心肌梗死指南课件

急性心肌梗死治疗指南北京大学第三医院心内科The

new

guidelines

accounted

for

the

variety

of

physicians

and

clinicians

involved

in

the

care

of

patients

with

acute

ischemic

heart

disease.

Advicewas

obtained

frommany

constituents

to

formulate

the

most

recent

guidelines.

The

key

players

include

the

American

Heart

Association,

AmericanCollege

of

Cardiology

under

the

guidance

of

the

Agency

of

Health

Research

Quality.

The

European

guidelines

were

issued

approximately

at

thesame

time

as

the

ACC/AHH

guidelines,

making

this

a

transatlantic

effort.

There

are

many

similarities

but

each

set

ofguidelines

recognizes

thedifferences

in

care

across

the

Atlantic.指南制定者The

weight

of

evidence

is

graded

on

three

levels

A,

B,

and

C,

with

anemphasis

on

randomized

clinical

trials.A-

the

data

is

obtained

frommany

large

randomized

clinical

trialsB-the

data

is

obtained

fromfewer,

smaller

randomized

clinical

trials

or

there

is

careful

analyses

ofnonrandomized

studies

including

observationalstudiesC-the

weakest

evidence

of

all

is

supplies

by

expert

consensus

or

opinionManystandard

medical

practices

carry

aweightof

“C”

and

were

never

exposed

to

arandomized

trial

(e.g.

supplying

oxygen).支持适应证建议的证据权重等级=证据来自多个随机临床试验。=证据来自单个随机试验或非随机研究。=专家的一致观点。The

weightof

effidence

is

applied

to

a

particular

area

and

aClassofRecommendations

is

formulated.

The

classes

range

from

I–

III,

and

Class

IIis

subdivided

into

a

and

b.Class

I-the

intervention

is

useful

and

effectiveClass

IIa-suggests

the

evidence

conflicts

or

there

is

a

difference

of

opinions

butleans

toward

efficacy

Class

IIb-suggests

the

evidence

conflicts

or

there

is

a

difference

of

opinions

butleans

against

efficacy

Class

III-suggests

the

intervention

is

notuseful/effective

and

may

be

harmfulMost

physicians

would

suggest

that:Class

I

and

IIa

should

be

practicedClass

IIb

should

be

given

careful

consideration

for

an

individual

patient.Class

III

should

not

be

practiced指南适应证建议分类I

IIaIIbIII指那些已证实有用、有益和有效的操作或治疗。指那些有关证据倾向于有用/有效。有关证据不能充分说明有用/有效。指那些已证实无效并且在有些病例可能是有害的操作或治疗。The

big

bang

for

the

buck

is

in

secondary

prevention

for

patients

previously

diagnosed

with

an

MI,

an

episode

of

angina,

orboth.Education

isa

keycomponent

in

the

emergency

room.

Acute

chest

pain

accounts

for

only10%of

all

emergency

roomvisits;

the

remaining

90%are

unrelated

to

ischemic

heart

disease.Prevention

is

another

key

component.

An

estimated

1.5

million

people

were

hospitalized

for

ischemic

heart

disease

in

1996

alone

and

close

to

aquarter

of

a

million

died

fromsudden

death

before

they

arrived

at

the

hospital.Ischemic

heart

disease

is

still

amajor

health

issue.

In

this

year

alone,

there

are

estimates

that

1

million

Americans

will

haveanew

or

repeatepisode

of

ischemic

heart

disease.指南内容√简介√入院前的任务√急诊诊断和治疗√住院治疗√药物治疗原理和方法√长期治疗The

big

bang

for

the

buck

is

in

secondary

prevention

for

patients

previously

diagnosed

with

an

MI,

an

episode

of

angina,

orboth.Education

isa

keycomponent

in

the

emergency

room.

Acute

chest

pain

accounts

for

only10%of

all

emergency

roomvisits;

the

remaining

90%are

unrelated

to

ischemic

heart

disease.Prevention

is

another

key

component.

An

estimated

1.5

million

people

were

hospitalized

for

ischemic

heart

disease

in

1996

alone

and

close

to

aquarter

of

a

million

died

fromsudden

death

before

they

arrived

at

the

hospital.Ischemic

heart

disease

is

still

amajor

health

issue.

In

this

year

alone,

there

are

estimates

that

1

million

Americans

will

haveanew

or

repeatepisode

of

ischemic

heart

disease.缺血性心脏病n

12,200,000

people

in

the

US

have

had

an

MI,angina

pectoris,

or

bothn

5,315,000

Americans

visited

EmergencyDepartments

for

chest

pain

in

1997n

1,433,000

Americans

hospitalized

for

IHD

in1996n

1,100,000

Americans

will

have

a

new

orrepeat

IHD

event

this

yearHospitalization

due

to

atherosclerotic

disease,

particularly

acute

coronary

syndromes,

accounts

for

well

over

one

million

admissions

to

U.S.hospitals

each

year.CoronaryAtherosclerosisAcute

MyocardialInfarction1,153,000Admissions829,000AdmissionsHospitalizations

Due

to

Atherosclerotic

DiseaseCerebrovascularDisease961,000AdmissionsVascular

Disease3.2

Million

Hospital

AdmissionsOther

IschemicHeart

Disease280,000Admissions不稳定心绞痛NQMIQ波MI心肌梗死急性冠脉综合征无ST段抬高

ST段抬高NSTEMI急性冠状动脉综合征概念Chronology

of

Atherosclerotic

VascularDisease

ProcessDevelopment

ofatherosclerosis

andvulnerableplaque

Acute

Coronary

Syndrome

Secondary

PreventionIschemic

Heart

DiseaseCerebrovascularDiseasePeripheral

VascularDisease急性冠状动脉综合征机制急性心肌梗死病理表现Unstable

plaques

are

characterized

by

a

large

lipid

core

and

thin

fibrous

cap.

Inflammatory

cells

and

activated

macrophages

are

believed

to

beinvolved

in

destabilizing

the

plaque

and

the

fibrous

cap.Characteristics

of

Unstable

and

Stable

PlaqueThinfibrous

capInflammatorycellsFewSMCsErodedendotheliumActivatedmacrophagesThickfibrous

capLack

ofinflammatorycellsFoam

cellsIntactendotheliumMore

SMCsUnstableStableIt

is

now

recognized

that

unstable

angina

(UA),

non-Q-wave

myocardial

infarction

(NQMI),

and

ST-segment

elevationmyocardial

infarction(STE-MI)

are

all

parts

of

the

spectrumof

clinical

manifestations

of

acute

coronary

syndrome

(ACS).

The

older

terminology

has

now

beenreplaced

with

terminology

that

divides

ACS

into

non-ST-elevation

ACS

(NSTE-ACS)

and

ST-segment-elevation.

All

the

slides

in

this

teachingset

deal

withNSTE-ACS.UANSTEMISTEMIPlaque

Disruption/Fissure/ErosionThrombus

FormationNon-ST-Segment

Elevation

AcuteCoronary

Syndrome

(ACS)ST-SegmentElevationAcuteCoronarySyndrome(ACS)急性冠状动脉综合征机制Platelets

are

recognized

to

play

an

integral

role

in

acute

coronary

syndromes

and

arterial

thrombosis.

After

plaque

fissure

or

rupture,

there

isplatelet

adhesion

and

activation.

This

leads

to

platelet

aggregation

within

the

coronary

artery,

and

ultimately

partial

orcomplete

occlusion

of

thecoronary

artery.The

integral

role

of

platelets斑块破裂血小板黏附血小板激活血小板聚集血栓阻塞There

are

multiple

mediators

which

can

result

in

platelet

activation,

including

ADP,

epinephrine,

collagen,

arachidonic

acid,

and

thrombin.

Aspirinblocks

activation

of

platelets

by

arachidonic

acid.

The

thienopyridines

(ticlopidine

and

clopidogrel)

block

ADP-mediated

plateletactivation.

Antithrombin

therapy

(heparin,

low-molecular-weight

heparin,

or

direct

thrombin

inhibitors)

block

thrombin-mediated

plateletactivation.

The

glycoprotein

IIb/IIIa

inhibitors

block

platelet

aggregation

by

inhibiting

fibrin

frombinding

to

the

GP

IIb/IIIa

receptorADPTiclopidineClopidogrelEpinephrineCollagenArachidonicAcidAspirinThrombinHeparinLMW

HeparinfibrinThePlateletIIb/IIIa

receptorsGP

IIb/IIIa

inhibitorsAlthough

there

are

a

variety

of

approaches

to

enhancing

anticoagulant

effects

none

are

completely

satisfactory

when

used

as

a

single

agent.Major

categories

of

anticoagulant

therapy

include

agents

that

target

any

one

of

three

maincomponents

of

the

thrombotic

process;

thrombin,platelets,

or

fibrin.Sites

ofAnti-thrombotic

Drug

ActionTissue

factorPlasma

clottingcascadeThrombinFibrinThrombusPlatelet

aggregationCollagenThromboxane

A2ADPATATAspirinTiclopidineClopidogrelConformationalactivation

of

GPIIb/IIIaGPIIb/IIIainhibitorsProthrombinFactorXaBivalirudinHirudinArgatrobanLMWHHeparinFibrinogenThrombo-lyticsCoagulationcascadePlateletcascadePatients

who

present

withST

segment

depressionhave

at

least

as

great

a

six-month

risk

of

mortalityas

those

who

present

withST-segment-elevationACS,

emphasizing

the

importance

of

aggressive

in-hospital

and

post-discharge

therapy.ACS患者6个月死亡率必须至少具备下列三条标准中的两条：√缺血性胸痛的临床病史；√心电图的动态演变；√血清心肌标记物浓度的动态改变。急性心肌梗死诊断心肌梗死新定义具备以下任一条可确定急性心梗的诊断：n

心肌坏死生化标记物的典型升高与回降（肌钙蛋白或CK－MB），同时合并至少下述一条：（a）：缺血症状（b）：ECG出现病理Q波（c）：ECG缺血表现（ST段升高或降低）（d）：冠脉介入操作（如PTCA）n

急性心肌梗死的病理学证据Use

of

Cardiac

Markers

in

ACSCardiac

troponin

after“classical”

AMICK-MB

after

AMICardiac

troponin

after“microinfarction”Days

After

Onset

of

AMIUpper

reference

limit01234567812Multiples

of

th5e

URL1020URL

=

99th

%tile

of

Reference

Control

Group50典型临床表现√持续胸痛>30

min√大汗淋漓√恶心呕吐√面色苍白心电图动态变化血清心肌标记物的测定主要包括CK、CK-MB、肌钙蛋白T/I和肌红蛋白，测定心肌标记物有助于AMI的确定诊断和评估梗死面积，但再灌注治疗不须等待测定的结果。AMI血清心肌标记物肌红蛋白TNTCKCK-MB出现时间（h）1-22-463-4敏感时间（h）4-88-128-12峰值时间（d）4-810-242416-24持续时间（d）15-143-42-4入院前的任务√AMI死亡患者中约50%在发病后1小时内于院外猝死，死因主要是可救治的致命性心律失常。√院前急救的基本任务是帮助AMI患者安全、迅速地转运到医院，以便尽早开始再灌注治疗。入院前的任务√停止任何主动活动和运动√立即舌下含服硝酸甘油1片，每5分钟可重复使用。若含服硝酸甘油3片仍无

效则应拨打急救电话。√入院前溶栓急诊诊断和治疗力争在10分钟内完成病史采集、临床检查和记录18导联心电图以明确诊断。对于ST段抬高

的AMI患者，应在30分钟内开始溶栓，或在90分钟内开始行急诊PCI治疗。急诊诊断和治疗-心电图急诊诊断和治疗（一）一般治疗√心电监测√卧床休息√建立静脉通道√吸氧√硝酸甘油√镇痛√阿司匹林√阿托品（二）再灌注治疗√静脉溶栓√溶栓辅助用药√急诊介入治疗√急诊CABG硝酸甘油√患者只要无禁忌证通常使用硝酸甘油静脉滴注24-48小时，然后改用口服硝酸酯制剂。√硝酸甘油的禁忌证有低血压（收缩压<

90mmHg）、严重心动过缓（<50次/分）或心动过速。阿司匹林√所有AMI患者只要无禁忌证均应立即口服水溶性阿司匹林或嚼服肠溶阿司匹林

150-300mg。镇痛√可给吗啡3mg静脉注射，必要时每5min重复1次，总量不宜超过15mg。√副作用有恶心、呕吐、低血压和呼吸抑制。阿托品√主要用于AMI特别是下壁AMI伴有窦性心动过缓、心室停搏和房室传导阻滞患者。√可给阿托品静脉注射0.5-1mg，必要时每

3-5min可重复使用，总量应<2.5mg。肯定是

ACS可能是

ACS按ACS诊治方案进行慢性稳定型心绞痛非心源性疾病药物治疗根据相应诊断治疗有提示ACS的症状12导联心电图Definite

ACSPossible

ACS非ST抬高>

12h<

12h适合溶栓 溶栓禁忌无再灌注适应证Symptoms

Suggestive

of

ACS静脉溶栓（D-N

<

30

m）PCI（D-B

<

90）药物治疗根据症状考虑再灌注

ST段抬高√心电监测，及时发现和处理心律失常√降低心肌耗氧量√维持血液动力学稳定√尽快再灌注治疗，使闭塞的IRCA迅速再通AMI的治疗原则急性心肌梗死治疗的最终目标·

尽早再通梗死相关血管·

完全改善缺血区的再灌注·

尽量减少心肌的坏死·

尽可能保护具有收缩功能的心肌细胞·

改善急性期和长期的疗效溶栓剂的使用方法√尿激酶：150万单位于30分钟内静脉滴注，配合肝素或低分子量肝素皮下注射每

12小时一次。√链激酶或重组链激酶：建议150万单位于

1小时内静脉滴注，配合肝素或低分子量肝素皮下注射应用。√重组组织型纤溶酶原激活剂：应用50mgrt-PA（8mg静脉注射，42mg在90min内静脉滴注），配合肝素静脉应用。急性心梗的溶栓疗法颅内出血病史近一年中有脑中风病史有脑肿瘤病史急性消化道出血怀疑有主动脉夹层动脉瘤一年前有过脑中风病史

恶性高血压(血压>180/110mmHg

)抗凝治疗中(INR 2

-

3

)近4周内有过消化道出血活动期溃疡病近2-4周有创伤、心肺复苏和手术史者近期内有过不易被压迫的血管穿刺妊娠期妇女绝对禁忌症

相对禁忌症Intracranial

haemorrhage

and

mortality

of

available

thrombolytic

agentsA

comparisonof

intracranial

haemorrhage

and

mortality

rates

reported

in

the

major

thrombolytic

trials

shows

that

tenecteplase

is

associated

withan

incidence

of

intracranial

haemorrhage

that

is

within

the

range

reported

within

all

major

thrombolytic

trials.溶栓剂的颅内出血和病死率溶栓再通指标√溶栓2h内或任何一个30min前后心电图ST段下降

50%√CK-MB或CK提前到14h或16h(距发病)√溶栓2h内胸疼迅速减轻(>70%)或消失√溶栓2h内出现再灌注心律失常静脉溶栓疗法的不足之处梗死相关血管再通率低50-85%缺乏TIMI

3级血流（<50%）起效在45-90分钟后无法确认疗效

0.5-1.5%的颅内出血仅30%的病人因无禁忌症可接受治疗溶栓治疗的疗效和时间之比挽救的千分比0

-

12

-

3 4

-

6 7

-

12症状出现的时间（小时）2519169研究(n=58.600):溶栓治疗35Thienoyridine

(clopidogrel

or

ticlopidine)

has

aweightof

evidence

is

B

because

there

has

been

no

direct

comparision

between

aspirin

andthienopyridine.Clopidogrel

is

preferred

over

ticlopidine

mainly

based

on

opinion,

but

supported

by

some

safety

data.Heparin

is

recommended,

but

the

guidelines

does

not

state

a

preference

for

IV

unfractionated

orLMW.溶栓治疗I

IIaIIbIII两个或两个以上相邻导联ST段抬高（胸导联 0.2mv，肢体导联

0.1mv），或提示AMI病史伴左束支传导阻滞，起病时间 12小时，年龄 75

岁。ST段抬高，年龄 75岁。ST段抬高，发病时间12-24小时。虽有ST段抬高，但起病时间 24，缺血性胸痛已消失或仅有ST段压低。AMI的PTCA:3种方案直接性PTCA补救性PTCA即刻性PTCA直接PTCA的优点快速和有效地祛除病变!适用于对溶栓疗法有禁忌症的病人！直接PTCA的指征√ST段抬高或新出现束支传导阻滞的AMI患者，直接PTCA作为溶栓治疗的替代治疗。√ST段抬高或新出现左束支传导阻滞的AMI并发心原性休克患者，年龄<75岁，发病在

36h内，并且血管重建术可在休克发生18h内完成者，应首选直接PTCA治疗。√适宜再灌注治疗而有溶栓治疗禁忌证者，直接PTCA可作为一种再灌注治疗手段。挽救性PTCA的指征接受溶栓疗法后持续有心绞痛者血液动力学不稳定者有持续性或增多性ST-段抬高者溶栓与介入治疗的选择溶栓治疗介入治疗发病 3小时介入治疗不能进行在有外科支持的有经验的PCI中心介入治疗有延误（door-to-balloon时间>90min，door-to-balloon减去door-to-needle时间>

1h）心源性休克溶栓禁忌发病超过3小时STEMI诊断可疑就地溶栓与转院PCI√新指南强调就地溶栓与转院PCI的比较。√在发病3小时内就地溶栓与转院PCI的预后相当，而发病超过3小时，转院PCI的预后显著优于就地溶栓。易化PCI√有计划地使用减量溶栓药物和糖蛋白

IIb/IIIa受体拮抗剂然后行PCI称为易化

PCI，是目前新的热点。冠脉搭桥手术Thienoyridine

(clopidogrel

or

ticlopidine)

has

aweightof

evidence

is

B

because

there

has

been

no

direct

comparision

between

aspirin

andthienopyridine.Clopidogrel

is

preferred

over

ticlopidine

mainly

based

on

opinion,

but

supported

by

some

safety

data.Heparin

is

recommended,

but

the

guidelines

does

not

state

a

preference

for

IV

unfractionated

orLMW.早期一般措施I

IIaIIbIII心电监测血流动力学稳定患者最初12小时卧床休息避免Valsalva动作最大程度减轻疼痛常规使用抗焦虑药无并发症的稳定患者延长卧床休息时间Thienoyridine

(clopidogrel

or

ticlopidine)

has

aweightof

evidence

is

B

because

there

has

been

no

direct

comparision

between

aspirin

andthienopyridine.Clopidogrel

is

preferred

over

ticlopidine

mainly

based

on

opinion,

but

supported

by

some

safety

data.Heparin

is

recommended,

but

the

guidelines

does

not

state

a

preference

for

IV

unfractionated

orLMW.吸氧I

IIaIIbIII严重肺淤血动脉氧饱和度<90%无并发症AMI患者，常规应用2-3小时无并发症AMI患者，常规应用3-6小时以上急性左心衰竭的处理（一）√适量利尿剂，静脉注射速尿20mg。√静脉滴注硝酸甘油，小剂量（10ug/min）开始，逐渐加量，直到收缩压下降10-15%，但不低于90mmHg。√尽早口服ACEI，急性期以短效为宜，小剂量开始，根据耐受情况逐渐加量。急性左心衰竭的处理（二）√肺水肿合并严重高血压时是静脉滴注硝普钠的最佳适应证。小剂量（10ug/min）开始，根据血压逐渐加量并调整至合适剂量。√在合并快速心房颤动时，可用西地兰或地高辛减慢心室率。√急性肺水肿伴严重低氧血症者可行人工机械通气治疗。心原性休克的处理√在严重低血压时，应静脉滴注多巴胺5-15ug/kg/min，如血压不升，使用大剂量多巴胺。大剂量多巴胺无效时，也可静脉滴注去甲肾上腺素。√AMI合并心原性休克时药物治疗不能改善预后，应使用主动脉内球囊反搏。√迅速使完全闭塞的梗死相关血管开通，恢复血流至关重要。漂浮导管适应证√严重或进行性充血性心力衰竭或肺水肿;√心原性休克或进行性低血压；√可疑的AMI机械并发症;√低血压而无肺瘀血，扩容治疗无效。主动脉内球囊反搏适应证√心原性休克药物治疗难以恢复时，作为冠状动脉造影和急诊血管重建术前的一项稳定措施。√并发机械性并发症，作为冠状动脉造影和修补手术前的一项稳定性治疗手段。√顽固性室性心动过速反复发作伴血流动力学不稳定。√AMI后顽固性心绞痛在冠状动脉造影和血管重建术前的一种治疗措施。AMI并发心律失常√首先应加强针对急性心肌梗死、心肌缺血的治疗。AMI并发室上性快速心律失常√房性早搏：与交感兴奋或心功能不全有关，本身不需特殊治疗。√阵发性室上性心动过速：伴快速心室率，必须积极处理。√心房扑动：少见且多为暂时性。√心房颤动：常见且与预后有关。AMI合并心房颤动√血流动力学不稳定的患者，如出现血压降低、脑供血不足、心绞痛或心力衰竭者需迅速作同步电复律。√血流动力学稳定的患者，以减慢心室率为首要治疗。√胺碘酮对中止心房颤动、减慢心室率及复律后维持窦性心律均有价值，可静脉用药并随后口服治疗。AMI合并心房颤动√无心功能不全、支气管痉挛或房室传导阻滞者，可静脉使用 受体阻滞剂如美多心安5mg在5min内静脉注入，必要时可重复，15min内总量不超过15mg。√洋地黄制剂，如西地兰静脉注入，其起效时间较慢。心功能不全者应首选洋地黄制剂。√如治疗无效或禁忌且无心功能不全者，可静脉使用维拉帕米或硫氮唑酮。AMI合并室性快速心律失常√心室颤动、持续性多形室性心动过速，立即非同步直流电复律，起始电能量200J，如不成功可给予300J重复。√持续性单形室性心动过速伴心绞痛、肺水肿、低血压，应予同步直流电复律，起始能量100J，如不成功可提高除颤能量。√持续性单形室性心动过速不伴上述情况，可首先给予药物治疗。AMI合并室性快速心律失常√利多卡因：快速静脉注射50mg，需要时每5-10

min可重复，最大负荷剂量150mg，然后1-4mg/min维持静脉滴注，时间不宜超过24h。√胺碘酮：10分钟内静脉注入150mg，必要时可重复，然后1mg/min静脉滴注6小时，再给予0.5mg/min维持滴注。√普鲁卡因酰胺：AMI合并室性快速心律失常√频发室性早搏、成对室性早搏、非持续性室速可严密观察或利多卡因治疗。√偶发室性早搏、加速的室性自主心律可严密观察，不作特殊处理。√短阵多形室性心动过速，酷似尖端扭转型室性心动过速，但QT间期正常，可能与缺血引起的多环路折返机制有关，治疗方法同上，如利多卡因、胺碘酮等。AMI合并缓慢性心律失常√无症状窦性心动过缓，可暂作观察，不予特殊处理。√症状性窦性心动过缓、二度I型房室传导阻滞、三度房室传导阻滞伴窄QRS波逸

搏心律，可先用阿托品静脉注射治疗。√出现下列情况，需行临时起搏治疗。Thienoyridine

(clopidogrel

or

ticlopidine)

has

aweightof

evidence

is

B

because

there

has

been

no

direct

comparision

between

aspirin

andthienopyridine.Clopidogrel

is

preferred

over

ticlopidine

mainly

based

on

opinion,

but

supported

by

some

safety

data.Heparin

is

recommended,

but

the

guidelines

does

not

state

a

preference

for

IV

unfractionated

orLMW.阿托品使用建议I

IIaIIbIII有症状的窦性心动过缓心室停搏有症状的房室结水平AVB房室结水平以下的AVB无症状的窦性心动过缓临时起搏治疗√三度房室传导阻滞伴宽QRS波逸搏、心室停搏；√症状性窦性心动过缓、二度I型房室传导阻滞或三度房室传导阻滞伴窄QRS波逸搏经

阿托品治疗无效；√二度II型房室传导阻滞；√双侧束支传导阻滞，新发生的右束支传导阻滞伴左前或左后分支阻滞和新发生的左束支传导阻滞并发一度房室传导阻滞。机械性并发症√急性游离壁破裂√亚急性游离壁破裂√室间隔穿孔√急性二尖瓣关闭不全√左心室室壁瘤特殊并发症√深静脉血栓形成和肺动脉栓塞√心室内血栓形成和体循环栓塞√心包炎√晚期室性心律失常√心肌梗死后心绞痛和缺血硝酸酯类药物√硝酸酯类药物的主要作用是松弛血管平滑肌产生血管扩张的作用，从而减少心脏做功和心肌耗氧量。√酸酯类药物还可直接扩张冠状动脉，增加心肌血流，预防和解除冠状动脉痉挛，对于已有严重狭窄的冠状动脉，可通过扩张侧支血管增加缺血区血流。硝酸酯类药物√常用的硝酸酯类药物包括硝酸甘油、硝酸异山梨酯和5-单硝山梨醇酯。√硝酸酯类药物的副反应有头痛、反射性心动过速和低血压等。√禁忌证为AMI合并低血压（收缩压<90mmHg）或心动过速（心率>100次），伴右室梗死时即使无低血压也应慎用。硝酸酯类药物√静脉滴注硝酸甘油应从低剂量开始，即

10ug/min，可酌情逐渐增加剂量，每5-10min增加5-10ug，直至症状控制、血压正常者收缩压降低10mmHg或高血压患者收缩压降低30mmHg为有效治疗剂量√静脉用药24-48h后可使用口服制剂如硝酸异山梨酯或5-单硝山梨醇酯继续治疗。抗血小板治疗√阿司匹林通过抑制血小板内的环氧化酶使血栓素A2合成减少，达到抑制血小板聚集的作用。√AMI急性期，阿司匹林剂量应在150-300mg/d之间，3天后改为小剂量50-150mg/d维持。√副作用主要是胃肠道症状，与剂量相关。抗血小板治疗√噻氯匹定和氯吡格雷主要抑制ADP诱导的血小板聚集。√主要副反应是中性粒细胞及血小板减少，应用时需监测血象。√氯吡格雷是新型ADP受体拮抗剂，口服后起效快，副反应明显减低。初始剂量

300mg，以后剂量75mg/d维持。Thienoyridine

(clopidogrel

or

ticlopidine)

has

aweightof

evidence

is

B

because

there

has

been

no

direct

comparision

between

aspirin

andthienopyridine.Clopidogrel

is

preferred

over

ticlopidine

mainly

based

on

opinion,

but

supported

by

some

safety

data.Heparin

is

recommended,

but

the

guidelines

does

not

state

a

preference

for

IV

unfractionated

orLMW.抗血小板治疗I

IIaIIbIIIAspirin

+

clopidogrel,for

up

to

1

monthAspirin

+

clopidogrel,for

up

to

9

months抗凝治疗√凝血酶是使纤维蛋白原转变为纤维蛋白最终形成血栓的关键环节，因此抑制凝血酶至关重要。√抑制途径包括抑制其生成即抑制活化的因子X和直接灭活已形成的凝血酶。√包括普通肝素和低分子量肝素。普通肝素√对于ST段抬高的AMI，肝素作为溶栓治疗的辅助用药，对于非ST段抬高的AMI，静脉滴注肝素为常规治疗。√溶栓前先静脉注射肝素5000U冲击量，继之以1000U/h维持静脉滴注48h，根据ACT或APTT调整肝素剂量。后改用皮下肝素

7500U每日2次，治疗2-3d。低分子量肝素√低分子量肝素为普通肝素的一个片段，预防血栓形成的总效应方面优于普通肝素。√鉴于低分子量肝素应用方便、不需监测凝血时间、出血并发症低等优点，建议可用低分子量肝素代替普通肝素。Recommendations

for

IIb/IIIa

inhibition

therapy

in

acute

coronary

disease

strongly

reflects

the

weigh

of

evidence.The

recommendations

and

highrisk

are

defined

broadly.

High

risk

is

defined

as

any

of

the

categories

listed

on

the

slide,

and

any

patient

that

ishemodynamically

compromised.Patients

that

would

benefit

from

IIa/IIIb

therapy

would

include

those

patients

with:Definitive

ECG

changes

during

an

episodeof

rest

pain,

even

if

the

pain

passedVentricular

arrhythmia

or

ventricular

tachycardia

with

chest

painA

positive

cardiac

markerThe

abciximab

recommendationis

a

subset

of

the

above.

Abciximab

should

only

be

given

if

there

is

a

planned

PCI

in

the

next

24

hours.受体阻滞剂I

IIaIIbIII无禁忌证患者应及早应用，无论是否同时做溶栓治疗或直接PTCA。中度左心室衰竭或相对禁忌证患者，密切监测下应用重度左心室衰竭患者受体阻滞剂√受体阻滞剂通过减慢心率，降低体循环血压和减弱心肌收缩力来减少心肌耗氧量，对改善缺血区的氧供需失衡，缩小心肌梗死面积，降低急性期病死率有肯定的疗效。√常用的受体阻滞剂为美托洛尔、阿替洛尔。受体阻滞剂的禁忌证√严重支气管痉挛性疾病√心动过缓（心率<60次）√二度及以上房室传导阻滞√明显低血压√中重度左心衰竭（>KillipIII级）√末梢循环灌注不良血管紧张素转换酶抑制剂√主要作用机制是通过影响心肌重塑、减轻心室过度扩张而减少充盈性心力衰竭的发生率和死亡率。√在无禁忌证的情况下，及早常规应用。√ACEI使用的剂量和时限应视患者情况而定。ACEI禁忌证√低血压（<90mmHg）√双侧肾动脉狭窄√血肌酐水平显著升高（>3mg/dL）√高血钾症（>5.5mmol/L）√妊娠、哺乳妇女√对ACEI制剂过敏者钙拮抗剂√钙拮抗剂在AMI治疗中不作为一线用药。√可能与硝苯地平反射性增加心率，抑制心脏收缩力和降低血压有关。在AMI常规治疗中钙拮抗剂被视为不宜使用的药物。Recommendations

for

IIb/IIIa

inhibition

therapy

in

acute

coronary

disease

strongly

reflects

the

weigh

of

evidence.The

recommendations

and

highrisk

are

defined

broadly.

High

risk

is

defined

as

any

of

the

categories

listed

on

the

slide,

and

any

patient

that

ishemodynamically

compromised.Patients

that

would

benefit

from

IIa/IIIb

therapy

would

include

those

patients

with:Definitive

ECG

changes

during

an

episodeof

rest

pain,

even

if

the

pain

passedVentricular

arrhythmia

or

ventricular

tachycardia

with

chest

painA

positive

cardiac

markerThe

abciximab

recommendationis

a

subset

of

the

above.

Abciximab

should

only

be

given

if

there

is

a

planned

PCI

in

the

next

24

hours.钙拮抗剂I

IIaIIbIII受体阻滞剂无效或禁忌时，地尔硫卓或维拉帕米可用于控制AMI后进行性缺血或心房颤动伴快速心室率。硝苯地平因其负性肌力作用，反射性交感神经兴奋，心动过速和低血压效应，禁忌在AMI中应用。对于AMI合并左心室功能不全、房室传导阻滞、严重窦性心动过缓及低血压者，禁忌使用地尔硫卓和维拉帕米。洋地黄制剂√24小时之内一般不使用洋地黄制剂，对于AMI合并左心衰竭的患者24小时后常规服用洋地黄制剂是否有益也一直存在争议。√对于AMI左心衰竭并发快速心房颤动的患者，可首次静脉注射西地兰0.4mg，此后根据情况追加0.2-0.4mg，然后口服地高辛维持。葡萄糖-胰岛素-钾溶液√研究结果提示，在AMI早期用GIK静脉滴注及进行代谢调整治疗是可行的。然而最终