心肌梗死指南課件

急性心肌梗死治療指南北京大學第三醫(yī)院心內(nèi)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).支持適應證建議的證據(jù)權(quán)重等級=證據(jù)來自多個隨機臨床試驗。=證據(jù)來自單個隨機試驗或非隨機研究。=專家的一致觀點。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指南適應證建議分類I

IIaIIbIII指那些已證實有用、有益和有效的操作或治療。指那些有關(guān)證據(jù)傾向于有用/有效。有關(guān)證據(jù)不能充分說明有用/有效。指那些已證實無效并且在有些病例可能是有害的操作或治療。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.指南內(nèi)容√簡介√入院前的任務√急診診斷和治療√住院治療√藥物治療原理和方法√長期治療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.缺血性心臟病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不穩(wěn)定心絞痛NQMIQ波MI心肌梗死急性冠脈綜合征無ST段抬高

ST段抬高NSTEMI急性冠狀動脈綜合征概念Chronology

of

Atherosclerotic

VascularDisease

ProcessDevelopment

ofatherosclerosis

andvulnerableplaque

Acute

Coronary

Syndrome

Secondary

PreventionIschemic

Heart

DiseaseCerebrovascularDiseasePeripheral

VascularDisease急性冠狀動脈綜合征機制急性心肌梗死病理表現(xiàn)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)急性冠狀動脈綜合征機制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斑塊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個月死亡率必須至少具備下列三條標準中的兩條：√缺血性胸痛的臨床病史；√心電圖的動態(tài)演變；√血清心肌標記物濃度的動態(tài)改變。急性心肌梗死診斷心肌梗死新定義具備以下任一條可確定急性心梗的診斷：n

心肌壞死生化標記物的典型升高與回降（肌鈣蛋白或CK－MB），同時合并至少下述一條：（a）：缺血癥狀（b）：ECG出現(xiàn)病理Q波（c）：ECG缺血表現(xiàn)（ST段升高或降低）（d）：冠脈介入操作（如PTCA）n

急性心肌梗死的病理學證據(jù)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典型臨床表現(xiàn)√持續(xù)胸痛>30

min√大汗淋漓√惡心嘔吐√面色蒼白心電圖動態(tài)變化血清心肌標記物的測定主要包括CK、CK-MB、肌鈣蛋白T/I和肌紅蛋白，測定心肌標記物有助于AMI的確定診斷和評估梗死面積，但再灌注治療不須等待測定的結(jié)果。AMI血清心肌標記物肌紅蛋白TNTCKCK-MB出現(xiàn)時間（h）1-22-463-4敏感時間（h）4-88-128-12峰值時間（d）4-810-242416-24持續(xù)時間（d）15-143-42-4入院前的任務√AMI死亡患者中約50%在發(fā)病后1小時內(nèi)于院外猝死，死因主要是可救治的致命性心律失常?！淘呵凹本鹊幕救蝿帐菐椭鶤MI患者安全、迅速地轉(zhuǎn)運到醫(yī)院，以便盡早開始再灌注治療。入院前的任務√停止任何主動活動和運動√立即舌下含服硝酸甘油1片，每5分鐘可重復使用。若含服硝酸甘油3片仍無

效則應撥打急救電話?！倘朐呵叭芩痹\診斷和治療力爭在10分鐘內(nèi)完成病史采集、臨床檢查和記錄18導聯(lián)心電圖以明確診斷。對于ST段抬高

的AMI患者，應在30分鐘內(nèi)開始溶栓，或在90分鐘內(nèi)開始行急診PCI治療。急診診斷和治療-心電圖急診診斷和治療（一）一般治療√心電監(jiān)測√臥床休息√建立靜脈通道√吸氧√硝酸甘油√鎮(zhèn)痛√阿司匹林√阿托品（二）再灌注治療√靜脈溶栓√溶栓輔助用藥√急診介入治療√急診CABG硝酸甘油√患者只要無禁忌證通常使用硝酸甘油靜脈滴注24-48小時，然后改用口服硝酸酯制劑。√硝酸甘油的禁忌證有低血壓（收縮壓<

90mmHg）、嚴重心動過緩（<50次/分）或心動過速。阿司匹林√所有AMI患者只要無禁忌證均應立即口服水溶性阿司匹林或嚼服腸溶阿司匹林

150-300mg。鎮(zhèn)痛√可給嗎啡3mg靜脈注射，必要時每5min重復1次，總量不宜超過15mg?！谈弊饔糜袗盒摹I吐、低血壓和呼吸抑制。阿托品√主要用于AMI特別是下壁AMI伴有竇性心動過緩、心室停搏和房室傳導阻滯患者。√可給阿托品靜脈注射0.5-1mg，必要時每

3-5min可重復使用，總量應<2.5mg?？隙ㄊ?/p>

ACS可能是

ACS按ACS診治方案進行慢性穩(wěn)定型心絞痛非心源性疾病藥物治療根據(jù)相應診斷治療有提示ACS的癥狀12導聯(lián)心電圖Definite

ACSPossible

ACS非ST抬高>

12h<

12h適合溶栓 溶栓禁忌無再灌注適應證Symptoms

Suggestive

of

ACS靜脈溶栓（D-N

<

30

m）PCI（D-B

<

90）藥物治療根據(jù)癥狀考慮再灌注

ST段抬高√心電監(jiān)測，及時發(fā)現(xiàn)和處理心律失?！探档托募『难趿俊叹S持血液動力學穩(wěn)定√盡快再灌注治療，使閉塞的IRCA迅速再通AMI的治療原則急性心肌梗死治療的最終目標·

盡早再通梗死相關(guān)血管·

完全改善缺血區(qū)的再灌注·

盡量減少心肌的壞死·

盡可能保護具有收縮功能的心肌細胞·

改善急性期和長期的療效溶栓劑的使用方法√尿激酶：150萬單位于30分鐘內(nèi)靜脈滴注，配合肝素或低分子量肝素皮下注射每

12小時一次?！替溂っ富蛑亟M鏈激酶：建議150萬單位于

1小時內(nèi)靜脈滴注，配合肝素或低分子量肝素皮下注射應用?！讨亟M組織型纖溶酶原激活劑：應用50mgrt-PA（8mg靜脈注射，42mg在90min內(nèi)靜脈滴注），配合肝素靜脈應用。急性心梗的溶栓療法顱內(nèi)出血病史近一年中有腦中風病史有腦腫瘤病史急性消化道出血懷疑有主動脈夾層動脈瘤一年前有過腦中風病史

惡性高血壓(血壓>180/110mmHg

)抗凝治療中(INR 2

-

3

)近4周內(nèi)有過消化道出血活動期潰瘍病近2-4周有創(chuàng)傷、心肺復蘇和手術(shù)史者近期內(nèi)有過不易被壓迫的血管穿刺妊娠期婦女絕對禁忌癥

相對禁忌癥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.溶栓劑的顱內(nèi)出血和病死率溶栓再通指標√溶栓2h內(nèi)或任何一個30min前后心電圖ST段下降

50%√CK-MB或CK提前到14h或16h(距發(fā)病)√溶栓2h內(nèi)胸疼迅速減輕(>70%)或消失√溶栓2h內(nèi)出現(xiàn)再灌注心律失常靜脈溶栓療法的不足之處梗死相關(guān)血管再通率低50-85%缺乏TIMI

3級血流（<50%）起效在45-90分鐘后無法確認療效

0.5-1.5%的顱內(nèi)出血僅30%的病人因無禁忌癥可接受治療溶栓治療的療效和時間之比挽救的千分比0

-

12

-

3 4

-

6 7

-

12癥狀出現(xiàn)的時間（小時）2519169研究(n=58.600):溶栓治療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.溶栓治療I

IIaIIbIII兩個或兩個以上相鄰導聯(lián)ST段抬高（胸導聯(lián) 0.2mv，肢體導聯(lián)

0.1mv），或提示AMI病史伴左束支傳導阻滯，起病時間 12小時，年齡 75

歲。ST段抬高，年齡 75歲。ST段抬高，發(fā)病時間12-24小時。雖有ST段抬高，但起病時間 24，缺血性胸痛已消失或僅有ST段壓低。AMI的PTCA:3種方案直接性PTCA補救性PTCA即刻性PTCA直接PTCA的優(yōu)點快速和有效地祛除病變!適用于對溶栓療法有禁忌癥的病人！直接PTCA的指征√ST段抬高或新出現(xiàn)束支傳導阻滯的AMI患者，直接PTCA作為溶栓治療的替代治療?！蘏T段抬高或新出現(xiàn)左束支傳導阻滯的AMI并發(fā)心原性休克患者，年齡<75歲，發(fā)病在

36h內(nèi)，并且血管重建術(shù)可在休克發(fā)生18h內(nèi)完成者，應首選直接PTCA治療?！踢m宜再灌注治療而有溶栓治療禁忌證者，直接PTCA可作為一種再灌注治療手段。挽救性PTCA的指征接受溶栓療法后持續(xù)有心絞痛者血液動力學不穩(wěn)定者有持續(xù)性或增多性ST-段抬高者溶栓與介入治療的選擇溶栓治療介入治療發(fā)病 3小時介入治療不能進行在有外科支持的有經(jīng)驗的PCI中心介入治療有延誤（door-to-balloon時間>90min，door-to-balloon減去door-to-needle時間>

1h）心源性休克溶栓禁忌發(fā)病超過3小時STEMI診斷可疑就地溶栓與轉(zhuǎn)院PCI√新指南強調(diào)就地溶栓與轉(zhuǎn)院PCI的比較?！淘诎l(fā)病3小時內(nèi)就地溶栓與轉(zhuǎn)院PCI的預后相當，而發(fā)病超過3小時，轉(zhuǎn)院PCI的預后顯著優(yōu)于就地溶栓。易化PCI√有計劃地使用減量溶栓藥物和糖蛋白

IIb/IIIa受體拮抗劑然后行PCI稱為易化

PCI，是目前新的熱點。冠脈搭橋手術(shù)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心電監(jiān)測血流動力學穩(wěn)定患者最初12小時臥床休息避免Valsalva動作最大程度減輕疼痛常規(guī)使用抗焦慮藥無并發(fā)癥的穩(wěn)定患者延長臥床休息時間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嚴重肺淤血動脈氧飽和度<90%無并發(fā)癥AMI患者，常規(guī)應用2-3小時無并發(fā)癥AMI患者，常規(guī)應用3-6小時以上急性左心衰竭的處理（一）√適量利尿劑，靜脈注射速尿20mg?！天o脈滴注硝酸甘油，小劑量（10ug/min）開始，逐漸加量，直到收縮壓下降10-15%，但不低于90mmHg?！瘫M早口服ACEI，急性期以短效為宜，小劑量開始，根據(jù)耐受情況逐漸加量。急性左心衰竭的處理（二）√肺水腫合并嚴重高血壓時是靜脈滴注硝普鈉的最佳適應證。小劑量（10ug/min）開始，根據(jù)血壓逐漸加量并調(diào)整至合適劑量。√在合并快速心房顫動時，可用西地蘭或地高辛減慢心室率?！碳毙苑嗡[伴嚴重低氧血癥者可行人工機械通氣治療。心原性休克的處理√在嚴重低血壓時，應靜脈滴注多巴胺5-15ug/kg/min，如血壓不升，使用大劑量多巴胺。大劑量多巴胺無效時，也可靜脈滴注去甲腎上腺素?！藺MI合并心原性休克時藥物治療不能改善預后，應使用主動脈內(nèi)球囊反搏。√迅速使完全閉塞的梗死相關(guān)血管開通，恢復血流至關(guān)重要。漂浮導管適應證√嚴重或進行性充血性心力衰竭或肺水腫;√心原性休克或進行性低血壓；√可疑的AMI機械并發(fā)癥;√低血壓而無肺瘀血，擴容治療無效。主動脈內(nèi)球囊反搏適應證√心原性休克藥物治療難以恢復時，作為冠狀動脈造影和急診血管重建術(shù)前的一項穩(wěn)定措施?！滩l(fā)機械性并發(fā)癥，作為冠狀動脈造影和修補手術(shù)前的一項穩(wěn)定性治療手段?！填B固性室性心動過速反復發(fā)作伴血流動力學不穩(wěn)定?！藺MI后頑固性心絞痛在冠狀動脈造影和血管重建術(shù)前的一種治療措施。AMI并發(fā)心律失?！淌紫葢訌娽槍毙孕募」Ｋ?、心肌缺血的治療。AMI并發(fā)室上性快速心律失常√房性早搏：與交感興奮或心功能不全有關(guān)，本身不需特殊治療?！剃嚢l(fā)性室上性心動過速：伴快速心室率，必須積極處理?！绦姆繐鋭樱荷僖娗叶酁闀簳r性?！绦姆款潉樱撼Ｒ娗遗c預后有關(guān)。AMI合并心房顫動√血流動力學不穩(wěn)定的患者，如出現(xiàn)血壓降低、腦供血不足、心絞痛或心力衰竭者需迅速作同步電復律?！萄鲃恿W穩(wěn)定的患者，以減慢心室率為首要治療?！贪返馔獙χ兄剐姆款潉印p慢心室率及復律后維持竇性心律均有價值，可靜脈用藥并隨后口服治療。AMI合并心房顫動√無心功能不全、支氣管痙攣或房室傳導阻滯者，可靜脈使用 受體阻滯劑如美多心安5mg在5min內(nèi)靜脈注入，必要時可重復，15min內(nèi)總量不超過15mg?！萄蟮攸S制劑，如西地蘭靜脈注入，其起效時間較慢。心功能不全者應首選洋地黃制劑?！倘缰委煙o效或禁忌且無心功能不全者，可靜脈使用維拉帕米或硫氮唑酮。AMI合并室性快速心律失?！绦氖翌潉印⒊掷m(xù)性多形室性心動過速，立即非同步直流電復律，起始電能量200J，如不成功可給予300J重復?！坛掷m(xù)性單形室性心動過速伴心絞痛、肺水腫、低血壓，應予同步直流電復律，起始能量100J，如不成功可提高除顫能量?！坛掷m(xù)性單形室性心動過速不伴上述情況，可首先給予藥物治療。AMI合并室性快速心律失?！汤嗫ㄒ颍嚎焖凫o脈注射50mg，需要時每5-10

min可重復，最大負荷劑量150mg，然后1-4mg/min維持靜脈滴注，時間不宜超過24h?！贪返馔?0分鐘內(nèi)靜脈注入150mg，必要時可重復，然后1mg/min靜脈滴注6小時，再給予0.5mg/min維持滴注。√普魯卡因酰胺：AMI合并室性快速心律失?！填l發(fā)室性早搏、成對室性早搏、非持續(xù)性室速可嚴密觀察或利多卡因治療?！膛及l(fā)室性早搏、加速的室性自主心律可嚴密觀察，不作特殊處理?！潭剃嚩嘈问倚孕膭舆^速，酷似尖端扭轉(zhuǎn)型室性心動過速，但QT間期正常，可能與缺血引起的多環(huán)路折返機制有關(guān)，治療方法同上，如利多卡因、胺碘酮等。AMI合并緩慢性心律失常√無癥狀竇性心動過緩，可暫作觀察，不予特殊處理。√癥狀性竇性心動過緩、二度I型房室傳導阻滯、三度房室傳導阻滯伴窄QRS波逸

搏心律，可先用阿托品靜脈注射治療。√出現(xiàn)下列情況，需行臨時起搏治療。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.阿托品使用建議I

IIaIIbIII有癥狀的竇性心動過緩心室停搏有癥狀的房室結(jié)水平AVB房室結(jié)水平以下的AVB無癥狀的竇性心動過緩臨時起搏治療√三度房室傳導阻滯伴寬QRS波逸搏、心室停搏；√癥狀性竇性心動過緩、二度I型房室傳導阻滯或三度房室傳導阻滯伴窄QRS波逸搏經(jīng)

阿托品治療無效；√二度II型房室傳導阻滯；√雙側(cè)束支傳導阻滯，新發(fā)生的右束支傳導阻滯伴左前或左后分支阻滯和新發(fā)生的左束支傳導阻滯并發(fā)一度房室傳導阻滯。機械性并發(fā)癥√急性游離壁破裂√亞急性游離壁破裂√室間隔穿孔√急性二尖瓣關(guān)閉不全√左心室室壁瘤特殊并發(fā)癥√深靜脈血栓形成和肺動脈栓塞√心室內(nèi)血栓形成和體循環(huán)栓塞√心包炎√晚期室性心律失?！绦募」Ｋ篮笮慕g痛和缺血硝酸酯類藥物√硝酸酯類藥物的主要作用是松弛血管平滑肌產(chǎn)生血管擴張的作用，從而減少心臟做功和心肌耗氧量?！趟狨ヮ愃幬镞€可直接擴張冠狀動脈，增加心肌血流，預防和解除冠狀動脈痙攣，對于已有嚴重狹窄的冠狀動脈，可通過擴張側(cè)支血管增加缺血區(qū)血流。硝酸酯類藥物√常用的硝酸酯類藥物包括硝酸甘油、硝酸異山梨酯和5-單硝山梨醇酯?！滔跛狨ヮ愃幬锏母狈磻蓄^痛、反射性心動過速和低血壓等。√禁忌證為AMI合并低血壓（收縮壓<90mmHg）或心動過速（心率>100次），伴右室梗死時即使無低血壓也應慎用。硝酸酯類藥物√靜脈滴注硝酸甘油應從低劑量開始，即

10ug/min，可酌情逐漸增加劑量，每5-10min增加5-10ug，直至癥狀控制、血壓正常者收縮壓降低10mmHg或高血壓患者收縮壓降低30mmHg為有效治療劑量√靜脈用藥24-48h后可使用口服制劑如硝酸異山梨酯或5-單硝山梨醇酯繼續(xù)治療。抗血小板治療√阿司匹林通過抑制血小板內(nèi)的環(huán)氧化酶使血栓素A2合成減少，達到抑制血小板聚集的作用?！藺MI急性期，阿司匹林劑量應在150-300mg/d之間，3天后改為小劑量50-150mg/d維持。√副作用主要是胃腸道癥狀，與劑量相關(guān)?？寡“逯委煛锑缏绕ザê吐冗粮窭字饕种艫DP誘導的血小板聚集?！讨饕狈磻侵行粤＜毎把“鍦p少，應用時需監(jiān)測血象?！搪冗粮窭资切滦虯DP受體拮抗劑，口服后起效快，副反應明顯減低。初始劑量

300mg，以后劑量75mg/d維持。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.抗血小板治療I

IIaIIbIIIAspirin

+

clopidogrel,for

up

to

1

monthAspirin

+

clopidogrel,for

up

to

9

months抗凝治療√凝血酶是使纖維蛋白原轉(zhuǎn)變?yōu)槔w維蛋白最終形成血栓的關(guān)鍵環(huán)節(jié)，因此抑制凝血酶至關(guān)重要?！桃种仆緩桨ㄒ种破渖杉匆种苹罨囊蜃覺和直接滅活已形成的凝血酶?！贪ㄆ胀ǜ嗡睾偷头肿恿扛嗡?。普通肝素√對于ST段抬高的AMI，肝素作為溶栓治療的輔助用藥，對于非ST段抬高的AMI，靜脈滴注肝素為常規(guī)治療?！倘芩ㄇ跋褥o脈注射肝素5000U沖擊量，繼之以1000U/h維持靜脈滴注48h，根據(jù)ACT或APTT調(diào)整肝素劑量。后改用皮下肝素

7500U每日2次，治療2-3d。低分子量肝素√低分子量肝素為普通肝素的一個片段，預防血栓形成的總效應方面優(yōu)于普通肝素?！惕b于低分子量肝素應用方便、不需監(jiān)測凝血時間、出血并發(fā)癥低等優(yōu)點，建議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.受體阻滯劑I

IIaIIbIII無禁忌證患者應及早應用，無論是否同時做溶栓治療或直接PTCA。中度左心室衰竭或相對禁忌證患者，密切監(jiān)測下應用重度左心室衰竭患者受體阻滯劑√受體阻滯劑通過減慢心率，降低體循環(huán)血壓和減弱心肌收縮力來減少心肌耗氧量，對改善缺血區(qū)的氧供需失衡，縮小心肌梗死面積，降低急性期病死率有肯定的療效。√常用的受體阻滯劑為美托洛爾、阿替洛爾。受體阻滯劑的禁忌證√嚴重支氣管痙攣性疾病√心動過緩（心率<60次）√二度及以上房室傳導阻滯√明顯低血壓√中重度左心衰竭（>KillipIII級）√末梢循環(huán)灌注不良血管緊張素轉(zhuǎn)換酶抑制劑√主要作用機制是通過影響心肌重塑、減輕心室過度擴張而減少充盈性心力衰竭的發(fā)生率和死亡率。√在無禁忌證的情況下，及早常規(guī)應用?！藺CEI使用的劑量和時限應視患者情況而定。ACEI禁忌證√低血壓（<90mmHg）√雙側(cè)腎動脈狹窄√血肌酐水平顯著升高（>3mg/dL）√高血鉀癥（>5.5mmol/L）√妊娠、哺乳婦女√對ACEI制劑過敏者鈣拮抗劑√鈣拮抗劑在AMI治療中不作為一線用藥?！炭赡芘c硝苯地平反射性增加心率，抑制心臟收縮力和降低血壓有關(guān)。在AMI常規(guī)治療中鈣拮抗劑被視為不宜使用的藥物。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

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hours.鈣拮抗劑I

IIaIIbIII受體阻滯劑無效或禁忌時，地爾硫卓或維拉帕米可用于控制AMI后進行性缺血或心房顫動伴快速心室率。硝苯地平因其負性肌力作用，反射性交感神經(jīng)興奮，心動過速和低血壓效應，禁忌在AMI中應用。對于AMI合并左心室功能不全、房室傳導阻滯、嚴重竇性心動過緩及低血壓者，禁忌使用地爾硫卓和維拉帕米。洋地黃制劑√24小時之內(nèi)一般不使用洋地黃制劑，對于AMI合并左心衰竭的患者24小時后常規(guī)服用洋地黃制劑是否有益也一直存在爭議。√對于AMI左心衰竭并發(fā)快速心房顫動的患者，可首次靜脈注射西地蘭0.4mg，此后根據(jù)情況追加0.2-0.4mg，然后口服地高辛維持。葡萄糖-胰島素-鉀溶液√研究結(jié)果提示，在AMI早期用GIK靜脈滴注及進行代謝調(diào)整治療是可行的。然而最終