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The
Management
of
AcuteMyocardial
InfarctionEarly
RepolarizationBrugada
SyndromePrinzmetal
AnginaPericarditisST
Segment
Elevation
(Transmural
ischemia)Anterior
AMI
Acute
Inf.
AMINon-infarct
ST
ElevationST
Segment
Depression
(Non-transmural
ischemia)ST
DepressionNSTEMIT
wave
inversionNSTEMINSTE
ACS
:
Key
ThemesNSTE
ACS:
a
high
risk
population
patient
risk benefit
from
treatmentwith
medications,
an
invasive
strategy
Interaction
between
invasive
strategy
andpharmacologic
txAntithrombotics
cornerstone
of
treatment
Anticoagulants:
heparin,
LMWH,
directthrombin
inhibitors
Antiplatelet
agents:
aspirin,
IIb/IIIa,
ADPinhibitorsAntman
EM
et
al
N
Engl
J
Med
1996;335:1342-9Invasive
vs.
Conservative
Strategy
for
ACSDeath
or
(re)-MITrialN
PCIConsRITA
31810
7.68.3VINO131
6.322.4TACTICS2220
7.39.5TRUCS148
7.616.7FRISC
II2451
10.414.1MATE201
9.96.7VANQUISH920
24.012.2Overall7876RR=
0.88,
p=0.05Intervention
better0.1
0.2
0.3
0.5
0.7
1.0
1.5
2.0Fox,
Lancet
360:743
‘03Death/(re)-MIDeath/(re)InfarctionCP971744-45%ConsInvTnT
cut
point
=
0.01
ng/mL(54%
of
pt
TnT
+)TACTICS–TIMI
18Troponin
T:
Death,
MI,
Rehosp
ACS,
6
MonthsOR=0.52*P<0.001InteractionP<0.001P=NS*n=414n=396n=463n=495Benefits
of
an
Invasive
Strategy
inNon-ST
Elevation
ACSOnly
shown
to
reduce
death
and
MI
in highrisk
ptsReduces
re-hospitalization,
angina
in many
othersShortens
hospitalization,
may
be
cost effectiveWhat
about
the
optimal
timing
of
an invasive
strategy?Medical
Tx
for
72-170
hrThen,
cath
labn=207Cath
lab
6
hrn=203ISAR-COOLCP1107655-467%
had troponin,65%
had
ST
depressionNeumann
FJ
et
al
JAMA
2004500
mg,
100
mg
bid600
mg,
75
mg
bid10
mg/kg
bolus,
0.10AspirinClopidogrelTirofibanmg/kg/min
infusionHeparin(PTT
60-85
seconds)Non-ST
Acute
Coronary
Syndrometroponin
or
ST
depressionn=410ISAR-COOLPrimary
EndpointCP1107655-230-dayevent
rate(%)Death
&
MIDeathNeumann
FJ
et
al
JAMA
2004Any
nonfatalMINonfatal
Q-wave
MIRR
1.96
(1.01-3.82)P=0.04
P=0.23Cooling
off
(n=207)Early
intervention(n=203)P=0.12
P=0.56Timing
of
an
Invasive
Strategy
inNon-ST
Elevation
ACSISAR-REACT
was
a
small,
singlecenter
study.Clinical
trials
are
still
gon.Other
analyses
also
indicate
that
cath within
24
hours
is
better
than
later
cathOught
to
use
intensive
antiplatelet therapy
with
a
veryearly
invasive
stratWhat
medical
therapy
ought
to
beused
in
ACS?Antithrombotic
Trialists’
Collaboration.
BMJ.
2002;324:71–86.Aspirin
DoseOR*No.
of
Trials
(%)Odds
RatioAspirin
Dose
and
Events
in
High-Risk
PtsFrequency
of
CV
Death,
MI,
Stroke500–1500mg3419160–325mg192675–150mg1232P=0.0001<750
0.5
1.01.5
2.0mg3Antiplatelet
B13
erettAntiplateletAnyWorseaspirin6523CURECP999547-2Non-ST
elevation
ACS12,562
patientsASA
75
to
325
mg
po
qdplacebon=6,3033-12
month
follow-up(average
9
mo)Yusuf
S
et
al
NEJM
2001;16:494-502ASA
+
clopidogrel(300
mg
load,
75
mg
qd)n=6,259CURECV
Death/MI/Stroke,
1
YearCP999731-3Placebo
(n=6,259)Clopidogrel
(n=6,303)ath,
MI,
stroke
(%)P=0.00003Days
after
enrollmentCUREEventrate(%)RR
0.80P=0.00005CP995058-6Aspirin
andPlacebo
(n=6,303)Clopidogrel
(n=6,259)CV
death,
CVMI,
stroke
deathMIStrokeNon-CVdeathRR
0.92P=NSRR
0.77P<0.001RR
0.85P=NSRR
0.96P=NSCUREMajor/Life-Threatening
Bleeds
in
the
7
Days
After
CABGPlaceboClopRRpN
=
476N
=
436Stopped
<
5
daysprior
to
CABG:Pts
with
Major
orLife
ThreateningBleeding6.3%
9.6%
1.53
0.06Major
Bleeds:
Significantly
disabling,
intraocular,or
transfusion 2
unitsLife
Threatening:
Hgb
>5g/dl,
hypotension(inotropes),
surgery
to
stop
bleeding,symptomatic
ICH
or
transfusion 4
unitsACC/AHA
ACS
Guideline
UpdateClass
I
Aspirin
75
to
325
mg/day
(level
ofevidence:
A)
ASA
and
clopidogrel
for
9
months
afterNSTE
ACS
(level
of
evidence:
B)Class
3
Do
not
administer
clopidogrel
in
the
5days
before
CABGBraunwald
E,
et
al.
Heparin
(UF
or
LMW)
in
ACS
Without
STDeath
or
MIUFH
or
LMWHControlOR95%
CITheroux
2/122
(1.6%)4/121
(3.3%)0.500.10-2.53Cohen
0/371/32
(3.1%)0.120.01-5.89RISC
3/210
(1.4%)7/189
(3.7%)0.400.11-1.39Cohen
4/105
(3.8%)9/109
(8.2%)0.460.15-1.41Holdright*
42/154
(27.3%)40/131
(30.5%)0.850.51-1.43Gurfinkel(UFH)4/70
(5.7%)
7/73
(9.6%)0.580.17-1.98Gurfinkel(LMWH)0/68
7/73
(9.6%)0.130.03-0.60FRISC
4/70
(5.7%)36/757
(4.8%)0.390.22-0.68UFH
vs55/698
(7.9%)
68/655
(10.4%)0.670.45-0.99placebo/coLMWH
vsplacebontrol13/809
(1.6%)
43/830
(5.2%)
0.340.20-0.58Total68/1507
(4.5%)
104/1412
(7.4%)0.530.38-0.73Only
RCTs,
placebo
or
untreated
controlsEikelboom
JW
et
al:
Lancet
55:1936-42,
2000CP951342-10.1Heparin
better1.010.0Control
betterFRAXIS(nadroparin;
n=2357)ESSENCE(enoxaparin;
n=3171)TIMI
IIB(enoxaparin;
n=3910).751.5(P=0.032)(P=0.029)Braunwald
E
et
al.Circulation
2000;102:1193-1209LMWHBetter1.0UFHBetterLMWH
versus
UFH
in
UA/NSTEMI
ManagedNon-invasively:Effect
on
Death,
MI,
Recurrent
IschemiaTrial:FRIC(dalteparin;
n=1482)CLASS
Ia
(Ia级推荐)一旦出现UA/NSTEMI,需尽快在抗血小板治疗的基础上给予患者抗凝药物。介入方案:证据级别A-包括依诺肝素和普通肝素;证据级别B-包括比伐 卢定和戊聚糖钠保守方案:药物选择可以是依诺肝素、普通肝素(证据级别A)或者戊聚 糖钠(证据级别B),有效性已经确立。对于选择保守治疗的病人,如果有较高的出血风险,倾向于选择戊聚糖钠(证据级别B)CLASS
IIa
(IIa级推荐)对于最初选择保守治疗策略的UA/NSTEMI病人,作为抗凝治疗,依诺肝素或者戊聚糖钠要优于普通肝素,除非计划在24小时内进行冠脉搭桥手术。(证据级别B)2007年ACC/AHA
UA/NSTEMI的指南抗凝治疗推荐ACC/AHA
2007更新的抗凝治疗指南高危或确诊ACS实行导管或PCI疑似/确诊ACS可能ACS阿司匹林+IV
UFH/LMWH*GP
IIb/IIIa拮抗剂阿司匹林+皮下LMWH
*或IV
UFH阿司匹林氯吡格雷氯吡格雷*证据等级Ia:依诺肝素优于IV
UFHACC/AHA治疗建议2007“不稳定型心绞痛/非ST段抬高心梗患者,除非计划在24小时内行冠脉搭桥手术,相对于普通肝素,依诺肝素(Enoxaparin)作为抗凝剂应优先选用。(证据级别A)”2002
update
ACC/AHA
guidelineACCP7指南对LMWH的治疗建议n
急性期LMWH优于UFH(1B级);n
LMWH治疗时不需常规监测(1C级);n
已使用LMWH的患者如需进行PCI,应继续使用LMWH(2C级);n
应用GPIIb/IIIa受体拮抗剂者,
LMWH安全性优于UFH(2B级)。n
NSTE
ACS患者中LMWH的疗程评价是:NSTE
ACS患者应早期介入治疗,如果冠脉干预延迟,可考虑延长LMWH治疗作为血运重建的“桥梁”。Rest
pain
>
5
min
andST
Δ
>
0.1
mVorDocumented
CADorCK-MBN=132Heparin70
U/kg
bolus+15
U/kg/hr
infusionBivalirudin0.1
mg/kg
bolus+0.25
mg/kg
infusionTIMI
-
8:
Bivalirudin
vs.
Placebo
in
ACSTIMI
-
8:
Bivalirudin
vs.
Placebo
in
ACS4-6wks7days4-6wks7daysp=0.008p=0.024p=NSp=NSBeta
Blockers
Reduce
CV
death,
MI,
stroke
by
25-30%
in
high
risk
ptsNot
well
studied
in
non-STE
ACS
Reduce
heart
rate,
blood
pressure,ischemia,
chest
discomfortClass
1
indication;
quality
indicator
Use
in
everyone
withoutcontraindications5.617.915.714.23.812.911.710.312.811.805101520ry
Endpoint
%PlaceboGP
IIb/IIIaPURSUIT30
daysPRISM48
hrsPRISMPLUS7
daysP
=
0.04P
=
0.01P
=
0.004PARAGON
A30
daysP
=
0.48PARAGON
B30
daysP
=
0.33Platelet
GP
IIb/IIIa
Inhibition
for
Non-ST
ACSPrimary
Endpoint
Results
from
the
5
Major
RCTsIIb/IIIa
Inhibitors
in
ACS
PatientsGreatest
benefit
is
during
PCI
If
pursuing
a
non-invasive
strategy,recommend
treating
pts
with
elevatedtroponins,
high
TIMIscores,
etc;probably
those
with
diabetes,
markedST
segment
shifts
Do
not
recommend
their
routineadministration
to
all
ACS
pts
in
whoma
non-invasive
strategy
is
plannedConclusions
Much
remains
to
be
learned
about
theoptimal
medical
therapy
for
ACS
pts
The
data
favor
an
invasive
strategy,and
suggest
different
medications
anddoses
ought
be
administered
ifpursuing
an
invasive
vs.
non-invasivestrategy,
and
in
high
vs.
low
risk
ptsUA
/
NSTEMI:Pharmacological
and
Mechanical
InterventionBraunwald
E
et
al.
J
AmColl
Cardiol
2000;36:970-1062Braunwald
E
et
al.Circulation2002;106:1893-1900危险分层(TIMI危险评分)高危TIMI评分5-7低危TIMI评分0-2中危TIMI评分3-4ASA+LMWH(普通肝素)+氯吡格雷依替巴肽/替罗非班ASA+LMWH
or普通肝素+氯吡格雷ASA+LMWH(普通肝素)+氯吡格雷依替巴肽/替罗非班Cath/PCI/CABG进行监测/危险评估缺血二级预防无缺血Algorithm
for
Patients
withUA/NSTEMI
Managed
byan
Initial
Invasive
StrategyProceed
to
Diagnostic
AngiographyASA
(Class
I,
LOE:
A)Clopidogrel
if
ASA
intolerant
(Class
I,
LOE:A)Diagnosis
of
UA/NSTEMI
is
Likely
orDefiniteInvasive
StrategyInitiate
A/C
Rx
(Class
I,
LOE:
A)Acceptable
options:
enoxaparin
or
UFH
(Class
I,
LOE:
A)bivalirudin
or
fondaparinux
(Class
I,
LOE:
B)Select
Management
StrategyProceed
with
anInitialConservativeStrategyAnderson
JL.
J
Am
Coll
Cardiol.
2007,
In
press.
Figure
7ABB1B2Prior
to
AngiographyInitiate
at
least
one
(Class
I,
LOE:
A)
orboth
(Class
IIa,
LOE:
B)
of
the
following:ClopidogrelIV
GP
IIb/IIIa
inhibitorFactors
favoring
admin
of
both
clopidogreland
GP
IIb/IIIa
inhibitor
include:Delay
to
AngiographyHigh
Risk
FeaturesEarly
recurrent
ischemic
discomfortInitiate
clopidogrel
(Class
I,
LOE:
A)Consider
adding
IV
eptifibatide
or
tirofiban
(ClassIIb,
LOE:
B)Conservative
StrategyInitiate
A/C
Rx
(Class
I,
LOE:
A):Acceptable
options:
enoxaparin
or
UFH
(Class
I,LOE:
A)
or
fondaparinux
(Class
I,
LOE:
B),
butenoxaparin
or
fondaparinux
are
preferable
(Class
IIA,LOE:
B)Select
Management
StrategyASA
(Class
I,
LOE:
A)Clopidogrel
if
ASA
intolerant
(Class
I,
LOE:
A)Diagnosis
of
UA/NSTEMI
is
Likelyor
DefiniteAlgorithm
for
Patients
with
UA/NSTEMIManaged
by
an
Initial
Conservative
StrategyProceed
withInvasiveStrategy(Continued)Anderson
JL.
J
Am
Coll
Cardiol.
2007.
In
press.
Figure
8C2C1AEvidence
for
Primary
PCI
asTreatment
of
Choice
for
STEMI
ACSp=0.0003p<0.0001p=0.0004p<0.0001OR=0.57Keeley
&
Grines
Lancet
2003PCILyticRisk
ReductionDeath28%Death/MI/CVA43%Primary
PCI:The
Preferred
Reperfusion
StrategySummary
of
23
Randomized
Trials
(n=7739)Primary,
Transfer,
Facilitated
&
Rescue
PCIfor
STEMIn
Primary
PCI
(PPCI)Direct
to
CVL
for
PCI
reperfusion
therapyn
Transfer
PCIPts
transferred
from
hospitals
without
PCI
facilities(no
lysis)
to
a
PCI
centren
Facilitated
PCIPatients
receiving
thrombolysis*
followed
byintentional
PCIn
Rescue
PCIPCI
after
failed
thrombolysis
(at
90
mins)*Thrombolysis
may
be
Pre-hospitalDoor-To-Balloon
(DTB)
Time&
Choice
of
Reperfusion
Therapy
in
STEMIn
Sx
onset
<3
hr:Fibrinolysis
only
if
estimated
DTB
>
60
minn
Sx
onset
>3
hrs
<12hr:Primary
PCI
withDTB
of
90min;
otherwiseFibrinolysis
is
acceptable
alternativen
Sx
onset
>12hr:No
lysis
but
PCI
may
still
be
beneficialEvidence
for
Pre-Hospital
Thrombolysisfor
Early
(
<2
Hour)
STEMIEvidence
to
support
Transfe
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