csim acs lecture
TRANSCRIPT
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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%