...

  28. Fibrinolíticos – Contra-indicações • Absolutas: Sangramento ativo; Disseccao de aorta; TCE recente (3 meses); Tumor cerebral ou Malformacao vascular; sangramento ativo(exceto menstruacao) ou diátese hemorrágica; AVE hemorrágico; AVCisq (3 meses) • Relativas: PA >180/110mmhg; úlcera péptica em atividade; uso de anticoagulantes; PCR > 10min;gestacao;sangramento interno recente (2-4s); puncao vascular não compressível; exposicao a estreptoquinase (5d – 9m).

  29. Critérios de Reperfusão • Desaparecimento da Dor • Redução de mais 50% do Supra-ST na derivação com maior supra-ST • Arritmias de Reperfusão • Pico precoce de CK-MB (<12h)

  30. Patencia da Coronaria após Trombólise (TIMI) • 0 : artéria ocluída • I: alguma penetração do contraste depois da artéria ocluída, sem perfundir seu leito distal • II: perfusão completa do leito distal, porém com lentidão • III: perfusão completa e rápida do leito distal • Após 1,5h: maior patência com rtpa • Após 3h: patência igual • Risco de reoclusão nas primeiras horas é maior com rtpa.

  31. Angioplastia Primária - PCI • Maior patência após 1,5h • Informações sobre a anatomia do leito coronariano • Menor taxa de morte precoce, reinfarto (3x7%) e AVC • Mesmo em grandes centros, somente 4-9% possui tempo porta balão <90%. • Exige centro de hemodinâmica e hemodinamicista experiente.

  32. Bypass • Lesão grave de tronco

  33. Reperfusão • STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 minutes of first medical contact (see Figure 1) as a systems goal. (Level of Evidence: A) • STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact (see Figure 1) should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated (Level of evidence:B)

  34. Facilitated PCI Classe IIb • Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of the following are present: a. Patients are at high risk, b. PCI is not immediately available within 90 minutes, and c. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight). (Level of Evidence: C) Classe III • A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI may be harmful. (Level of Evidence: B)

  35. Angioplastia de Resgate • Tentativa de recanalização em pacientes onde o trombolítico não foi eficaz • Indicações: - Presença de sinais de ICC/Choque cardiogênico/EAP - Arritmias/instabilidade elétrica que comprometam a função ventricular - Persistência de sintomas isquêmicos - Preferencialmente em pac. < 75ª (B)

  36. Angioplastia de Resgate • In the Wijeysundera meta-analysis there was a trend toward reduced: • mortality rates with rescue PCI from 10.4% to 7.3% (RR 0.69 [95% confidence interval (CI) 0.46 to 1.05]; p0.09), • reduced reinfarction rates from 10.7% to 6.1% (RR 0.58 [95% CI 0.35 to 0.97]; p0.04), • reduced heart failure rates from 17.8% to 12.7% (RR 0.73 [95% CI 0.54 to 1.00]; p0.05).

  37. Angiplastia de Resgate • There was an excess occurrence of stroke in 2 trials (10 events vs. 2 events), but the majority of the strokes were thromboembolic rather than hemorrhagic, and the sample size was small, so more data are needed to define this risk. • There also was an increase in absolute risk of bleeding of 13%, suggesting that adjustments in antithrombotic medication dosing are needed to improve safety. It should be noted that the majority of patients who underwent rescue PCI received fibrinolytic therapy with streptokinase.

  38. Angioplastia de Resgate • Elective PCI of an occluded infarct artery 1 to 28 days after MI in stable patients had no incremental benefit beyond optimal medical therapy with aspirin, beta blockers, ACE inhibitors, and statins in preserving LV function and preventing subsequent cardiovascular events.

  39. Anticoagulantes • Classe I • Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than UFH are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparininduced thrombocytopenia with prolonged UFH treatment). (Level of Evidence: A)

  40. Anticoagulantes • UFH (initial intravenous bolus 60 U per kg [maximum 4000 U]) followed by an intravenous infusion of 12 U per kg per hour (maximum 1000 U per hour) initially, adjusted to maintain the activated partial thromboplastin time at 1.5 to 2.0 times control (approximately 50 to 70 seconds) (Level of Evidence: C).

  41. Anticoagulantes • Enoxaparin (provided the serum creatinine is less than 2.5 mg per dL in men and 2.0 mg per dL in women): - for patients less than 75 years of age, an initial 30 mg intravenous bolus is given, followed 15 minutes later by subcutaneous injections of 1.0 mg per kg every 12 hours; - for patients at least 75 years of age, the initial intravenous bolus is eliminated and the subcutaneous dose is reduced to 0.75 mg per kg every 12 hours. - Regardless of age, if the creatinine clearance (using the Cockroft-Gault formula) during the course of treatment is estimated to be less than 30 mL per minute, the subcutaneous regimen is 1.0 mg per kg every 24 hours. - Maintenance dosing with enoxaparin should be continued for the duration of the index hospitalization, up to 8 days. (Level of Evidence: A)

  42. Anticoagulantes • Fondaparinux (provided the serum creatinine is less than 3.0 mg per dL): initial dose 2.5 mg intravenously; - subsequently subcutaneous injections of 2.5 mg once daily. Maintenance dosing with fondaparinux should be continued for the duration of the index hospitalization, up to 8 days. (Level of Evidence: B) - Because of the risk of catheter thrombosis, fondaparinux should not be used as the sole anticoagulant to support CI. An additional anticoagulant with anti-IIa activity should be administered

  43. Anticoagulantes • For patients undergoing PCI after having received an anticoagulant regimen, the following dosing recommendations should be followed: • For prior treatment with UFH, administer additional boluses of UFH as needed to support the procedure, taking into account whether GP IIb/IIIa receptor antagonists have been administered. (Level of Evidence: C) Bivalirudin may also be used in patients treated previously with UFH. (Level of Evidence: C) • b. For prior treatment with enoxaparin, if the last subcutaneous dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last subcutaneous dose was administered at least 8 to 12 hours earlier, an intravenous dose of 0.3 mg per kg of enoxaparin should be given. (Level of Evidence: B) • c. For prior treatment with fondaparinux, administer additional intravenous treatment with an anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa receptor antagonists have been administered.(Level of Evidence: C)

  44. Tienopiridinos • Classe I • Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Level of Evidence: A) Treatment with clopidogrel should continue for at least 14 days. (Level of Evidence: B) • In patients taking clopidogrel in whom CABG is planned, the drug should be withheld for at least 5 days and preferably for 7 days unless the urgency for revascularization outweighs the risks of excess bleeding. (Level of Evidence: B)

  45. Tienopiridinos • Classe IIa • In patients less than 75 years of age who receive fibrinolytic therapy or who do not receive reperfusion therapy, it is reasonable to administer an oral loading dose of clopidogrel 300mg. (Level of Evidence: C) (No data are available to guide decision making regarding an oral loading dose in patients 75 years of age or older.) • Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Level of Evidence: C)

  46. IECA e ARBs • The initiation of ACE inhibitors was recommended in all STEMI patients who are not at lower risk. • For patients at lower risk, which was defined as a normal left ventricular ejection fraction (LVEF), well-controlled cardiovascular risk factors, and performance of revascularization, ACE inhibitor therapy was considered reasonable. • ARBs were recommended in patients who are intolerant of ACE inhibitors and have clinical or radiologic signs of heart failure, an LVEF ≤40 percent, or hypertension

  47. Inibidores da Aldosterona • Are receiving therapeutic doses of an ACE inhibitor • Have an LVEF ≤40 percent • Have either HF or diabetes • Have a serum creatinine ≤2.5 mg/dL in men and ≤2.0 mg/dL in women • Have a serum potassium <5.0 meq/L

  48. Statin •  Statin therapy should be initiated prior to hospital discharge, and perhaps as early as possible, in all patients with an STEMI. • We recommend therapy with atorvastatin 80 mg/day, which was used in the PROVE IT-TIMI 22 and MIRACL trials

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