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    Acute coronary syndromes

    Iftikhar Ul HaqConsultant Cardiologist

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    Learning outcomes

    • Demonstrate ability to both describe and recogniseappropriate features in clinical presentation (includingrele ant history! e"amination and in estigation# found inpatients $ith AC% s& other causes of chest pain&

    • Demonstrate ability to interpret in estigations sufficientto establish a differential diagnosis of acute coronarysyndrome' including non %) ele ation *C+ changesand biomarkers&

    • Demonstrate kno$ledge and understanding of the

    pathophysiological processes contributing to thede elopment of acute coronary syndrome

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    %elf directed learning

    • )he *C+• ,ascular endothelial cell function• %hock• -uscle cell biology• Illness pre ention and smoking

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    Uni ersal Definition of -I

    • .)he term -I should be used $hen there ise idence of myocardial necrosis in a clinicalsetting consistent $ith myocardial ischaemia/ 0 )n 1 22th percentile of U3L ()ype 4 -I#

    5LU% at least one of' 0 %ymptoms of ischaemia 0 *C+ changes indicating ischaemia 0 *C+ e idence of necrosis' ne$ pathological 6 $a es 0 Imaging ne$ loss of myocardium! or ne$ 37-A

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    Uni ersal Definition of -I

    • )ype 4 0 8usual -I9• )ype : imbalance in myocardial ; : supply and

    demand → ischaemia $ithout definite CAD

    • )ype < %udden death' other e idence of A-I orocclusi e thrombus

    • )ype = 5CI associated -I' )n >"< U3L

    • )ype ? CA@+ associated' )n >"? U3L ne$ 6$a esBL@@@! or angiographicBimaging e idence

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    ACUTE CORONARY SYNDROMEACUTE CORONARY SYNDROME

    No ST ElevationNo ST Elevation ST ElevationST ElevationST ElevationST Elevation

    Unstable Angina NQMI QwMI Myocardial In arction

    NSTEMI

    Definitions

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    Lipidpool Lipid-rich

    plaque

    Fissure Plaque

    disruption

    Occlusivethrombus

    Subocclusivethrombus

    Acute MI,Q-wave

    nstablean!ina"

    #on-Q-waveMI

    5laque 3upture

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    Days from randomi ation%a onitto % et al. JAMA& 4222 :E4'FGF

    - o r t a

    l i t y

    ( H #

    4EGG :G =G G EG 4GG 4 GG

    E

    4G

    :

    =

    4:G 4=G

    T!wave inversion"#$% &n'()*("+

    ST elevation wit, co!e-istingde.ression /#0% &n'0)*1/+

    ST de.ression2#/% &n'$)(1"+

    ST elevation

    1#2% &n'")"1/+

    AC%' mortality at months+U%); :@' %) segment depression 0 a high risk population

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    Chest pain hospital admissions

    • Chest pain is the biggest cause ofpresentation to A * in the UJ'

    0 GG!GGG patients per year

    0 4:?!GGG ha e K%)* AC% (4 in =# 4

    0# airbairn I5& J R Coll Physicians Edinb :GG<

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    Immediate assessments

    • irst 0 5atient history 0 *C+ 0

    5hysical e"amination• )hen 0 3isk stratification 0 @lood marker tests

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    Diagnosis of AC%

    3equires the presence of at least t$o of the follo$ingcriteria'

    4& Chest pain (clinical manifestation#

    :& *C+ changes consistent $ith ischaemia ornecrosis

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    AC%' classical clinical symptoms at presentation

    • Classical 0 DiscomfortBpain in the centre of the chest 0 Lasts for more than a fe$ minutes or recurs 0 3adiation to other areas! e&g& armsBMa$BneckBback

    • Atypical presentations elderly or diabetic patients' 0 @reathlessness 0 )achycardia 0 Kausea or omiting

    0 %$eating and clamminess

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    3eat4res o stable angina

    • Anginal pain is' 0 constricting discomfort in the front of the chest! neck! shoulders! Ma$ or arms

    0 precipitated by physical e"ertion 0 relie ed by rest or +)K in about ? minutes&•5eople $ith typical angina ha e all the abo e anginal pain features! people $ith atypical anginaha e t$o of the features and people $ith non anginal chest pain ha e one or none of the features&•Do not define typical and atypical features of anginal and non anginal chest pain differently inmen and $omen or among ethnic groups&• actors making stable angina more likely'

    0 increasing age 0 $hether the person is male 0 cardio ascular risk factors 0 a history of established CAD (e&g& pre ious -I! coronary re ascularisation#&• %table angina is unlikely if the pain is'

    0 continuous or ery prolonged and5or 0 unrelated to acti ity and5or 0 brought on by breathing in and5or

    0 associated $ith di iness! palpitations! tingling or difficulty s$allo$ing&

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    Cardiac 3isk actors

    • -odifiable 0 @5 0 Lipids

    0 Diabetes 0 %moking status

    • i"ed 0 5atients se" 0 Age

    0 amily history 0 *thnicity 0 5re ious anginaB-I

    0 C,AB5,D

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    Chest 5ain 0 differential diagnosis

    CA3DIAC

    Angina

    -yocardial Infarction

    5ericarditis

    Aortic dissection

    5UL-;KA3N

    5ulmonary *mbolus

    5leurisy

    5neumothora" +A%)3;

    Ulcer or 3eflu"

    +allstones5ancreatitis

    -U%CUL;%J*L*)AL

    Chostochondritis

    )rauma

    K;K ;3+AKIC

    An"iety

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    S4s.ected ACS• Check immediately if chest pain is current! or $hen the last episode $as! particularly if in the last4: hours&• Check if the chest pain may be cardiac& Consider'

    0 history of the painO any cardio ascular risk factorsO history of ischaemic heart disease and any pre ious treatmentO pre ious in estigations for chest pain&• Check if any of the follo$ing symptoms of ischaemia are present& )hese may indicate an AC%'

    0 5ain in the chest andBor other areas (for e"ample! the arms! back or Ma$# lasting longer than4?minutes&

    0 Chest pain $ith nausea and omiting! marked s$eating or breathlessness (or a combination of

    these#! or $ith haemodynamic instability& 0 Ke$ onset chest pain! or abrupt deterioration in stable angina! $ith recurrent pain occurringfrequently $ith little or no e"ertion and often lasting longer than 4? minutes&

    • Central chest pain may not be the main symptom&• Do not use response to glyceryl trinitrate (+)K# to make a diagnosis of AC%&• Do not assess symptoms of an AC% differently in men and $omen or among different ethnicgroups&• Ad ise people about seeking medical help if they ha e further chest pain&• If the chest pain is non cardiac! e"plain this to the person and refer for further in estigation ifappropriate&

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    Diagnosis of AC%

    3equires the presence of at least t$o of the follo$ingcriteria'

    4& Chest pain (clinical manifestation#

    :& *C+ changes consistent $ith ischaemia ornecrosis

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    5erform an *C+ immediately especially if thepatient is still in pain

    0 If *C+ is normal or non diagnostic in a patient $ithcontinuing symptoms repeat after

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    3isk %tratification by *C+

    )he risk of death or -I at

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    Kormal *C+

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    Anterolateral %) depression

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    Anterior %) segment depression

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    A $ith infero lateral %) depression and L,H

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    %) depression , : , ! ) in ersion in a,L

    L l %) d i

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    Lateral %) segment depression

    ) $

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    Anterior ) $a e in ersion

    $ $

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    Deep arro$head anterolateral ) $a e in ersion

    A t i di l i f ti $ith g %) g t l ti

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    Anterior myocardial infarction $ith gross %) segment ele ation(sho$ing PtombstoneP 3 $a es#

    An inferolateral myocardial infarction $ith reciprocal changes in

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    An inferolateral myocardial infarction $ith reciprocal changes inleads I! a,L! ,4! and ,:

    L f b dl b h bl k

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    Left bundle branch block

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    Diagnosis of AC% (K%)*-I#

    3equires the presence of at least t$o of the follo$ingcriteria'

    4& Chest pain (clinical manifestation#

    :& *C+ changes consistent $ith ischaemia ornecrosis

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    G 4: 4E := : < = ? F E 2 4G

    3elatie concentration

    DaysHours)ime after infarct

    Kormal

    )roponin-yoglobin

    CJ! A%)

    LDH

    )roponin I Le els and -ortality in 5atients

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    ) p y$ith K%)* AC%

    G

    :

    =

    E

    G QG&= G&= Q4&G 4&G Q :&G :&G Q?&G ?&G Q2&G 12&G

    H -

    o r t a l i t y a

    t = : D a y s

    Antman *A! )anasiMe ic -R! )hompson @! et al& Cardiac specific troponin I le els to predict the risk of mortalityin patients $ith acute coronary syndromes& N Engl J Med. 422

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    )roponin 5itfalls

    )roponin can be ele ated in• 5*• %epsis•

    5ost op• A• L,

    3ate of death or -I in relation to %)

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    3ate of death or I in relation to %)de iation and troponin

    %abatine et al. Am Heart J :GG

    5QG&GGG4 (globalχ:

    test

    1G&4G G&G4 G&4GQG&G4

    Kone

    %) de G&G? G&G2 m,

    %) de 1 G&4G m,

    0"#*%06#$%

    07#7%

    0(#2%0(#6%

    "#0%

    /#1%

    1#7%

    $#0%

    G

    :

    =

    E

    4G

    4:

    4=

    4

    D e a

    t , o r

    M I

    a t 1 8 o n

    t , s

    & % +

    Tro.onin T &ng58l+

    EC9

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    3isk and 3isk %tratification

    )I-I risk score for K%)* AC%

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    *Entry criteria: UA or NSTEMII defined as ischemic pain at rest within past 24H, withe idence of !A" #ST se$ment de iation or positi e mar%er&

    Antman et a' JAMA 2000; 2(4: () +(42

    # +-&.IS/ S!0.E 1 Tota' oints

    43356-3ST de iation 7 8 mm

    25323 !ardiac mar%ers

    2-43.ecent #924H& se ere an$ina

    3)).ESENTATI0N

    ()23ASA se in past - days

    )633/nown !A" #stenosis ;

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    7hat is the riskS

    A : year old $oman presents $ithunstable angina& ;n e"amination! the pulseis 4GGbpm! blood pressure 44GBFG! and shehad crepitations at the lung bases& )he*C+ sho$ed some %) depression in theanterior leads& @lood tests sho$ed serumcreatinine $as 4=? µmolBL& )n) $as

    undetectable

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    Acute Coronary %yndromes

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    Acute Coronary %yndromes)herapeutic +oals

    • 3educe myocardial ischaemia

    • Control of symptoms

    • 5re ention of -I and death

    Acute Coronary %yndromes

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    Acute Coronary %yndromes -edical -anagement

    • Anti ischaemic agents • Anti platelet agents

    • Anti thrombin agents

    • ( ibrinolytics#

    • Coronary re ascularisation

    5athogenesis of AC%'

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    5athogenesis of AC%)he integral role of platelets

    5laqueissure or

    3upture

    5latelet Aggregation

    5latelet Acti ation

    5latelet Adhesion

    )hrombotic;cclusion

    E ine rine Collagen Arac,idonic

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    AD;

    •)iclopidine•Clopidogrel

    •Heparin•L-7 Heparin

    •Direct )hrombinInhibitors

    • Aspirin

    E.ine.,rine g ,Acid

    T,ro8bin

    IIbBIIIareceptors

    fibrin

    )he5latelet

    •+5 IIbBIIIa inhibitors

    Drug therapies in K%)* AC% management

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    Drug therapies in K%) AC% management

    • Aspirin• Clopidogrel• L-7H• +5IIbBIIIa receptor antagonists

    • @eta blockers• Kitrates (if ongoing painBL,D#• %tatins

    *%C AC% )ask orce& Eur Heart J :GG: :

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    • ;ffer a single loading dose of

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    Use established scoring system such as +3AC* to predict month mortality and assess risk

    of future ad erse cardio ascular e ents 4 & Assess bleeding risk and pertinent comorbiditybefore considering treatments and at each stage of management

    • Lo$est risk ( ≤ 4&? #• Lo$ risk (14&? 0

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    Lo$est risk (T 4&? # 4(1 4&?0

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    Highest risk(1 2&G #4

    Intermediate risk(1

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    ;ffer coronary angiography ($ith follo$ on 5CI if indicated# $ithin 2 hours of firstadmission unless contraindicated& 5erform as soon as possible if patient is clinically

    unstable or at high ischaemic risk

    Discuss management strategy $ith inter entional cardiologist and cardiac surgeon

    -anagement of intermediate risk! high riskand highest risk continued

    Coronary angiogram

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    3CA stenosis

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    5ost Hospital Discharge Care

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    5ost Hospital Discharge Care

    A Antiplatelets and AC* I@ @eta blockers and @lood 5ressureC Cholesterol and CigarettesD Diet and Diabetes* *ducation and *"ercise

    Learning outcomes

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    Learning outcomes

    • Clinical presentation of AC% 0 History! *"amination

    • In estigations

    0 *C+! biomarkers• 5athophysiology• 3isk assessment in AC%