Síndromes coronarios agudos

Presentación del tema: "Síndromes coronarios agudos"— Transcripción de la presentación:

1 Síndromes coronarios agudos
Prof. Dr. Hugo Ramos Cátedra de Clínca Médica Facultad de Ciencias Médicas Universidad Nacional de Córdoba

2 Clasificación de los síndromes coronarios agudos

3 IAM con elevación del ST

4 Acute coronary syndromes
Acute coronary syndromes. The longitudinal section of an artery depicts the time line of atherogenesis from a normal artery (1), to lesion initiation and accumulation of extracellular lipid in the intima (2), to the evolution to the fibrofatty stage (3), and to lesion progression with procoagulant expression and weakening of the fibrous cap (4). An ACS develops when the vulnerable or high-risk plaque undergoes disruption of the fibrous cap (5); disruption of the plaque is the stimulus for thrombogenesis. Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth (6). Following disruption of a vulnerable or high-risk plaque, patients experience ischemic discomfort resulting from a reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a completely occlusive thrombus (bottom half, right) or subtotally occlusive thrombus (bottom half, left). Patients with ischemic discomfort may present with or without ST-segment elevation on the ECG. Of patients with ST-segment elevation, most ultimately develop a Q- wave MI (QwMI), whereas a few develop a non–Q-wave MI (NQMI). Patients who present without ST-segment elevation are suffering from unstable angina or NSTEMI, a distinction that is ultimately made on the presence or absence of a serum cardiac marker such as CK-MB or a cardiac troponin detected in the blood. Most patients presenting with NSTEMI ultimately develop an NQMI on the ECG; a few may develop a QwMI. The spectrum of clinical presentations ranging from unstable angina through NSTEMI and STEMI are referred to as the acute coronary syndromes. Dx = diagnosis.  
(Modified from Libby P: Circulation 104:365, 2001; Hamm CW, Bertrand M, Braunwald E: Lancet 358:1533, 2001; Davies MJ: Heart 83:361, 2000; and Antman EM, Anbe DT, Armstrong PW, et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction]. Circulation 110:e82, 2004.) 4

5 Fisiopatologia

6 Adhesión firme pero reversible Adhesión irreversible
Micrografia electronica de plaquetas discoides latentes Plaquetas activadas, agregadas, con hebras de fibrina Plaquetas que fluyen en forma de disco Plaquetas en forma de bola Plaquetas de forma hemisferica Plaquetas desplegadas

7 coronarias epicárdicas
Trombosis de arterias coronarias epicárdicas Trombina Fibrina Tx litico Antitrombinas Flujo Antiplaquetarios Plaquetas Vasoespasmo

8 Progresión de la lesión en el tiempo
FIGURE 52-21 Wave front of necrosis in infarction in the absence of collaterals. Total occlusions shorter than 20 minutes do not cause irreversible injury but can cause myocardial stunning as well as precondition the heart and protect it against recurrent ischemic injury. Irreversible injury begins after 20 minutes and progresses as a wave front from endocardium to epicardium. After 60 minutes, the inner third of the LV wall is irreversibly injured. After 3 hours, there is a subepicardial rim of tissue remaining, with the transmural extent of infarction completed between 3 and 6 hours after occlusion. The most important factor delaying the progression of irreversible injury is the magnitude of collateral flow, which is primarily directed to the outer layers of the heart.  
(Modified from Kloner RA, Jennings RB: Consequences of brief ischemia: Stunning, preconditioning, and their clinical implications: Part 1. Circulation 104:2981, 2001.) Kloner RA, Jennings RB. Circulation 2001; 104:2981 8

9 Diagnóstico del IAM con elevación del ST

10 Infarto de cara inferior
V1 V2 V3 V4 V5 V6 DI DII DIII aVR aVL aVF Elevación del punto J >0.1 mV

11 Infarto de cara anterior
V1 V2 V3 V4 V5 Elevación del punto J >0.2 mV en hombres >40 años >0.25 en hombres <40 años >0.15 mV en mujeres

12 Complicaciones

13 Arritmias Inestabilidad Eléctrica
EV, TV, FV, RIA, Taq unión atrioventricular no paroxística Falla de bomba, estimulación simpática Taq sinusal, FA, Flutter, TPSV Bradiarritmias y trast de conducción Bradicardia sinusal, ritmo de escape de la unión, bloqueos AV, bloqueos IV

14 Insuficiencia cardíaca aguda
Clasificación de Killip-Kimball Shock cardiogénico

15 Clasificación de Killip-Kimball
KK 1 No rales - no 3º ruido KK 2 Rales, 3º ruido, PV yugular aumentada KK 3 Edema Agudo de Pulmón KK 4 Shock cardiogénico Killip T, Kimball J. Am J Cardiol 1967;20:457

16 Ruptura de VI Robbins & Cotran, 8th ed., 2010, pp 529-587
Cardiac rupture syndromes complicating STEMI. A, Anterior myocardial rupture in an acute infarct. B, Rupture of the ventricular septum. C, Complete rupture of a necrotic papillary muscle.  
(From Schoen FJ: The heart. In Kumar V, Abbas AK, Fausto N [eds]: Robbins & Cotran Pathologic Basis of Disease. 8th ed. Philadelphia, Saunders, 2010, pp ) Robbins & Cotran, 8th ed., 2010, pp 16

17 Aneurisma y pseudoaneurisma de VI
Differences between a pseudoaneurysm and a true aneurysm. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.  
(From Shah PK: Complications of acute myocardial infarction. In Parmley W, Chatterjee K [eds]: Cardiology. Philadelphia, JB Lippincott, 1987.) Shah PK. Cardiology, JB Lippincott, 1987 17

18 Factores de riesgo de shock cardiogénico
Edad >75 años TAS <120 mmHg FC >110 lpm ó <60 lpm Tiempo prolongado desde el comienzo de los síntomas Braunwald´s, 9th Edition 2012

19 Tratamiento del IAM con elevación del ST

20 Tiempos a tratamiento en IAM
10 10 10 min Total 30 min 10 10 70 min Total 90 min Antman EM et al: JACC 2004;44: O´Gara P et al. Circulation 2013;127:e362-e425

21 Tiempos para el tratamiento
<10 min 1er ECG 10 a 20 min Diagnóstico Tx inicial Crit para Tx Reperfusión 20 a 30 min Trat de reperfusión con ATC/Fibrinolíticos O´Gara P et al. Circulation 2013;127:e362-e425 Steg G et al. Eur Heart J 2012; 33, 2569–2619 Guías Fed Arg Cardiol 2012 :

22 Bases del tratamiento M onitoreo (Morfina?) O2 N itratos A spirina

23 Dx + Monitoreo + O2 + NTG + AAS
Primeros 20 min!

24 Monitoreo/Desfibrilación = Droga Dosis de electrones transcutánea
IAM con ST = TV/FV potencial

25 Tratamiento de SCA con ST
NTG + Antiag Plaquetarios ATCp / Fibrinoliticos Heparina B Bloqueantes IECA / ARA Eplerenona Estatinas

26 Angioplastia primaria (ATCp)

27 Angioplastia primaria en IAM
Tratamiento preferido pero no siempre disponible

28 Fibrinoliticos

29 Indicaciones clase I Si no hay disponibilidad de ATCp dentro de los 120 min < 30 min desde el ingreso Hasta 12 hs del inicio de los síntomas Guías Fed Arg Cardiol 2014: O´Gara P et al. Circulation 2013;127:e362-e425 Steg G et al. Eur Heart J 2012; 33, 2569–2619

30 Preguntas?

31 Oxigeno Medir saturación Hb O2 4 L/min Sat Hb <90%
Insuficiencia cardiaca (KK > 2) Dificultad respiratoria Antman EM et al: JACC 2004;44: Van de Werf F et al: Eur Heart J 2003;24:28-66 Anderson JL et al: Circulation 2007;116:e148-e304

32 Nitratos 1º dosis sublingual (hasta tres dosis) 2º dosis IV
Vasoespasmo HTA Insuficiencia cardiaca Antman EM et al: JACC 2004;44: Van de Werf F et al: Eur Heart J 2003;24:28-66

33 Antiagregantes plaquetarios

34 Mecanismos de accion de la antiagregacion plaquetaria
Clopidogrel C ADP ADP Colageno Trombina TXA2 Inh GP IIb/IIIa Receptor Trombina Activacion The key to understanding atherothrombosis is that the benefit in event reduction from clopidogrel is additive not duplicative of the ASA benefit. As ASA and clopidogrel inhibit different pathways of platelet activation, there is potential for synergy between the two agents. Clopidogrel is a potent, non-competitive inhibitor of ADP-induced platelet aggregation, irreversibly inhibiting the binding of ADP to its platelet membrane receptors.1,2 The inhibition is specific and does not significantly affect cyclo- oxygenase or arachidonic acid metabolism.3 ADP binding is necessary for activation of the GPIIb/IIIa receptor, which is the binding site for fibrinogen. Fibrinogen links different platelets together thus forming the platelet aggregate.1 Therefore, clopidogrel ultimately inhibits the activation of the GPIIb/IIIa receptor and its binding to fibrinogen. ASA inhibits the cyclo-oxygenase enzyme, preventing the production of prostaglandin and thromboxane A2 (TxA2) from arachidonic acid. TxA2 activates the GPIIb/IIIa binding site on the platelet, allowing fibrinogen to bind.1 ASA COX TXA2 Schaffer AJ: Am J Med 1990;101: 34

35 Aspirina 1º dosis 162 a 325 mg masticada
Continuar 100 mg/d indefinidamente Alergia a AAS: Clopidogrel / Prasugrel / Ticagrelor Antman EM et al: JACC 2004;44: Van de Werf F et al: Eur Heart J 2003;24: Krumholz H et al: JACC 2006;47: Guías Fed Arg Cardiol 2011: - Guidelines ACC/AHA 2013

36 <90´ <30´ <30´ 3-24hs Comité Cardiopatía Isquémica FAC

37 Clopidogrel 1º dosis Siguientes dosis 75 mg/día con FBL con ATCp
<75 a 300 mg VO >75 a 75 mg VO con ATCp 600 mg Siguientes dosis 75 mg/día Yusuf S et al: NEJM 2001;45: Chen ZM: Lancet 2005;366: Guías Fed Arg Cardiol 2011: - Guidelines ACC/AHA 2013

38 Prasugrel Dosis de carga 60 mg Dosis de mantenimiento 10 mg/d Cuidado:
no dar hasta 24 hs después de un FBL fibrinoespecífico y 48 hs después de un FBL no fibrinoespecífico Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

39 Ticagrelor Dosis de carga 180 mg Mantenimiento 90 mg/d c/ 12 hs
Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

40 Bypass AoCo de urgencia
Anatomía no adecuada para ATCp con Isquemia recurrente Shock cardiogénico Insuficiencia cardíaca severa Otros hallazgos de alto riesgo Guidelines ACC/AHA 2013

41 Indicaciones clase I Síntomas <12 hs de duración
Contraindicaciones para FBL Shock cardiogénico o insuf cardíaca, independiente del tiempo de demora Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

42 Indicaciones Clase II Clase III
Evidencia clínica o ECG de isquemia en curso12-24 hs del comienzo de los síntomas Clase III ATC en arteria no relacionada con el IAM si está clínicamente estable Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

43 Indicaciones Clase IIa:
Cuando ATC no está disponible si hay evidencia clínica o ECG de isquemia en curso hs desde el inicio de los síntomas Si hay una gran área de miocardio en riesgo o inestabilidad hemodinámica Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

44 Fibrinolisis fallida o reoclusión
Clase IIa Derivación urgente para ATCp de rescate En pac estables para realizar CCG Tan pronto como sea logísticamente factible (idealmente dentro de las 24 hs) Pero > 3 hs postfibrinolisis Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

45 Hubo signos de reperfusión?
Dolor <50% Descenso del ST del ECG >50% Elevación enzimática precoz

46 Heparinas

47 Antitrombóticos difieren en la cadena larga de sacáridos
HNF: Media, 50 unidades de sacaridos 35% pentasacaridos PM: 15000 Heparina NF PS LMWH: Media, 18 unidades de sacaridos 20% pentasacaridos PM: 5000 PS LMWH LMWH Pentasacarido: 5 unidades de sacaridos 100% pentasacaridos Paolasso E 47

48 (> 90% no < 18 sacáridos)
LMC TROMBINA INACTIVADA • • HNF • • • PMM 15K (> 90% no < 18 sacáridos) X veces 33% PS ••••••• ••••• •••• TROMBINA AT Xa Xa IVFT X 1:1 X veces LMC (<50% 18 sacáridos) • • HBPM • • • FONDAPARINUX (PS) • • • • • PMM 5K 15% PS • • • • • • • • 100% PS TROMBINA AT AT Xa Xa IVFT PS TROMBINA INACTIVADA D>N>E X X 2:1-4:1 E>N>D Paolasso E, 2002

49 Indicaciones Mínimo de 48 hs o hasta el alta
HNF: KPTT >1.5 a 2 basal Enoxaparina: 1 mg/kg bolo IV seguido 15 min después por dosis SC c/ 12 hs Fondaparinux: 2.5 mg bolo IV, seguido 24 hs después por 1 dosis SC c/ 24 hs Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

50 Beta Bloqueantes

51 Beta Bloqueantes Dentro de las 24 horas Sin contraindicaciones
Post Fibrinoliticos / ATC Sin contraindicaciones Insuf Cardiaca Bloqueos AV Bradicardia Alergia Shock Antman EM et al: JACC 2004;44: Van de Werf F et al: Eur Heart J 2003;24:28-66 Krumholz H et al: JACC 2006;47:

52 Inhibidores de la ECA o Bloqueadoes del Receptor de Aldosterona

53 Inhibidor de la ECA IECA Dentro de las 24 hs si hay
IAM de cara anterior Insuficiencia cardíaca FEVI <40% En la convalescencia del IAM sin contraindicaciones Antman EM et al: JACC 2004;44: Van de Werf F et al: Eur Heart J 2003;24:28-66 Krumholz H et al: JACC 2006;47:

54 Bloqueador del receptor de angiotensina
ARA No tolerantes a IECA Guías Fed Arg Cardiol 2011: Guidelines ACC/AHA 2013

55 Patogenia de la placa Schematic of the evolution of the atherosclerotic plaque. 1, Accumulation of lipoprotein particles in the intima. The modification of these lipoproteins is depicted by the darker color. Modifications include oxidation and glycation. 2, Oxidative stress, including products found in modified lipoproteins, can induce local cytokine elaboration. 3, The cytokines, thus induced, increase expression of adhesion molecules for leukocytes that cause their attachment and chemoattractant molecules that direct their migration into the intima. 4, Blood monocytes, on entering the artery wall in response to chemoattractant cytokines such as monocyte chemoattractant protein 1 (MCP-1), encounter stimuli such as macrophage colony-stimulating factor that can augment their expression of scavenger receptors. 5, Scavenger receptors mediate the uptake of modified lipoprotein particles and promote the development of foam cells. Macrophage foam cells are a source of mediators, such as further cytokines and effector molecules like hypochlorous acid, superoxide anion (O2−), and matrix metalloproteinases. 6, SMCs migrate into the intima from the media. 7, SMCs can then divide and elaborate extracellular matrix, promoting extracellular matrix accumulation in the growing atherosclerotic plaque. In this manner, the fatty streak can evolve into a fibrofatty lesion. 8, In later stages, calcification can occur (not depicted) and fibrosis continues, sometimes accompanied by SMC death (including programmed cell death or apoptosis), yielding a relatively acellular fibrous capsule surrounding a lipid-rich core that may also contain dying or dead cells and their detritus. 55

56 Eplerenona

57 Eplerenona en IAM Adamopoulos C et al: Eur J Heart F Clin 2009;11:

58 Eplerenona en IAM Indicaciones Dosis 25-50 mg/día
FE VI<40% Insuficiencia cardíaca sintomática Diabetes Dosis mg/día < Mortalidad < 3 días Adamopoulos C et al: Eur J Heart F Clin 2009;11:

59 Estatinas

60 Estatinas en los SCA Mono citos LDL Endotelio LDL macro- Ox fagos LDL
HDL Inhibicion de adhesion de monocitos Mono citos HDL HDL LDL Endotelio LDL Eflujo de Colesterol Inhibicion de Oxid de LDL Ox LDL macro- fagos foam cell HDL 26 60 25

61 Cardiodesfibrilador implantable

62 Myeburg R: NEJM 2008;359:2245-2253 Guidelines ACC/AHA 2013
Remodelamiento Infarto Agudo de miocardio Cicatriz Isquemia transitoria Paro cardíaco y Muerte súbita cardíaca Myeburg R: NEJM 2008;359: Guidelines ACC/AHA 2013

63 Cardiodesfibrilador implantable
Clase I TV / FV >48 hs por arritmia que no es debida a isquemia transitoria o reversible reinfarto Anormalidades metabólicas Guidelines ACC/AHA 2013

64 Gracias