Scasest

REPUBLICA BOLIVARIANA DE VENEZUELA
MINISTERIO DEL PODER POPULAR PARA LA SALUD

HOSPITAL CENTRAL UNIVERSITARIO DR. ANTONIO MARIA PINEDA
DEPARTAMENTO DE MEDICINA
SERVICIO DE CARDIOLOGIA
TRATAMIENTO INICIAL
HOSPITALARIO DEL
SCASEST
Dr Jos G. Hernndez C
Residente Asistencial Cardiologa
MEDIDAS GENERALES DE APOYO

OXIGENOTERAPIA
Debe administrarse oxigeno cuando la saturacin arterial
de oxigeno es < 90% o si el paciente tiene insuficiencia
respiratoria.
Guia ESC 2015 sobre el tratamiento de los sindromes coronarios agudos en pacientes sin elevacion persistente del segmento ST
Rev Esp Cardiol. 2015;68(12):1125.e1-e64
MEDIDAS GENERALES DE APOYO

OXIGENOTERAPIA
AVOID Study: Air versus oxygen in ST-segment elevation
myocardial infarction.
Conclusiones
La terapia de oxgeno suplementario en pacientes con
STEMI pero sin hipoxia puede aumentar la lesin
miocrdica temprana y se asoci con el tamao del infarto
de miocardio mayor evaluado a los seis meses .
AVOID Study: Air versus oxygen in ST-segmentelevation myocardial infarction. Stub D, Smith K, Bernard S, Nehme Z, Stephenson M,
Bray JE, Cameron P, Barger B, Ellims AH, Taylor AJ, Meredith IT, Kaye DM. Circulation. 2015;131:214350.
TERAPIA ANTIISQUEMICA
El objetivo del tratamiento farmacolgico antiisqumico es
disminuir la demanda miocrdica de oxgeno o aumentar el
aporte de oxgeno al miocardio.
Fisiopatologa
deldel
miocardio
isqumico.
dede
la frecuencia
cardiaca
Jos
Moreu-Burgosa
Fisiopatologa
isqumico.
Importancia
la frecuencia
cardiaca
Jos
Moreu-Burgosa
Guia
ESC 2015 sobre
elmiocardio
tratamiento
de los Importancia
sindromes
coronarios
agudos
en
pacientes
sin
elevacion y y
Carlos
Macaya-Miguel
Rev
Esp
Cardiol
Supl.
2007;7:19D-25D
Carlos
Macaya-Miguel
Rev
Esp
Cardiol
Supl.
2007;7:19D-25D
persistente
del segmento
ST
Rev
Esp
Cardiol.
2015;68(12):1125.e1-e64
NITRATOS
Los nitratos intravenosos son mas eficaces que los nitratos
sublinguales *
NTG EV 50mg/10ml
10-200mcg/min 3 cc/h
DNIS SL
c/5min x 3 dosis
5mg
NITRATOS
GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly

and together on 6-week mortality and ventricular function after acute
myocardial infarction. Gruppo Italiano per lo Studio della
Sopravvivenza nell'infarto Miocardico.
Mortalidad a las 6 semanas era 6.5% entre los pacientes tratados
con nitratos y 6.9% entre los pacientes que no recibieron nitratos
(2p=0.28, OR 0.94, 95%CI: 0.84-1.05);
Con respecto al evento combinado (mortalidad y disfuncion
ventricular severa): nitratos 15.9% vs no nitratos 16.7% (2p=0.12,
OR 0.94, 95%CI: 0.87-1.02)
GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after
acute myocardial infarction. Gruppo Italiano per lo Studio della Sopravvivenza nell'infarto Miocardico. Giulio Zuanetti, MD; Roberto
Latini, MD; Aldo P. Maggioni, MD; MariaGrazia Franzosi, PhD; Luigi Santoro, MSc; Gianni Tognoni, MD Lancet. 1994 May
7;343(8906):1115-22.
NITRATOS
GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate
singly and together on 6-week mortality and ventricular function
after acute myocardial infarction. Gruppo Italiano per lo Studio
della Sopravvivenza nell'infarto Miocardico.
Lisinopril antes de las 24h del IM: Reduce

significativamente la mortalidad a las 6 semanas en un
11%; No hubo beneficio de supervivencia del uso de NTG.
7;343(8906):1115-22.
NITRATOS
Drug Interactions With Phosphodiesterase-5 Inhibitors
Used for the Treatment of Erectile Dysfunction or
Pulmonary Hypertension
Coadministration OF PDE5Is and nitrates can trigger
marked vasodilation and severe hypotension.
Overview of the cardiovascular effects of tadalafil. Emmick JT, Stuewe SR, Mitchell M. Eur Heart J Suppl. 2002;4:H32H47
Drug Interactions With Phosphodiesterase-5 Inhibitors Used for the Treatment of Erectile Dysfunction or Pulmonary Hypertension
Bryan G. Schwartz, MD; Robert A. Kloner, MD, PhD (Circulation. 2010;122:88-95.
BETABLOQUEANTES
Inhiben competitivamente los efectos miocrdicos de las
catecolaminas circulantes
Reducen el consumo miocrdico de oxgeno al disminuir:
Frecuencia cardiaca
Presin arterial
Contractilidad miocrdica
Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy David E. Golan MD,
Principles
Guia
ESC
of 2015
Pharmacology:
sobre el tratamiento
The Pathophysiologic
de los sindromes
Basiscoronarios
of Drug
agudos en pacientes sin elevacion persistente del segmento ST
PhD,
Second
Edition
Therapy
Rev Esp
David
Cardiol.
E. Golan
2015;68(12):1125.e1-e64
MD, PhD, Second Edition
BETABLOQUEANTES
Overview of results of randomized clinical trials in heart
disease. I. Treatments following myocardial infarction
Metanlisis de 27 estudios
Tratamiento con bloqueadores beta se asoci a una
reduccin del riesgo relativo (RR) del 13% en la mortalidad
durante la primera semana tras el infarto de miocardio
Overview of results of randomized clinical trials in heart disease. I. Treatments following myocardial infarction. Yusuf S, Wittes
J, Friedman L. JAMA 1988 Oct 14;260(14):2088-93.
BETABLOQUEANTES
Early intravenous beta-blockers in patients with acute
coronary syndrome - a meta-analysis of randomized trials.
Mortalidad intrahospitalaria se redujo 8% con
betabloqueantes EV, RR=0.92 (95% CI, 0.86-1.00; p=0.04)
comparado con controles.
Early intravenous beta-blockers in patients with acute coronary syndrome--a meta-analysis of randomized trials. Chatterjee
S, Chaudhuri D, Vedanthan R, Fuster V, Ibanez B, Bangalore S, Mukherjee D. Int J Cardiol. 2013 Sep 30;168(2):915-21. doi:
10.1016/j.ijcard.2012.10.050. Epub 2012 Nov 17.
BETABLOQUEANTES
coronary syndrome - a meta-analysis of randomized trials.
Beta bloqueante EV redujo el riesgo de taquiarritmias
STROKE
ventriculares (RR=0.61; 95 % CI 0.47-0.79;
p=0.0003) y reIM
SHOCK
(RR=0.73, 95 % CI 0.59-0.91; p=0.004)
reIM sin incrementar el
riesgo de shock cardiogenico, (RR=1.02; 95% CI 0.77-1.35;
p=0.91) o ecv (RR=0.58; 95 % CI TAQUIARRITMIAS
0.17-1.98; p=0.38).
S, Chaudhuri D, Vedanthan R, Fuster V, Ibanez B, Bangalore S, Mukherjee D. Int J Cardiol. 2013 Sep 30;168(2):915-21. doi:
10.1016/j.ijcard.2012.10.050. Epub 2012 Nov 17.
BETABLOQUEANTES
coronary syndrome--a meta-analysis of randomized trials.
CONCLUSIONES:
Administracion temprana de Betabloqueantes EV en los pacientes
apropiados con SCA parece estar asociada con una reduccin
significativa en el riesgo de resultados cardiovasculares a corto plazo ,
incluyendo una reduccin en el riesgo de mortalidad por todas las
causas
S1, Chaudhuri D, Vedanthan R, Fuster V, Ibanez B, Bangalore S, Mukherjee D. Int J Cardiol. 2013 Sep 30;168(2):915-21. doi:
10.1016/j.ijcard.2012.10.050. Epub 2012 Nov 17.
BETABLOQUEANTES
Impact of acute beta-blocker therapy for patients with non-ST-segment
elevation myocardial infarction.
CONCLUSIONS:
La mayoria de los pacientes con NSTEMI recibio terapia temprana con
beta bloqueantes.
Debido a que el tratamiento con beta-bloqueantes aguda se asoci con
mejores resultados clnicos en casi todos los subgrupos de pacientes
evaluados , un uso ms amplio en pacientes con IMSEST parece
justificado
Impact of acute beta-blocker therapy for patients with non-ST-segment elevation myocardial infarction. Miller CD 1, Roe MT, Mulgund
J, Hoekstra JW, Santos R, Pollack CV Jr, Ohman EM, Gibler WB, Peterson ED. Am J Med. 2007 Aug;120(8):685-92.
BETABLOQUEANTES
Debe evitarse la administracin precoz de bloqueadores
beta a pacientes con riesgo de shock cardiognico si se
desconoce la funcin ventricular.
Riesgo de shock cardiognico:
Edad > 70 aos
Frecuencia cardiaca > 110 lpm
Presin arterial sistlica < 120 mmHg
BETABLOQUEANTES
No se debe administrar bloqueadores beta a pacientes con
sntomas relacionados con vasoespasmo coronario (fenmeno de
Raynaud) o que consuman cocana.
El pronstico a largo plazo para los pacientes con angina variante

es relativamente buena
El uso de antagonistas del calcio lo mejora .
Long-term prognosis for patients with variant angina and influential factors.Yasue H 1, Takizawa A, Nagao M, Nishida S, Horie
M, Kubota J, Omote S, Takaoka K, Okumura K. Circulation. 1988 Jul;78(1):1-9.
BETABLOQUEANTES
Contraindicaciones absolutas : FC < 60 lpm , PAS < 100
mmHg, insuficiencia cardiaca moderada o severa ,
trastornos de la conduccin AV , enfermedad severa de las
vas respiratorias .
Contraindicaciones relativas : asma, uso actual de
bloqueador del canal del calcio y / o B -bloqueante ,
enfermedad vascular perifrica grave con isquemia crtica
del miembro , IM inferior que implica el ventrculo derecho
Oxford Handbook of Cardiology SECOND EDITION 2012 Edited by Punit Ramrakha and Jonathan Hill Oxford University Press
INHIBICION PLAQUETARIA
DRUGS FOR THE HEART 8th edition 2013 Opie elsevier saunders
ASPIRINA
Veterans Administration Study
1384 pacientes con AI aleatorizados, 325mg dia vs placebo por
12 semanas
La incidencia de muerte o infarto agudo de miocardio fue del
51% menor en el grupo de aspirina que en el grupo placebo: 31
pacientes (5,0%) en comparacin con 65 ( 10,1%) ; P = 0,0005 .
Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans
Administration Cooperative Study. Lewis HD Jr, Davis JW, Archibald DG, Steinke WE, Smitherman TC, Doherty JE 3rd, Schnaper
HW, LeWinter MM, Linares E, Pouget JM, Sabharwal SC,Chesler E, DeMots H. N Engl J Med. 1983 Aug 18;309(7):396-403.
ASPIRINA
Infarto agudo de miocardio no fatal fue del 51% menor en el
grupo de aspirina : 21 pacientes ( 3.4%) en comparacin con 44
( 6,9%) ; P = 0,005.
La reduccin de la mortalidad en el grupo de aspirina fue
tambin el 51% - 10 pacientes ( 1,6 %) en comparacin con 21
( 3,3 %) - aunque no fue estadsticamente significativa ; P =
0,054.
ASPIRINA
No hubo diferencias en los sntomas gastrointestinales o
evidencia de la prdida de sangre entre los grupos de
tratamiento y control .
Nuestros datos muestran que la aspirina tiene un efecto
protector contra el infarto agudo de miocardio en los hombres
con angina inestable, y sugieren un efecto similar sobre la
mortalidad.
CLOPIDOGREL
Cure Study
Aleatorizado, prospectivo, doble ciego, que incluy a 12,562
pacientes que recibieron ASA 75-325 mg y fueron asignados a
clopidogrel (300 mg de carga seguido de 75 mg diarios) o
placebo por tres meses a un ao.
El punto final combinado primario fue la incidencia de muerte
cardiovascular, IAM o ACV. El 75% de los pacientes tena AI.
Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation.
Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK; Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial
Investigators. N Engl J Med. 2001 Aug 16;345(7):494-502.
TRATAMIENTO ANTIAGREGANTE
CLOPIDOGREL
Cure Study
El primer evento primario muerte de causa cardiovascular, IM no
fatal, ecva - occurri en 9.3 % de los pacientes del grupo con
copidogrel y en 11.4 % de los pacientes en el grupo placebo (RR
con clopidogrel comparado con placebo, 0.80; 95 % IC, 0.72 to
0.90; P<0.001).
El segundo evento primario - primer evento primario o isquemia
refractaria occuri en 16.5 % de los pacientes del grupo con
copidogrel y en 18,8 % de los pacientes en el grupo placebo (RR
0.86; 95 % IC, 0.79 to 0.94; P<0.001).
CLOPIDOGREL
Cure Study
Los porcentajes de pacientes con isquemia refractaria o grave en
el hospital , insuficiencia cardaca, y los procedimientos de
revascularizacin tambin fueron significativamente menores con
clopidogrel.
Hubo un nmero significativamente mayor de pacientes con
hemorragia mayor en el grupo de clopidogrel que en el grupo
placebo ( 3,7 % frente al 2,7 %; RR, 1,38 ; P = 0,001 ) , pero no hubo
significativamente muchos pacientes con episodios de
hemorragia potencialmente mortal ( un 2,2 %[ corregido ] frente a
1,8 %, p = 0,13 ) o ecv hemorrgicos ( 0,1 % frente a 0,1 %) .
CLOPIDOGREL
Cure Study
CONCLUSIONES :
El agente antiplaquetario clopidogrel tiene efectos
beneficiosos en pacientes con sndromes coronarios
agudos sin elevacin del segmento ST .
Sin embargo , el riesgo de hemorragia grave se incrementa
en los pacientes tratados con clopidogrel.
CLOPIDOGREL
CURRENT-OASIS Study
Estudio doble ciego, randomizado, factorial 2 X 2, que incluy
25,087 pacientes con SCA (71% AI/IAM no Q y 29% IAM con SST)
a quienes se deba realizar PCI con stent dentro de las 72 horas
de la randomizacin.
Clopidogrel 600mg & 150mg vs. 300mg & 75mg
Aspirina 300mg & 75-100mg vs. 300mg & 300-325mg
Punto final primario: Muerte CV, IAM y ACV
Punto de seguridad: Hemorragia mayor al mes.
CLOPIDOGREL
CURRENT-OASIS Study
Resultado:
No se evidenci beneficio en punto final primario con
mayores dosis.
Se observ beneficio en grupo que finalmente fue
angioplastiado y tendencia a perjuicio en el grupo tratado
medicamente.
Menor tasas de hemorragias en el grupo de dosis estndar.
CLOPIDOGREL
FARMACOCINETICA
Inhibidor de la GP IIb/IIIa
Platelet glycoprotein IIb/IIIa inhibition in acute coronary syndromes.
Gradient of benefit related to the revascularization strategy
Meta-anlisis de ensayos clnicos aleatorizados de la terapia con
inhibidores de la glucoprotena plaquetaria IIb / IIIa en el tratamiento
mdico de sndromes coronarios agudos sin elevacin del ST.
Entre 29570 pacientes, el bloqueo de la integrina IIb / IIIa se asoci
con una reduccin de muerte o infarto de miocardio no fatal a los 30
das, desde el 11,5% hasta el 10,7% (OR 0,91, P = 0,02).
Platelet glycoprotein IIb/IIIa inhibition in acute coronary syndromes. Gradient of benefit related to the revascularization strategy. Roffi
M1, Chew DP, Mukherjee D, Bhatt DL, White JA, Moliterno DJ, Heeschen C, Hamm CW, Robbins MA, Kleiman NS, Throux P, White
HD, Topol EJ. Eur Heart J. 2002 Sep;23(18):1441-8.
Platelet glycoprotein IIb/IIIa inhibition in acute coronary syndromes.
Gradient of benefit related to the revascularization strategy
Los pacientes sometidos a intervencin coronaria percutnea durante la
hospitalizacin se mantuvo una mayor reduccin de los eventos isqumicos
(odds ratio 0,82; p = 0,01) que los pacientes tratados mdicamente (odds ratio
0,95, P = 0,27).
Entre los pacientes sometidos a intervencin, el beneficio fue ms pronunciado
si el procedimiento se llev a cabo durante la infusin de inhibidor de
glicoprotena IIb / IIIa (odds ratio 0,74; P = 0,02), que si la revascularizacin se
realiz despus de la interrupcin del tratamiento (odds ratio 0,87, P = 0,17).
Platelet glycoprotein IIb/IIIa inhibition in acute coronary syndromes. Gradient of
benefit related to the revascularization strategy
CONCLUSIN:
Este anlisis, que incluye toda la experiencia de ensayos a gran escala de los
inhibidores de la glucoprotena IIb / IIIa por va intravenosa en pacientes con
sndromes coronarios agudos principalmente tratados mdicamente,
demuestra una por demas significativa, aunque moderada, reduccin de 30
das de muerte o infarto de miocardio asociado con la terapia.
Aunque no se basa en una hiptesis definido prospectivamente, los hallazgos
sugieren un gradiente de beneficio obtenido por estos agentes en funcin de
la estrategia de revascularizacin utilizado.
ANTICOAGULACIN
Inhibidores indirectos de la coagulacin
1. Inhibidores indirectos de la trombina: HNF; heparinas de bajo
peso molecular (HBPM).
2. Inhibidores indirectos del factor Xa: HBPM; fondaparinux.
. Inhibidores directos de la coagulacin.
1. Inhibidores directos del factor Xa: apixabn, rivaroxabn.
2. Inhibidores directos de la trombina: Bivalirudina, dabigatrn.
ANTICOAGULACIN
HNF VS ENOXAPARINA
Meta anlisis de 5 estudios (ESSENCE, TIMI 11-B, FRAXIS, FRIC,
GURFINKEL). Incluy 12,169 pacientes y compar la HNF vs HBPM.
Reduccin de un 17% del evento combinado IAM/muerte a 6 y 14 das a favor
de las heparinas de bajo peso molecular (3,9% vs 5,06%).
El mayor peso de la evidencia estuvo determinado por los estudios
ESSENCE y TIMI 11-B, en los cuales se emple la enoxaparina como droga
de comparacin.
No hubo diferencias en la tasa de hemorragia mayor. En cambio hubo un
exceso de hemorragias menores para las HBPM (10% vs 4,3%).
ANTICOAGULACIN
HNF VS ENOXAPARINA
Efficacy and safety of enoxaparin versus unfractionated heparin during
percutaneous coronary intervention: systematic review and meta-analysis
23 ensayos que representan a 30,966 pacientes, incluyendo 10.243
pacientes (33,1%) sometidos a ICP primaria para el IM con elevacin del
ST, 8750 (28,2%) sometidos a intervencin coronaria percutnea
secundaria despus de la fibrinlisis, y 11.973 (38,7%) con sndrome
coronario agudo sin elevacin del ST o pacientes estables programados
para una intervencin coronaria percutnea.
Un total de 13.943 pacientes (45,0%) recibieron enoxaparina y 17.023
(55,0%) de heparina no fraccionada.
Efficacy and safety of enoxaparin versus unfractionated heparin during percutaneous coronary intervention: systematic review and
meta-analysis. Silvain J1, Beygui F, Barthlmy O, Pollack C Jr, Cohen M, Zeymer U, Huber K, Goldstein P, Cayla G, Collet JP, Vicaut
E, Montalescot G. BMJ. 2012 Feb 3;344:e553. doi: 10.1136/bmj.e553.
ANTICOAGULACIN
HNF VS ENOXAPARINA
Efficacy and safety of enoxaparin versus unfractionated
heparin during percutaneous coronary intervention:
systematic review and meta-analysis
La enoxaparina se asoci con reducciones significativas en
muerte (RR: 0,66; IC del 95%: 0,57 a 0,76; p <0,001),
combinacin de muerte o infarto de miocardio (0,68, 0,57 a la
0,81; p <0,001), y las complicaciones del infarto de miocardio
(0,75, 0,6 a la 0,85; p <0,001), y una reduccin en la incidencia
de hemorragia mayor (0,80, 0,68 a la 0,95; p = 0,009).
ANTICOAGULACIN
HNF VS ENOXAPARINA
Efficacy and safety of enoxaparin versus unfractionated
heparin during percutaneous coronary intervention:
systematic review and meta-analysis
En pacientes en quienes se practico ICP primaria, la
reduccin en muerte (0.52, 0.42 to 0.64; P<0.001) es
particularmente significativa y asociada con reduccion de
sangrado mayor (0.72, 0.56 to 0.93; P=0.01).
ANTICOAGULACIN
HNF VS ENOXAPARINA
Efficacy and safety of enoxaparin versus unfractionated heparin
during percutaneous coronary intervention: systematic review
and meta-analysis
CONCLUSIN:
La enoxaparina parece ser superior a la heparina no fraccionada
en la reduccin de la mortalidad y los resultados de hemorragia
durante la intervencin coronaria percutnea y en particular en
los pacientes sometidos a intervencin coronaria percutnea
primaria para infarto de miocardio con elevacin del ST.
ANTICOAGULACIN
FONDAPARINUX
Comparison of Fondaparinux and Enoxaparin in Acute Coronary
Syndromes The Fifth Organization to Assess Strategies in Acute Ischemic
Syndromes Investigators*
Multicntrico, aleatorizado, doble ciego, de no inferioridad entre
fondaparinux y enoxaparina.
Incluy 28,078 pacientes con AI o IAM no Q dentro de las 24 horas de
comenzado los sntomas y que cumplieran con dos de tres criterios:
1. Al menos 60 aos de edad.
2. Elevacin de troponina y/o CK.
3. Cambios ECG compatibles con isquemia miocrdica.
.Punto
final primario
combinado
deSyndromes
muerte,TheIAM
o anginatorefractaria.
Comparison
of Fondaparinux
and Enoxaparin
in Acute Coronary
Fifth Organization
Assess Strategies in Acute
Ischemic Syndromes Investigators* (Salim Yusuf, D.Phil., M.B., B.S., Shamir R. Mehta, M.D., Susan Chrolavicius, B.A., Rizwan Afzal,
M.Sc., Janice Pogue, M.Sc., Christopher B. Granger, M.D., Andrzej Budaj, Ph.D., Ron J.G. Peters, M.D., Jean-Pierre Bassand, M.D.,
Lars Wallentin, Ph.D., Campbell Joyner, M.D., and Keith A.A. Fox, F.R.C.P N Engl J Med 2006;354:1464-76
ANTICOAGULACIN
FONDAPARINUX
Comparison of Fondaparinux and Enoxaparin in Acute Coronary
Syndromes The Fifth Organization to Assess Strategies in Acute
Ischemic Syndromes Investigators
No inferioridad del fondaparinux frente a la enoxaparina

(5,8% vs 5,7%).
La mortalidad total se redujo con fondaparinux
La incidencia de hemorragia mayor se redujo con
fondaparinux (2,2% vs 4,1%)
Mayor tasa de trombosis durante la ICP vs la enoxaparina.
Comparison of Fondaparinux and Enoxaparin in Acute Coronary Syndromes The Fifth Organization to Assess Strategies in Acute
Ischemic Syndromes Investigators* (Salim Yusuf, D.Phil., M.B., B.S., Shamir R. Mehta, M.D., Susan Chrolavicius, B.A., Rizwan Afzal,
M.Sc., Janice Pogue, M.Sc., Christopher B. Granger, M.D., Andrzej Budaj, Ph.D., Ron J.G. Peters, M.D., Jean-Pierre Bassand, M.D.,
Lars Wallentin, Ph.D., Campbell Joyner, M.D., and Keith A.A. Fox, F.R.C.P N Engl J Med 2006;354:1464-76
FUNCION ENDOTELIAL
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with statins after acute coronary syndromes.
RESULTADOS
La mediana del nivel de LDL-cholesterol alcanzada durante el
tratamiento era 95 mg por decilitro en el grupo pravastatina a dosis
standard y 62 mg por decilitro en el grupo de altas dosis de
atorvastatina (P<0.001).
KaplanMeier refleja una tasa del evento primario a los dos aos en
26.3 % en el grupo de pravastatina y 22.4 % en el grupo de
atorvastatina, lo que representa un 16 % de reduccion en el hazard
ratio en favor de la atorvastatina (P=0.005; 95 % IC, 5 a 26 %).
El studio no mostro criterio preespecificado para la equivalencia pero
identifico la superioridad del regimen intensivo.
Intensive versus moderate lipid lowering with statins after acute coronary syndromes. Cannon CP 1,Braunwald
E,McCabe CH,Rader DJ,Rouleau JL,Belder R,Joyal SV,Hill KA,Pfeffer MA,Skene AM;Pravastatin or
Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. N Engl J
KaplanMeier
of the Levels
Incidence
ofthe
the
Primary
Median Low-Density
LipoproteinEstimates
(LDL) Cholesterol
during
Study.
End Point of Death
from Any Cause or a Major Cardiovascular Event.
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with statins after

acute coronary syndromes.
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with statins after acute
coronary syndromes.
CONCLUSIONES
Entre los pacientes quienes han tenido un SCA reciente, un
regimen intensive hipolipemiante con estatina prove una
proteccion mayor contra eventos CV mayors y muerte que con
un regimen estandar
Estos hallazgos indicant que tales pacientes se benefician de
una disminucion temprana y continua del LDL cholesterol a
niveles muy por debajo de los meta actuals.
ALDOSTERONA
IECA
ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate,
and intravenous magnesium sulphate in 58,050 patients with suspected acute
myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival)
Collaborative Group.
58,050 pacientes ingresados en 1086 hospitales hasta 24 h (promedio 8 h)
despues de haber presentado clinica sospechosa de IM si CI para los
tratamientos del estudio (sin shock cardiogenico o hypotension severa y
persistente).
Fueron aleatorizados en un studio factorial "2 x 2 x 2 factorial". Los tratamientos
comparados fueron: (i) Captopril DI 6,25 mg titulada hasta 50 mg VO BID por un
mes versus placebo; (ii) Mononitrato de liberacion prolongada DI 30 mg titulada
hasta 60 mg VO OD por un mes versus placebo; y (iii) Sulfato de Magnesio DI 8
mmol seguido de 72 mmol por 24 horas versus control.
ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050
patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group.
Lancet. 1995 Mar 18;345(8951):669-85.
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with statins after acute coronary syndromes
Se incluy a 4162 pacientes que haban sido hospitalizados por un sndrome coronario agudo dentro de los 10 das anteriores
y se comprar 40 mg de pravastatin a al da (tratamiento estndar) con 80 mg de atorvastatina al da (terapia intensiva) .
ANTIINFLAMATORIO VASCULAR PLEIOTROPICO ESTABILIZAN LA PLACA AUMENTA COLAGENO DISMINUYEN ESTATINAS
EN PACIENTES CON SCA
ANGIOGENESIS Y VASCULOGENESIS
NIVELES LDL DISMINUYEN Y AUMENTAN HDL
ANTIACTIVANTE PLAQUETARIO CD 40
IM-PRUBET
TNT
EPHESUS
RECIFE
FLORIDA SCACEST
PACT
MIRACLE SCASEST
TIMI 22
IDEAL
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with statins
after acute coronary syndromes
La mediana del nivel de colesterol LDL alcanzado durante el
tratamiento fue 95 mg/dL (2,46 mmol/L) en el grupo de
pravastatina y 62 mg/dL(1,60 mmol/L) en el grupo de alta dosis
de atorvastatina (P <0,001).
reduccin del 16 %en el HR en favor de la atorvastatina (p =
0,005; 95 % IC, de 5 a 26%).
El estudio no cumple el criterio predefinido para la equivalencia,
pero s identific la superioridad del rgimen ms intensivo.
FUNCION ENDOTELIAL
ATORVASTATINA
Intensive versus moderate lipid lowering with
statins after acute coronary syndromes
CONCLUSIONES:
Entre los pacientes que han sufrido recientemente un sndrome
coronario agudo, un rgimen de estatina hipolipemiante intensivo
ofrece una mayor proteccin contra la muerte o eventos
cardiovasculares mayores que hace un rgimen estndar.
Estos hallazgos indican que tales pacientes se benefician de la
temprana y continua disminucin del colesterol LDL a niveles muy
inferiores a los niveles mximos actuales.
ALDOSTERONA
IECA
ISIS-4: a randomised factorial trial assessing early oral captopril, oral
mononitrate, and intravenous magnesium sulphate in 58,050 patients with
suspected acute myocardial infarction. ISIS-4 (Fourth International Study of
Infarct Survival) Collaborative Group.
Captopril (vs placebo) tuvo pequea pero significante reduccion en la
mortalidad a las 5 semanas, mantenida por un ao
Pacientes de alto riesgo mas favorecidos
No hubo beneficio en la supervivencia con MNIS ni con MgSO 4 a las 5
semanas
MNIS fue bien tolerado
ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050
patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group.
Lancet. 1995 Mar 18;345(8951):669-85.
ALDOSTERONA
IECA
GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly

and together on 6-week mortality and ventricular function after acute
myocardial infarction. Gruppo Italiano per lo Studio della
Sopravvivenza nell'infarto Miocardico.
Mortalidad a las 6 semanas era 6.5% entre los pacientes tratados
con nitratos y 6.9% entre los pacientes que no recibieron nitratos
(2p=0.28, OR 0.94, 95%CI: 0.84-1.05);
Con respecto al evento combinado (mortalidad y disfuncion
ventricular severa): nitratos 15.9% vs no nitratos 16.7% (2p=0.12,
OR 0.94, 95%CI: 0.87-1.02)
7;343(8906):1115-22.
ALDOSTERONA
IECA
GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate
singly and together on 6-week mortality and ventricular function
after acute myocardial infarction. Gruppo Italiano per lo Studio
della Sopravvivenza nell'infarto Miocardico.
Lisinopril antes de las 24h del IM: Reduce

significativamente la mortalidad a las 6 semanas en un
11%; No hubo beneficio de supervivencia del uso de NTG.
7;343(8906):1115-22.
Problem
Suspected acute MI
Format
Double-blinded multi-center RCT
Treatment
Oral ISMN (MR) OR oral captopril OR IV magnesium
Control
Standard therapy
Population
58050
PAPER: ISIS-4: a randomised factorial trial assessing early oral captopril,

oral mononitrate, and intravenous magnesium sulphate in 58,050
patients with suspected acute myocardial infarction.
Within 24 h of the onset of symptoms of suspected acute MI
No clear indications for, or contraindications to, any one of the study treatments
Inclusion criteria
Exclusion criteria
Follow-up
Primary endpoint
Date
18 Mar 1995
Journal
Lancet. 1995 Mar 18;345(8951):669-85.
The only exception was that patients who were to be given non-study nitrate for just a few days could still be entered.
(Such use of non-study nitrates was recorded at randomisation to allow separate analysis of the effects of the 1-month
study nitrate regimen among patients who were not, at the time of randomisation, being given non-study nitrates.)
Captopril (vs placebo)

-Small but significant reduction in 5 week mortality,
maintained
for 1 year
Specified not by the protocol but by the responsible
physician
Information
Suggested that caution
should be taken with hypotension, cardiogenic shock, poor peripheral perfusion, or cases
-Greatest
advantage in high risk patients
whether the chance of death was either very low
or very high.
No survival benefit for ISMN or magnesium at 5 weeks
5 weeks
ISMN well tolerated
5-week mortality
Secondary endpoint(s) Details
Brief summary:
Captopril shows benefit post-MI within 5 weeks, no nitrate/magnesium benefit
The immediate therapeutic objectives in treating P.H. are to

minimize the amount of myocardial necrosis that develops,
to alleviate his symptoms, and to prevent his death. These
objectives are achieved primarily by restoring coronary
blood flow (administering a thrombolytic and/or performing a
PCI) and lowering myocardial oxygen demand. Any lifethreatening ventricular arrhythmias that develop must be
treated. The long-term therapeutic objectives are to prevent
or minimize recurrent ischemic symptoms, reinfarction, heart
failure, and sudden cardiac death. The specific therapeutic
regimens are discussed in the questions that follow.
trials have shown unequivocally that if used appropriately, thrombolytics

can reduce the mortality associated with an AMI
Alteplase 15 mg bolus followed by a 50 mg infusion over 30 minutes and
then the remaining 35 mg over 60 minutes.
The Global Utilization of Streptokinase and t-PA for Occluded Arteries
(GUSTO) trial used this accelerated or front-loaded regimen for
administration of t-PA. In this trial, t-PA was compared to streptokinase and
a combination of streptokinase and t-PA. The results showed that t-PA alone
was the most effective in reducing mortality. The 30-day mortality rate for the
accelerated t-PA group was 6.3% compared to 7.3% in the streptokinase
group. In GUSTO, the t-PA regimen was also weight adjusted, such that after
the 15 mg bolus dose, the infusion was 0.75 mg/kg over 30 minutes followed
by 0.5 mg/kg over 60 minutes. The maximum dose received was 100 mg.
Reteplase was compared to t-PA in the GUSTO-III trial. Reteplase

has a slower clearance from the body, allowing the drug to be
given as a bolus without the need for a constant infusion. In the
GUSTO-III trial, reteplase was administered in two bolus doses of
10 MU, given 30 minutes apart. The mortality rate and incidence of
stroke were the same in the two groups of patients.
TNK was compared to t-PA in the Second Assessment of Safety
and Efficacy of a New Thrombolytic (ASSENT-2) trial. TNK was
administered as a bolus of 30 to 50 mg over 5 to 10 seconds,
based on body weight (Table 17-3). No difference existed between
TNK and t-PA in 30-day mortality and stroke.
The Second International Study of Infarct Survival (ISIS-2)

trial showed that aspirin 160 mg/day alone and in
combination with streptokinase reduced mortality in
patients with AMI by 23% and 42%, respectively, when
compared to a control group of patients who received
neither aspirin nor streptokinase. In doses of 160 mg or
more, aspirin generates a prompt clinical antithrombotic
effect as a result of its inhibition of thromboxane A2
production.
The use of UFH as adjunct therapy to prevent reocclusion

has been evaluated in many studies
The 2004 ACC/AHA guidelines recommend a 60 U/kg bolus
of UFH at the initiation of t-PA, followed by a maintenance
infusion of 12 U/kg/hour or a maximum of a 4,000 U bolus,
followed by 1,000 U/hour. The target activated partial
thromboplastin time should be 1.5 to 2.0 control
(generally 5075 seconds). UFH should always be
considered in patients at high risk for systemic or venous
embolism.
Similar results were seen in the Adjunctive Reperfusion Therapy (PCI-CLARITY) study in which STEMI
patients scheduled for PCI received pretreatment with either placebo or clopidogrel (300600 mg load,
then 75 mg daily) up to and including the day of angiography.30 Those receiving clopidogrel had a 38%
reduction in the MI or stroke prior to PCI (p = 0.028), as well as a 46% reduction in the incidence of
cardiovascular death, MI, or stroke 30 days following the procedure (p = 0.008). No difference in the
rate of major bleeding was seen between groups.
Finally, the Clopidogrel and Metoprolol in Myocardial Infarction Trial (COMMIT) evaluated the effect of
administrating either clopidogrel 75 mg daily with no loading dose or placebo in 45,852 patients
presenting with STEMI.31 The initial clopidogrel dose was given within 24 hours of symptom onset and
continued until hospital discharge or up to 4 weeks in the hospital. Compared to placebo, the
allocation to clopidogrel was associated with a 9% reduction in death, reinfarction, or stroke (p =
0.002) and a 7% reduction in all-cause mortality (p = 0.03). No significant excess in bleeding was
noted in the treatment group or in those who received concomitant thrombolytic therapy or who were
younger than 70 years.
Based on the data from COMMIT, P.H. could safely receive clopidogrel 75 mg daily as an inpatient.
However, long-term clopidogrel use in patients with STEMI remains questionable, unless the patient
receives a stent. As discussed later in the chapter, most of the data with maintenance clopidogrel use
are documented in patients with acute coronary syndromes (NSTE-ACS) and PCI.
In the Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Study25 (ExTRACT-TIMI 25), 20,506 patients with STEMI scheduled for thrombolytic therapy
were randomized to receive either enoxaparin throughout the index hospitalization or
continuous infusion UFH for 48 hours.32 Enoxaparin was dosed according to age and
renal function. For patients younger than 75 years, enoxaparin was dosed as a fixed 30
mg bolus followed 15 minutes later by 1 mg/kg subcutaneously (SQ) twice daily. For
patients older than 75 years, the bolus was eliminated, and the dose reduced to 0.75
mg/kg SQ twice daily. If the creatinine clearance was <30 mL/minute, the dose was
modified to 1.0 mg/kg SQ daily. UFH was dosed according to weight (60 U/kg bolus,
followed by 12 U/kg/hour) and adjusted to achieve an aPTT 1.5 to 2.0 control. The
composite end point of death or nonfatal MI through 30 days occurred in 12.0% in the
UFH group and 9.9% in the enoxaparin group, representing a 17% risk reduction (p
<0.001). Although no difference was noted in mortality between the two groups,
treatment with enoxaparin did reduce the 30-day risk of nonfatal reoccurrence of AMI by
33% compared to UFH (p <0.001). However, major bleeding was higher in the enoxaparin
group compared to those receiving UFH (2.1% vs. 1.4%, respectively, p <0.001). 2,3
The Enoxaparin as Adjunctive Antithrombin Therapy for STElevation Myocardial Infarction (ENTIRE-TIMI 23) trial
evaluated the use of a thrombolytic in combination with a
GP IIb/IIIa inhibitor and either UFH or LMWH. In this trial,
483 AMI patients were randomized to full-dose TNK or halfdose TNK + abciximab. Each group was then randomized to
receive either UFH or enoxaparin. Patients receiving fulldose TNK plus enoxaparin exhibited lower 30-day
mortality/recurrent MI rates compared to those receiving
TNK + UFH. Rates of major bleeding were highest with the
TNK, abciximab, and enoxaparin combination.2,3
The Organization for the Assessment of Strategies for Ischemic Syndromes (OASIS) 6 was a
complex, randomized double-blind trial of 12,092 patients with STEMI designed to assess the
effect of early initiation of fondaparinux with primary PCI and medical therapy.34 The study
compared the effects of fondaparinux (2.5 mg/day for up to 8 days) with two different control
arms: stratum 1, in which placebo was used if UFH was not indicated; and stratum 2, in which
UFH was administered for up to 48 hours followed by placebo for up to 8 days. Each control
group included a mix of the different treatment strategies, with essentially all primary PCI
patients receiving UFH. Compared to the control group, those receiving fondaparinux had a
significant reduction in the composite of death or reinfarction at 30 days (11.2% vs. 9.7%,
respectively, p = 0.008). Significant reductions in this end point were also observed at 9 days
(7.4% for the fondaparinux group vs. 8.9% for the controls, p = 0.003), and at the end of the
study (13.4% vs. 14.8%, p = 0.008). Specifically, in stratum 1, fondaparinux reduced the
incidence of death or MI compared to the control group (11.2% vs. 14.0%, p <0.05), but in
stratum 2, demonstrated no difference in this end point when compared to UFH. Fondaparinux
did not appear to offer benefit in patients who were managed with primary PCI. Although the
rates of death, MI, and severe bleeds did not differ in these patients, there was a higher rate of
catheter thrombosis with fondaparinux.
Determination of Reperfusion
Performing coronary angiography following thrombolytic therapy will reveal whether the
infarcted artery is open, how vigorous the blood flow is, and the extent of residual stenosis.
There are several clinical indicators that correspond with reperfusion, one of which is the
resolution of chest pain. Some investigators have found the development of reperfusion
arrhythmias to be associated with infarct-related artery patency, but neither of these
clinical markers is very reliable.
Two other methods used to estimate reperfusion are the ECG and laboratory changes.
Because the extent of the reduction of ST segment elevation may be related to the extent of
patency, 12-lead ECGs should be obtained frequently. ECGs have the advantage of being
readily available and noninvasive.
Early peaking of total CK and the CK-MB isoenzyme levels may also differentiate patients
who have achieved reperfusion from those in whom thrombolytic therapy has failed. Lewis
et al. found an absolute rise in CK activity of 480 U/L or a relative rise of 34% within the first
hour following successful thrombolysis. CK-MB activity was found to have a relative rise of
27% during the first hour. In the absence of reperfusion, CK activity was only increased by
15 U/L or had a relative rise of 3% over the first 2.5-hour period. 2,3
The Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in

Myocardial Infarction 28 (CLARITY-TIMI 28) evaluated 3,497 patients (1875
years of age) with STEMI who received standard thrombolytic therapy,
aspirin, and UFH, and were scheduled for angiography within 2 days.
Patients received either clopidogrel (300 mg loading dose, followed by 75
mg daily) or placebo within 10 minutes of thrombolytic administration.
Clopidogrel was continued up to and including the day of angiography and
stopped. The primary end point was the composite of an occluded infarctrelated artery on predischarge angiography or death or an MI up to the start
of coronary angiography. Compared to placebo, patients in the clopidogrel
group demonstrated a 36% reduction in the primary end point (p <0.001). By
30 days, the clopidogrel treatment group had a 20% reduction in
cardiovascular death, recurrent MI, or recurrent ischemia (p = 0.03). No
difference in the rate of major bleeding was seen between groups.
In the SAVE (Survival and Ventricular Enlargement) trial,

captopril (up to 50 mg TID) had a statistically significant
beneficial effect on mortality when given to asymptomatic
patients with an EF <40% who were 3 to 16 days post MI.
This 4-year follow-up study also showed significant
decreases in morbidity from heart failure and recurrent AMI
in the captopril group. Data from the ISIS-4, GISSI-3,
Trandolapril cardiac evaluation (TRACE), Infarction Ramipril
Efficacy (AIRE), and Second Survival of Myocardial
Infarction Long-term Evaluation (SMILE) trials have also
shown a benefit with the use of ACE inhibitors post MI.
As with thrombolytics, -blockers offer significant benefits to the MI patient in both the acute infarct period and/or several
days later as initial oral therapy. Several large trials were designed to give early IV -blockers (up to 24 hours after
symptom onset), followed by oral therapy; other studies used oral therapy alone beginning days after the infarct. Early IV
administration appears to be most beneficial, with a reduction of mortality of around 25% in the first 2 days when the
results of these trials are pooled. However, late oral therapy alone, up to 21 days post-MI in the -Blocker in Heart Attack
Trial, was also associated with a substantial reduction in mortality (around 10%). 2,3
Propranolol, metoprolol, timolol, and atenolol have been studied extensively. All have been given by early IV
administration. Typically, metoprolol and atenolol are used in the acute setting due to their -1 selectivity, ease of dosing
and administration, and weight of evidence. Oral carvedilol, a nonselective - and -blocker, has been used in the periinfarction period, specifically in patients with left ventricular dysfunction. In the Carvedilol Post-Infarction Survival Control
in Left Ventricular Dysfunction (CAPRICORN) trial, carvedilol reduced all-cause and cardiovascular mortality as well as
recurrent nonfatal MI.2,3
In general, if a patient has transient cardiac decompensation (e.g., hypotension, bradycardia, or worsening symptoms
P.17p19
of heart failure) during the acute infarct period, early IV -blockers are withheld. The patient's condition is then observed
for a few days; if it stabilizes, oral therapy is initiated and titrated slowly. Data from COMMIT highlight the importance of
tailored -blockade therapy.45 In this study, 45,852 patients were randomized to receive placebo or metoprolol (up to 15 mg
IV, then 200 mg orally daily) within 24 hours of AMI. Although metoprolol use reduced reinfarction (p <0.001) and
ventricular fibrillation rates (p <0.001) compared to placebo, the drug was also associated with a significant increase in
episodes of cardiogenic shock (p <0.00001). In a subgroup analysis, patients with hemodynamic instability at
randomization appeared to bear the brunt of early cardiogenic shock associated with metoprolol.
If the patient cannot tolerate an ACE inhibitor due to cough,

an ARB may be an alternative. In the Optimal Therapy in
Myocardial Infarction with the Angiotensin II Antagonist
Losartan (OPTIMAAL) Trial and Valsartan in Acute
Myocardial Infarction Trial (VALIANT), losartan and
valsartan demonstrated similar reductions in all-cause
mortality compared to captopril, with a nonsignificant trend
in favor of captopril. Dual therapy of captopril with
valsartan offered no additional benefits but increased side
effects.2,3
Historically, the presence of diabetes was a relative

contraindication for -blockade due to the adverse effects
on insulin release and blunting of the hypoglycemiaassociated tachycardia. However, diabetics comprise a
large portion of AMI patients, and many -blocker trials
contained diabetic AMI patients. Gottlieb et al. found that
post-MI diabetic patients treated with -blockers
experience a 36% reduction in mortality.46
Furthermore, data from the Glycemic Effects in Diabetes Mellitus:

Carvedilol-Metoprolol Comparison in Hypertensives (GEMINI) trial
suggest that in hypertensive, diabetic patients receiving RAS blockade,
carvedilol does not affect glycemic control and may improve insulin
sensitivity compared to metoprolol. 47 Due to these positive data, blockers would have to possess major negative effects on the diabetic
condition to be considered contraindicated. Diabetic patients who are
given -blockers should receive nonintrinsic sympathomimetic activity,
cardioselective agents (e.g., metoprolol, atenolol) or a more
cardioselective - blocker (e.g., carvedilol). Patients should be
advised to monitor their blood glucose levels carefully for both hypoand hyperglycemia after the -blocker is initiated, making adjustments
to their insulin or oral hypoglycemic therapy as needed.
Like angiotensin II, aldosterone also plays an important role in left ventricular remodeling. (See Chapter 18 for further
discussion of aldosterone.) Inhibiting aldosterone directly in addition to ACE inhibitor therapy was first evaluated in
the heart failure patients in the Randomized Aldactone Evaluation Study (RALES). 64 Patients who received
spironolactone exhibited a 30% reduction in mortality compared to placebo (p <0.001). Another aldosterone
antagonist, eplerenone, is a selective inhibitor of the mineralocorticoid receptor with fewer sexual side effects.
In the Eplerenone Post Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), 6,600
patients with AMI and an EF <40% were allocated to optimal medical therapy with either eplerenone or placebo. After
16 months, a 15% risk reduction in mortality (p = 0.008), 13% reduction in sudden death (p = 0.002), and 21% reduction
in cardiovascular death or hospitalization (p = 0.02) was seen in the eplerenone group compared to placebo. 64
Based on these data, the 2004 ACC/AHA guidelines recommend an aldosterone antagonist in STEMI patients without
significant renal dysfunction (creatinine <2.5 mg/dL in men and <2.0 mg/dL in women) or hyperkalemia (potassium <5
mEq/L) who are already receiving therapeutic doses of an ACE inhibitor, have an EF <40%, and have either
symptomatic heart failure or diabetes.2,3
P.17p24
Because our patient does not have heart failure or diabetes, he is not a candidate for aldosterone antagonism.
However, if his EF was <40%, either spironolactone or eplerenone would be an option. Serum potassium and renal
function would need to be carefully checked 3 days and at 1 week after therapy initiation and every month for the first
3 months. ACE inhibitor and potassium supplement doses may need to be adjusted. 64
The Myocardial Ischemia Reduction with Aggressive Cholesterol

Lowering (MIRACL) trial, which enrolled NSTEMI patients,
reported a 16% lower rate of death and nonfatal major cardiac
events at 4 months follow-up in patients receiving atorvastatin 80
mg/day within 24 to 96 hours of hospitalization when compared
with placebo (p = 0.048). The A to Z trial, showed a favorable
trend toward major cardiovascular event reduction during 624
months follow-up in AMI patients receiving an intensive
simvastatin regimen (40 mg/day for 1 month followed by 80
mg/day thereafter) initiated within 12 hours of stabilization when
compared with those receiving a less intensive regimen (placebo
for 4 months followed by simvastatin 20 mg/day).

Scasest

Caricato da

Informazioni sul documento

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Scasest

Caricato da

Copyright:

Formati disponibili

REPUBLICA BOLIVARIANA DE VENEZUELA

MINISTERIO DEL PODER POPULAR PARA LA SALUD

MEDIDAS GENERALES DE APOYO

MEDIDAS GENERALES DE APOYO

GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly

Lisinopril antes de las 24h del IM: Reduce

El pronstico a largo plazo para los pacientes con angina variante

No inferioridad del fondaparinux frente a la enoxaparina

Intensive versus moderate lipid lowering with statins after

GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly

Lisinopril antes de las 24h del IM: Reduce

Double-blinded multi-center RCT

Oral ISMN (MR) OR oral captopril OR IV magnesium

PAPER: ISIS-4: a randomised factorial trial assessing early oral captopril,

Lancet. 1995 Mar 18;345(8951):669-85.

Captopril (vs placebo)

Secondary endpoint(s) Details

Captopril shows benefit post-MI within 5 weeks, no nitrate/magnesium benefit

The immediate therapeutic objectives in treating P.H. are to

trials have shown unequivocally that if used appropriately, thrombolytics

Reteplase was compared to t-PA in the GUSTO-III trial. Reteplase

The Second International Study of Infarct Survival (ISIS-2)

The use of UFH as adjunct therapy to prevent reocclusion

The Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in

In the SAVE (Survival and Ventricular Enlargement) trial,

If the patient cannot tolerate an ACE inhibitor due to cough,

Historically, the presence of diabetes was a relative

Furthermore, data from the Glycemic Effects in Diabetes Mellitus:

The Myocardial Ischemia Reduction with Aggressive Cholesterol

Potrebbero piacerti anche