Sindromes Coronarios Agudos Dr. Javier N. Guetta Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke. Pepine CJ. The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol. 1998; 82(suppl 10A):244-275. 9

La enfermedad comienza aquí El riesgo comienza aquí Aterotrombosis Lesión Complicada/ Ruptura Células Espumosas Estrías Grasas Lesión Intermedia Ateroma Placa Fibrosa La enfermedad comienza aquí El riesgo comienza aquí Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke. Pepine CJ. The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol. 1998; 82(suppl 10A):244-275. Arteria sana Aterosclerosis precoz Inflamación Lesión precoz Placa vulnerable Placa estable 9

Ruptura de Placa / Erosión / Fisura Oclusivo SCAST No – Oclusivo AI / SCASEST Trombo Plaquetario Flujo TIMI 2 Embolización Vasoconstricción Edema Inflamación Flujo TIMI 0 Slide 9 ACS: Possible Link Between Platelets and Troponin and Benefit of GP IIb/IIIa Inhibition This diagram suggests the process by which platelet thrombus formation with microembolization may lead to necrosis in the microvasculature and elevated troponin levels. Agents that inhibit platelet aggregation by blockade of GP IIb/IIIa receptors may impede this process in 2 ways: preventing initial platelet thrombus formation at the site of plaque rupture and preventing microvascular thrombus formation. Deterioro de la perfusión tisular MIOCARDIO Necrosis tiempo dependiente Troponina + / CK + Arritmias / ICC Muerte

DOLOR PRECORDIAL EVALUACION Y TOMA DE DECISIONES Unidad de Dolor Torácico - Examen Clínico: Interrogatorio Examen Físico - ECG - Marcadores Bioquímicos

SCA Definido SCA Dudoso No SCA Paciente consulta en Guardia por Dolor Torácico Evaluación Básica ECG Interrogatorio Examen Físico Médico Cardiólogo ECG inmediato Clase II Clase I Disponibilidad de Laboratorio SCA Definido SCA Dudoso No SCA Alteraciones Isquémicas del ECG y / o Angina Definida Evaluación Avanzada DPCV Coronario ACE o ARC CF I-II Clase I DPCV no Coronario Pericarditis TEP, Aneurisma de Ao Periodo de Observación 8-12 horas Determinación / es Bioquímica / s ECG seriado Otras evaluaciones DP no CV Pulmonar Abdominal etc Conducta según diagnóstico y riesgo clínico Conducta según diagnóstico y riesgo clínico Unidad de Dolor Torácico

Cuatro Preguntas Clave Los datos de la historia clínica ¿Sugieren probabilidad intermedia a alta de padecer EAC? Si la respuesta es no, deberán realizarse otros tests diagnósticos para evaluar causas no cardíacas de dolor precordial. ¿Está cursando una angina inestable de intermedio a alto riesgo?

Cuatro Preguntas Clave 3. El paciente sufrió recientemente un IAM (<30 días) o se le realizó en los últimos 6-9 meses ATC o CRM? 4. Presenta condiciones comórbidas como ser anemia severa que pueda precipitar isquemia en ausencia de obstrucción coronaria significativa?

Clasificación del Dolor Precordial Angina Típica (definida) 1- Molestia precordial característica 2- Provocada por ejercicio o stress emocional 3- Mejora con el reposo o NTG. Angina Atípica (probable) Dos de las características mencionadas previamente Dolor precordial no cardíaco Una o ninguna de las características de la angina típica J Am Coll Cardiol. 1983;1:574, Letter

Sindromes Coronarios Agudos Angina Estable Angina Inestable IAM no Q IAM Q SCA sin elevación del ST Elevación ST ECG - ST ECG - ST CK-MB Troponina - PCR - NT Pro BNP? PCR – ¿HDL? Cannon CP. 1999

DOLOR TORACICO Examen Clínico, ECG Angina Definida CF III IV < 24 hs Cambios ST-T > 1mm Arritmia compleja Angina Probable No angina con antec. de enf. coronaria No angina con FRC (no DBT) ECG normal No antecedentes ACE ARC CF I-II SI SI SI OBSERVACION CONS. EXT. Evaluación Clínica ECG y Marcadores Bioquímicos seriados + ALTA UNIDAD CORONARIA - - + TEST FUNCIONAL

Evaluación en Guardia + – + – + Presentación Dolor Torácico Normal Depresión ST Elevación ST ECG Marcadores – + – + + Patients presenting with chest pain are first evaluated for the presence of ECG changes in the emergency department to determine if the chest pain is caused by coronary disease. The final diagnosis of a specific ACS incorporates both the ECG findings and results of assays for cardiac markers, such as CK-MB and troponins. Patients with persistent ST-segment elevation on ECG are diagnosed as having an ST-segment elevation MI (STEMI), regardless of whether their cardiac markers are elevated. In the larger group of patients who have ischemic ECG changes other than persistent ST-segment elevation (e.g., ST-segment depression, transient ST-segment elevation, T-wave inversions), measurement of cardiac markers is essential for distinguishing those who have unstable angina (no elevation of cardiac markers) and those with non-ST-segment elevation MI (elevated cardiac markers). Diagnóstico Angina Inestable No SCA IAM Braunwald E,2002 http://www.acc.org/clinical/guidelines/unstable/unstable

SCA sin Elevación ST Trombo Plaquetario no oclusivo Flujo TIMI 2 Embolización Vasoconstricción Edema Inflamación Flujo TIMI 0 Slide 9 ACS: Possible Link Between Platelets and Troponin and Benefit of GP IIb/IIIa Inhibition This diagram suggests the process by which platelet thrombus formation with microembolization may lead to necrosis in the microvasculature and elevated troponin levels. Agents that inhibit platelet aggregation by blockade of GP IIb/IIIa receptors may impede this process in 2 ways: preventing initial platelet thrombus formation at the site of plaque rupture and preventing microvascular thrombus formation. Deterioro de la perfusión tisular MIOCARDIO Necrosis tiempo dependiente Troponina + / CK + Arritmias / ICC Muerte

Clasificación de Riesgo TROPONINA: >0.01<0.1 ng/ml ACC-AHA 2000  BAJO. ARC III-IV 2 sem y med/ alta posibilidad de EC. ECG: normal/ sin cambios. TROPONINA: normal  MEDIANO. Angina > 20’,resuelta o < 20’ en curso y med/ alta posib. de EC. Edad >70. IAM, ACV, CRM, AAS. ECG: ondas T invertidas >0.2 mV/ Q anormales TROPONINA: >0.01<0.1 ng/ml  ALTO. Angina>20’ en curso. ARP<48 hs. EAP, nuevo soplo, rales, hipotensión. Edad >75. ECG: cambios ST>0.5 mV/ nuevo BRI/ TVS. TROPONINA:>0.1 ng/ml

TIMI SCORE 14 días 0/1 3 5 2 3 8 3 5 13 4 7 20 5 12 26 6/7 19 41 Score M/IAM % M/IAM/R % Edad  65 FRC  3 Enf. Coronaria conocida Uso previo AAS  7 d  2 episodios de angina en  24hs Elevación marcadores ST  0.5 mm 0/1 3 5 2 3 8 3 5 13 4 7 20 5 12 26 6/7 19 41

A. Piombo, J. Gagliardi, J. Guetta, J. Fuselli, C. Bertolasi Desarrollo de un Nuevo Sistema de Score para Clasificar el Riesgo en la Angina Inestable A. Piombo, J. Gagliardi, J. Guetta, J. Fuselli, C. Bertolasi Variables Score M/IAM % M/IAM/R % Angina de Reciente 1 Comienzo Angina Progresiva 2 Desnivel de ST 3 Trop. T o PCR + 4 Edad > 65 años 4 1-5 5 11 6-10 5.5 11 11-14 14 23 Grupo DIC

Manejo médico de Angina Inestable e IAM no-Q Trombo Blanco rico en plaquetas Reposo, oxígeno, monitoreo ECG Terapia antiplaquetaria (AAS, clopidogrel,) Heparina/heparina de bajo peso Inhibidores GP IIb IIIa Nitroglicerina Beta bloqueantes Revascularización (ATC/CRM) Vasoespasmo Slide 15 Current Medical Management of Unstable Angina and Non-Q-wave MI Medical treatment for unstable angina is primarily directed at controlling the symptoms of ischemia and inhibiting thrombus formation, in addition to routine supportive therapy. The efficacy of antiplatelet therapy has been well documented and ASA is regarded as standard treatment. Intravenous glycoprotein (GP) IIb/IIIa inhibitors may be used in selected high-risk patients, particularly those proceeding to angiography and possible revascularization. Heparin is regarded as standard therapy, particularly in higher risk patients. However it is increasingly being replaced by low-molecular-weight heparin (LMWH). Direct thrombin inhibitors such as hirudin are still being evaluated in clinical trials. Anti-ischemic treatment consists of nitroglycerin and, provided there are no contraindications, a beta-blocker. In some patients, a calcium channel blocker may be given. After the acute episode, aggressive management of risk factors is required and the patient should be advised about lifestyle changes including smoking cessation. The patient should be discharged on a beta-blocker and possibly a statin and an ACE inhibitor. Long-term antiplatelet therapy should also be an integral component of treatment.

Sindromes Coronarios Agudos sin Elevación ST - Tratamiento % Cambio de riesgo (con 95% CI) de muerte o IAM No. de trials No. de pacientes Tratamiento AAS 4 3114 Heparina 4 1547 Betabloqueantes 5 4700 Terapia Trombolítica 12 2376 Bloqueantes Cálcicos 5 956 Slide 18 Overall Effect of Therapies for Unstable Angina in Reducing Death or MI This slide summarizes the pooled results of various clinical trials in unstable angina and shows the relative benefit of various therapies. ASA, heparin and beta-blockers all significantly reduce the risk of death or MI. There is no evidence of additional benefit with thrombolytic therapy. Taken together, the trials of early intervention also show an overall benefit. -100 -50 50 < Disminuye Aumenta > Basado en datos combinados de ensayos clínicos randomizados Granger CB. In: Califf RM (Ed) Acute Coronary Care. Mosby, Philadelphia, PA,1995; Chap 42 Reference Grange CB. In: Califf RM (Ed) Acute Coronary Care. Mosby, Philadelphia, PA, 1995; Chap 42, pp 525–541.

CURE Study Clopidogrel en SCA Eventos (IAM, Stroke, o Muerte Cardiovascular 0.14 Placebo* (n = 6,303) 0.12 0.10 0.08 Clopidogrel* (n = 6,259) 20% Relative risk reduction p = 0.00009 Cummulative hazard rate 0.06 The combination of clopidogrel and ASA was also studied in the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial. A total of 12,562 patients with acute coronary syndromes without ST-segment elevation were randomized to receive either 75 mg once daily clopidogrel or placebo in addition to ASA (75 mg-325 mg daily) and followed for 12 months. Clopidogrel demonstrated a highly significant 20% relative risk reduction in the primary end point of vascular events of MI, stroke, or vascular death: 95% CI, 0.72–0.90; p = 0.00009.1,2 Overall, in the placebo group there were 719 (11.4%) vascular events experienced for the first time and 582 (9.3%) in the clopidogrel group. The hazard rate curves began to diverge within the first few hours after initiation of therapy and continued to diverge over the entire 12 months of treatment follow-up period.1 A significant reduction in relative risk of approximately 20% was observed during the first 30 days with this reduction being similar to the value observed during the chronic phase (from 30 days until the end of follow-up at 12 months). Thus, clopidogrel when used on top of standard therapy (including ASA) provides both an early and a long-term clinical benefit.1 0.04 0.02 0.00 3 6 9 12 Months of follow-up *On top of standard therapy (including ASA) 1. The CURE Trial Investigators. N Engl J Med 2001; 345: 494–502. References: 1. The CURE Trial Investigators. N Engl J Med 2001; 345: 494–502. 2. Data on file, 2002, p73 internal CSR-EFC 3307.

Resultados de los pacientes tratados con Inhibidores IIb/IIIa en PTCA no planeada Muerte/IAM dentro de los 30 días Inhibidor IIb/IIIa Control Reducción ±SD Odds ratio 95% Cl n PARAGON-A* 1513 10.6% 11.7% 11±15 PARAGON-A† 1526 12.0% 11.7% -2±16 PRISM 3232 5.8% 7.1% 19±13 PRISM-PLUS‡ 1570 8.7% 11.9% 30±14 PRISM-PLUS§ 695 13.6% 11.7% -19±25 PURSUIT 9461 14.2% 15.7% 11±5 PARAGON-B 5169 10.5% 11.5% 9±8 GUSTO-IV 7800 8.7% 8.0% -8±9 Total 30 966 10.6% 11.8% 8±4 Slide 17 Outcome of Patients Treated with IIb/IIIa Inhibitors where Percutaneous Revascularization was Not Planned This slide provides outcome data (combined incidence of death and MI after 30 days) of patients treated with GP IIb/IIIa inhibitors in the 5P* trials and GUSTO IV. These trials compared GP IIb/IIIa inhibitors with control treatment in patients with unstable angina who were also receiving aspirin therapy and in whom immediate percutaneous revascularization was not planned. In conclusion, these studies suggest that early, potent therapy with GP IIb/IIIa inhibitors leads to improved outcomes, but a number of issues are unresolved such as optimal length of therapy, the dosage that provides maximal platelet inhibition with minimal risk of bleeding complications and the most effective agent overall. *5P trials: PARAGON-A, PARAGON B, PRISM, PRISM-Plus and PURSUIT. Test de heterogenicidad: x2=9.07 Efecto Tratamiento : 2p=0.027 0.0 0.5 1.0 1.5 2.0 IIb/IIIa Mejor Control Mejor *bajas dosis de lamifiban, †Altas dosis lamifiban, ‡ tirofiban más heparina vs heparina sola, § tirofiban sola vs heparina sola Curr Opin Cardiol 2000;15:441–482

SCA sin Elevación ST y Tratamiento Intervencionista Cuatro grandes estudios compararon la estrategia conservadora vs invasiva : TIMI-IIIb No hubo diferencias significativas en Muerte /IAM VANQWISH Alta incidencia de Muerte / IAM en el grupo invasivo FRISC II Significativa reducción en Muerte / IAM con la estrategia invasiva TACTICS precoz Slide 16 The Place of Coronary Intervention in Unstable Angina and Non-Q-wave MI Controversies still exist regarding the optimal approach. There are two alternate approaches to intervention in unstable angina: an invasive strategy with early routine coronary angiography followed by revascularization if appropriate, or a more conservative strategy in which angiography is only undertaken in patients with refractory angina or a positive exercise test. Four randomized trials have compared the two strategies, although they differ in the design and in the patients included. TIMI-IIIb showed no difference in death/MI between the two arms, while in VANQWISH, the risk of death/MI was higher in the invasive group. In particular there were more deaths in the CABG patients. In FRISC II, all patients were treated with LMWH with the intention of stabilizing the patients. In the invasive arm, revascularization, when indicated, was undertaken after a mean of 4 days (PCI) or 8 days (CABG). At 1 year follow-up, there was a significant advantage in favor of the invasive approach. TACTICS is the most recent trial and showed a significant benefit for early routine intervention (angiography within 4–48 hours). Conclusions: these data suggest a need to: update the ACC/AHA guidelines modify the clinical approach with broader use of early invasive strategy/use of GP IIb/IIIa inhibitors TIMI IIIB Circulation 1999;89:1545–1556; Boden WE N Engl J Med 1998;338:1785–1792; FRISC II Lancet 1999;354:708–715; Cannon CP AHA Nov 2000

AAS, nitratos, betabloqueantes, heparina SCA sin Elevación ST Todos los pacientes AAS, nitratos, betabloqueantes, heparina Pacientes de Alto Riesgo GP IIb/IIIa Clopidogrel Coronariografía Heparina hasta coronariografía Continuar con GP IIb/IIIa 12–24 horas después de la coronariografía Pacientes de Bajo Riesgo Manejo médico (antiplaquetarios, nitratos, betabloqueantes) Stress test antes o después del alta Slide 19 Overview of Unstable Angina Guidelines The new US and European guidelines for the management of unstable angina and non-Q-wave MI have recently been published. The two sets of guidelines are very similar, with some minor differences. Once acute ST-elevation MI has been excluded, patients should receive appropriate medical therapy including ASA, beta-blockers, nitrates and heparin. High-risk patients, including those with recurrent ischemia, elevated cardiac markers, hemodynamic instability or major arrhythmias should undergo angiography. High-risk patients should also receive an intravenous GP IIb/IIIa inhibitor. Low-risk patients should be managed with aggressive medical therapy and then undergo a stress test. Bertrand ME et al Eur Heart J 2000;21:1406–1432 Braunwald E et al J Am Coll Cardiol 2000;36:970–1062 References Bertrand ME, Simoons ML, Fox AA. Recommendations of the Task Force of the European Society of Cardiology. Eur Heart J 2000;21:1406–1432. Braunwald E, Antman EM, Beasley JW et al. J Am Coll Cardiol 2000;36:970–1062.

SCA con Elevación ST Trombo oclusivo / Plaquetas - Fibrina Flujo TIMI 2 Embolización Vasoconstricción Edema Inflamación Flujo TIMI 0 Slide 9 ACS: Possible Link Between Platelets and Troponin and Benefit of GP IIb/IIIa Inhibition This diagram suggests the process by which platelet thrombus formation with microembolization may lead to necrosis in the microvasculature and elevated troponin levels. Agents that inhibit platelet aggregation by blockade of GP IIb/IIIa receptors may impede this process in 2 ways: preventing initial platelet thrombus formation at the site of plaque rupture and preventing microvascular thrombus formation. Deterioro de la perfusión tisular MIOCARDIO Necrosis tiempo dependiente Troponina + / CK + Arritmias / ICC Muerte

Sindromes Coronarios Agudos Con Elevación ST

IAM Mortalidad a través del tiempo Mortalidad a corto plazo % Desfibrilador Monitoreo Hemodinámico b-Bloqueantes Aspirina Trombolisis ATC Adapted from Antman, Braunwald In:Braunwald ed. Heart Disease p 1184.

Reperfusión y Beneficio Dependiente del Tiempo Lecture Notes In the GISSI-I trial, patients who received fibrinolytic therapy within 1 hour of symptom onset had a 47% reduction in 21-day mortality compared with placebo; benefit declined as the interval increased. Initiation of treatment between 1 and 3 hours after symptom onset was associated with a mortality reduction of 14%. (GISSI, 1986) The benefit of therapy for patients treated beyond 2 hours is more modest but still significant, and may reflect the ability of the late reperfusion to prevent ventricular enlargement or improve electrophysiologic stability as well as salvage myocardium. The results of other controlled clinical trials of fibrinolytic therapy also support the dramatic relationship between early restoration of patency and myocardial salvage. Using data from the studies by Reimer et al, Bergmann et al, and the GISSI-I clinical trial, Tiefenbrunn and Sobel constructed a reperfusion time-benefit curve that depicts the time-dependent benefit of intervention for AMI. A nonlinear curve provided the best fit for the data. A similar curve was developed by Boersma and colleagues in their analysis of a data set of 22 randomized clinical trials of fibrinolytic therapy. (Reimer et al, 1977; Bergmann et al, 1982; Boersma et al, 1996; Tiefenbrunn and Sobel, 1992) Adapted from Tiefenbrunn AJ, Sobel BE. Circulation. 1992;85:2311-2315.

Las Cuatro “D” Objetivo < 30 min Lecture Notes Tiempo de Inicio Tempo 1: DOOR Tiempo 2: DATA Tiempo 3: DECISION Tiempo 4: DRUG Intervalo III Decisión a la droga Intervalo II ECG a decisión para tratar Intervalo I Puerta a ECG Objetivo < 30 min Lecture Notes In an effort to reduce the time from symptom onset to the initiation of fibrinolytic therapy, the National Heart Attack Alert Program (NHAAP) has identified four critical and recordable time points, called “the four Ds.” These are identified as: Door (Time Point 1): The patient arrives at the emergency department (ED). Data (Time Point 2): An initial electrocardiogram (ECG) is obtained. Decision (Time Point 3): A decision is made to initiate fibrinolytic therapy. Drug (Time Point 4): Fibrinolytic therapy is initiated. The intervals between these time points were designated intervals I through III for the purpose of identifying and reducing in-hospital delays in treatment. NHAAP Recommendations. U.S. Department of Health NIH Publication: 1997:97-3787.

Guías de Manejo IAM ACC/AHA Guidelines (1999) Door-to-treatment time: < 30 minutes NHAAP Recommendations (1997) Door-to-treatment time: 30 minutes ACLS Recommendations (1992) Door-to-treatment time: 30 to 60 minutes Lecture Notes The 1999 ACC/AHA guidelines for the management of patients with AMI recommends a door-to-drug time that is less than 30 minutes. The NHAAP (1997) recommended that EDs should strive for initiation of fibrinolytic therapy in AMI patients within 30 minutes of arrival at the ED. The 1992 ACLS guidelines also recommended that fibrinolytic therapy be initiated for all eligible patients with AMI within 30 to 60 minutes of their arrival in the ED.

Candidatos para Reperfusión Miocárdica Sospecha de IAM: Presencia de síntomas (angor o equivalentes) persistentes (más de 20 min) que no ceden con nitritos, asociado con supradesnivel del ST/BRI u otro confundidor electrocardiográfico ECG Supradesnivel del ST  1 mm al menos en 2 derivaciones contiguas y  2 mm de V1 a V3 Ventana de tiempo Depende de la persistencia de isquemia, la extensión del infarto y el compromiso hemodinámico

Estratificación de Riesgo Subgrupos Hemodinámicos - Killip GISSI-1 (%) Killip Definición Incidencia Control Lítico Mortalidad Mortalidad I No ICC 71 7.3 5.9 II R3 ó 23 19.9 16.1 rales basales III Edema pulmonar 4 39.0 33.0 (rales >1/2 sup) IV Shock Cardiogénico 2 70.1 69.9

Trombolíticos Criterios ECG para el Tratamiento Estudios Randomizados Odds Ratio & 95% CI 0.33 1 3 Placebo Mejor Lisis Mejor Placebo Lisis 23.6% BBB 18.7% 16.9% ST Anterior 13.2% 8.4% ST Inferior 7.5% 13.4% ST Otros 10.6% 13.8% ST 15.2% 5.8% Otras Alt. 5.2% 2.3% Normal 3.0% Fibrinolytic Therapy Trialists. Lancet 1994;343:311.

ISIS-2 Collaborative Group, Lancet 1988;2:349. IAM: Aspirina ISIS-2 4300 4295 4300 4292 ISIS-2 Collaborative Group, Lancet 1988;2:349.

Estudios Randomizados Beta Bloqueantes Estudios Randomizados Studio Agente N ISIS-1 16,027 Atenolol During MI MIAMI 5,778 Metoprolol TIMI IIB 1,434 Metoprolol Norwegian 1,884 Timolol Post MI BHAT 3,837 Propranolol Hennekens et al. NEJM 1996;335:1660.

Metaanálisis Estudios Randomizados IAM: IECA Metaanálisis Estudios Randomizados Study Agent N Mortality Odds Ratio & 95% CI 1 2 ISIS-4 58,050 Captopril During MI GISSI-3 19,394 Lisinopril CONSEN II 6,090 Enalaprilat SAVE 2,231 Captopril Post MI AIRE 2,006 Ramipril TRACE 1,749 Trandolapril Rx Better Control Better Hennekens et al. NEJM 1996;335:1660.

ACC/AHA Manejo de Pacientes con Infarto Agudo de Miocardio Elevación Segmento ST Aspirina, beta-bloqueantes 12 h >12 h Elegible tratamiento Fibrinolítico Contraindicación Fibrinolíticos No Candidato a Reperfusión Síntomas Persistentes? Terapia Fibrinolítica ATC primaria o CRM No Si Otros tratamientos: IECA, Nitratos Considerar Reperfusión Lecture Notes Prompt recanalization of an infarct-related artery by fibrinolytic therapy or mechanical means and consequent restoration of myocardial perfusion have been shown to limit infarct size, reduce mortality, and improve left ventricular function. Delay in treatment is a critical factor in decreasing overall survival. The delay may be patient-related (ie, delay in seeking treatment) or due to the time required for diagnosis and initiation of treatment. This slide presents a suggested schema for the management of AMI with ST-segment elevation.

Consenso SCA con Supradesnivel ST: Trombolíticos Clase II Sospecha de IAM extenso entre 12 y 24 hs del inicio de los síntomas con dolor persistente y supradesnivel ST (B) Sospecha de IAM no extenso entre 6 y 12 hs del inicio de los síntomas con dolor persistente y supradesnivel ST (B) Congreso Argentino de Cardiología, Octubre 2001

Congreso Argentino de Cardiología, Octubre 2001 Consenso SCA con Supradesnivel ST: Estrategia Intervencionista Primaria Clase I Sospecha de IAM extenso, como alternativa al tratamiento trombolítico, en los que se puede tratar la arteria responsable, dentro de las 12 hs del inicio de los síntomas * (A) Sospecha de IAM extenso, como alternativa al tratamiento trombolítico, entre las 12 y 24hs con evidencia de isquemia persistente (dolor y supradesnivel ST/BRI * (A) Congreso Argentino de Cardiología, Octubre 2001

Congreso Argentino de Cardiología, Octubre 2001 Consenso SCA con Supradesnivel ST: Estrategia Intervencionista Primaria Clase I En pacientes que se hallan dentro de las 24 hs de un IAM con supradesnivel ST/BRI, con shock cardiogénico, menores de 75 años de edad y en los que la revascularización pueda realizarse dentro de las 18 hs del shock * (A) Como estrategia de reperfusión en pacientes con contraindicaciones absolutas para tratamiento trombolítico (C) Congreso Argentino de Cardiología, Octubre 2001

Congreso Argentino de Cardiología, Octubre 2001 Consenso SCA con Supradesnivel ST: Estrategia Intervencionista Primaria Tiempo aceptado: Tiempo puerta - balón 60 ( 30) min Operador experto: más de 75 angioplastias anuales Si KK > 2 el centro debe disponer de cirugía cardiovascular y balón de contrapulsación intraaórtica Congreso Argentino de Cardiología, Octubre 2001

Consenso SCA con Supradesnivel ST: Trombolíticos Clase I Sospecha de IAM extenso de menos de 12 hs de evolución, sin contraindicaciones, menores de 75 años, sin Edema Agudo de Pulmón (EAP) o shock cardiogénico (A) Sospecha de IAM no extenso de menos de 6 hs de evolución, sin contraindicaciones, menores de 75 años, sin Edema Agudo de Pulmón (EAP) o shock cardiogénico (A) Congreso Argentino de Cardiología, Octubre 2001

Enfermedad Coronaria A pesar de los avances, sigue siendo la principal causa de muerte Muertes por enfermedad Cardiovascular (%) Estados Unidos: mortalidad 1998 17% ACV 48% Enfermedad coronaria 5% HTA 5% ICC 2% Aterosclerosis 0,5% Enfermedad Reumática 0,5% Cardiopatías Congénitas 23% Otras Causas American Heart Association. 2001 Heart and Stroke Statistical Update. Dallas, Tex. American Heart Association, 2001

Unidad de Dolor Torácico Visión del Clínico ECG de ingreso Elevación ST Sin elevación ST El tiempo es músculo Marcadores Bioquímicos ECG seriado, Observación, Causas no cardíacas El tiempo está de nuestro lado

Unidad de Dolor Torácico Visión del AdministradorHospitalario ECG de ingreso Sin elevación ST Elevación ST Time is money El tiempo es músculo UCO UDT Alto riesgo Bajo Riesgo IIb IIIa inh. Revasc. precoz Alta

Unidad de Dolor Torácico Visión del representante legal Como evitar demandas por altas inadecuadas

Clasificación Angina Inestable: Braunwald Severidad Clase 1: < a 2 meses. Sin angina de reposo Clase 2: Angina de reposo < 1 mes. Sin angina de reposo en últimas 48hs Clase 3: Angina de reposo en las últimas 48hs Circunstancia clínica Clase a: Secundaria Clase b: Primaria Clase c: Post IAM (2 semanas) Tratamiento 1: Tratamiento mínimo o ausente 2: Tratamiento standard para ACE 3: Máximo tratamiento incluso NTG IV