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Acute Coronary Syndrome: Patsadee Nachom MD

1) Acute coronary syndrome (ACS) describes a range of conditions caused by reduced blood flow in the coronary arteries and includes unstable angina and myocardial infarction (MI). 2) ACS presents with prolonged chest pain and can have atypical symptoms. Evaluation involves ruling out life-threatening conditions and using sensitive tools to diagnose ACS. 3) Treatment depends on the type of ACS, with ST-elevation MI requiring immediate reperfusion through fibrinolysis or percutaneous coronary intervention to limit heart muscle damage.
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0% found this document useful (0 votes)
91 views58 pages

Acute Coronary Syndrome: Patsadee Nachom MD

1) Acute coronary syndrome (ACS) describes a range of conditions caused by reduced blood flow in the coronary arteries and includes unstable angina and myocardial infarction (MI). 2) ACS presents with prolonged chest pain and can have atypical symptoms. Evaluation involves ruling out life-threatening conditions and using sensitive tools to diagnose ACS. 3) Treatment depends on the type of ACS, with ST-elevation MI requiring immediate reperfusion through fibrinolysis or percutaneous coronary intervention to limit heart muscle damage.
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Acute coronary syndrome

Patsadee Nachom MD
Jonathan Abrams. N Engl J Med 2005;352:2524-33
ACS vs stable IHD
Both have “angina” = retrosternal pressure w
hich may radiate to arm or jaw

ACS (STEMI & NSTE-ACS)


• Onset & duration
– Prolonged (>20 min) angin
al pain at rest : 80% of cas
e
– New onset angina CCS II o
r III (1 month)
– Increasing angina CCS III
– Post-MI angina
Stable IHD
• “Typical angina”
• Associated symptoms (su 1)Substernal chest discomfort
2) Provoked by exertion or emoti
ggest MI) : Diaphoresis, n onal stress and
ausea, abdominal pain, d 3) Relieved by rest or NTG (withi
yspnea n 5-10 min).
Approach to chest pain
• R/O Life threatening condition
– Acute coronary syndrome
– Pulmonary embolism
– Aortic dissection
– Other : tension pneumothorax, esophageal rupture
• Using sensitive tools (symptoms , signs , lab) to
R/O
Angina equivalent / atypical presentation

• Absence of angina BUT


– Shortness of breath
– Arm /Jaw/ epigastric pain (dyspepsia)
– Diaphoresis, nausea/vomiting
• Chest pain with stabbing /pleuritc feature

• In older patient (>75 years), women, DM,


CRF, dementia.
Definition of myocardial infarction
= evidence of myocardial necrosis in clinical
setting consistent with acute MI

Detection of a rise and/or fall of cardiac biomarker values [


preferably cTn)] with at least one value above the 99th
percentile URL + at least one of :
• Symptoms of ischaemia.
• New or presumed new significant ST–T changes or new LBBB
• Development of pathological Q waves in the ECG.
• Imaging evidence of new loss of viable myocardium or new RWMA.
• Identification of an intracoronary thrombus by CAG or autopsy.

3rd universal definition of myocardial infarction ESC/ACCF/AHA/WHF 2012


Universal classification of MI
• Type 1: Spontaneous MI
• Type 2: MI secondary to an ischaemi
c imbalance
• Type 3: MI resulting in death when bi
omarker values are unavailable
• Type 4a: MI related to percutaneous
coronary intervention (PCI)
• Type 4b: MI related to stent thrombo
sis
• Type 5: MI related to coronary artery
bypass grafting (CABG)
Laboratory
High sensitivity-cardiac Troponin (hs-cTn)

Definition : Assay for cTn measurement


• in the single digit range of ng/L (=picogram/mL)
• with CV (coefficient of variation) <10% at 99th percentile (URL) of re
ference subject

European Heart Journal doi:10.1093/eurheartj/ehs154


Rapid early rule-in AMI with hs-TnT
(not for STEMI !)

= Increase hs-TnT> 7 ng/L (50% of 14)


(eg. From 10 => 17) Need 20% change
(eg. From 20 =>24ng/L)

European Heart Journal doi:10.1093/eurheartj/ehs154


Differential diagnosis
If low pretest probability for A
CS but TnT +ve  w/u oth
er cause

European Heart Journal doi:10.1093/eurheartj/ehs154


STEMI

EKG in STEMI
Fibrinolytic Rx & Pharmacoinvasive strategy
AMI complication
LV aneurysm
LBBB (not known to be old): Sgarb
ossa’s criteria
LBBB alone  acute MI (need clinical setting)

Repolarization pattern Acute MI


ST elevation (in absence of LVH and LBBB)

• New ST elevation at J point i


n 2 contiguous leads
– Cut-points:  0.1 mV in all lea
ds other than V2-V3
– In V2-V3 :

 0.2 mV in men ( 0.25mv if a


ge< 40 years),
 0.15 mV in women
• STE > 20 min + clinical = ST
EMI
Hyperacute T-wave
• DDx from hyperkalemia (which show no QT prolong)
• Should F/U EKG 5-10 minute apart if not sure
STE in other condition

Normal (male pattern)

Early repolarization

STE of normal variant

N Engl J Med 2003;349:2128-35.


Pericarditis AMI

DDx S
TE

LVH LBBB HyperK Brugada


N Engl J Med 2003;349:2128-35.
Time is myocardium
fibrinolysis

Harm!

PCI
Fibrinolytic Rx
•  Death 10%  8% (I
SIS-2)
• In-hospital death 5-6
%
• NNT 20-100 ,RRR 15-
20%
• ICH ~ 0.6 -1% (usuall
y occur in first 24 hr)
but half will death if oc
cur
Adjunctive anti-platelet & anti-
coagulation for fibrinolytic Rx

2013 ACCF/AHA STEMI guideline


Adjunctive anti-platelet & anti-coagulati
on for fibrinolytic Rx
• Start within 30 minute after initiate fibrinolytic Rx
Assessment of reperfusion after fibrinolysis
Reliability : STE resolution > relief of chest pain

EKG : resolution at least 50% in the worst lead at 60 – 90 minutes aft


er initiate fibrinolysis
Medication
• Oral beta blocker :should be initiated in first 24 hr if DO NOT have any of:
– HF
– Evidence of low output state
– Increase risk for cardiogenic shock : age > 70 years, SBP < 120 mmHg, presenti
ng HR > 110 bpm
– C/I : PR > 0.24 sec, 2-3 heart block, reactive airway disease
 Reevaluate for initiate beta-blocker after stable

• Statin : High intensity statin Rx (Atorvastatin 80/40 mg daily)  keep LDL <
70 mg/dL in long term

• ACEI (ARB if ACEI intolerant) : (class IIa)


– if LVEF  40%, anterior MI, HF (class I)

• Aldosterone antagonist if LVEF  40% + either symptomatic HF or DM


Complication after STEMI
Cardiogenic shock
RV infarction
Mechanical complication :
Electrical complication
Pericarditis
Cardiogenic shock
• Loss > 40% LV myocardial Killip classification
• Frank pulmonary edema wit
h hypoperfusion , SBP < 90
mmHg
• CI <2.2 L/min/sq.m., PCWP
> 18 mmHg,

Rx
• Revascularization
• Inotrope
• IABP
Intra-aortic balloon counterpulsatio
n
Inferior MI with RV infarct
• BP drop after NGT with lung clear, high JVP
• STE  1mm in V1, V3r & V4r ( most sensitive)
• Rx : Reperfusion :NSS load  inotropic drug  cardiov
ersion if AF  IABP
All need
surgical
repair
Inferior wall MI with HF
• DDx :
– Mechanical complication : Papillary muscle ru
pture, VSR
– On top pre-existing LV systolic dysfunction
– Severe multi-vessel CAD
– Bradycardia / VT
Electrical complication :ventricul
ar arrhythmia
• Sustained VT/VF (5-10% of AMI case)
– 90% occur in first 48 hr
– Rx : cardioversion / defibrillation
– Prevention : correction of electrolyte & acid/base, HF ,
shock, decrease inotrope
• early beta-blocker (within 24 hr) if no C/I

• NSVT / PVC :
– no need to Rx (prophylaxis lidocaine is harmful !)
– Correction of electrolyte (K 4.5, Mg 2),
Stress induce cardiomyopathy (Takotsu
bo, broken heart syndrome
• Catecholamine exce
ss state
• Post-menopausal wo
men
• Ischemic like chest p
ain / HF
• ECG : anterior preco
rdial STE
• Low peak TnT level (
but high BNP)
• Dx by R/O (CAG)
NSTE-ACS
(unstable angina & NSTEMI)
Likelihood of ACS
Clinical presentation

Lab
Known CAD EKG :
•dynamic ST change
/ CAD risks •Marked (3 mm) inverted-T
in multiple precordial lead
TnT : rising /falling
Likelihood of ACS
High likelihood
• Known coronary disease (
particularly recent PCI)  Intermediate likelihood 
• Typical angina reproducin Absence of high-likelihood Low likelihood   
g prior documented angin features + any of : Absence of high- & i
a   • Typical angina in a patient ntermediate-likel
• Hemodynamic or ECG ch ihood features b
anges during pain   without prior documented ut may have:  
• Dynamic ST-segment ele angina     • Chest discomfort
vation or depression of ≥1 • Atypical anginal symptoms in reproduced by p
mm   alpation  
diabetics or in nondiabetics • T waves flat or i
• Marked symmetric T-wav with  2 other risk factors    
e inversion in multiple pre nverted <1 mm  
cordial leads   • Male gender  /  Age > 70 y     • Normal ECG
• Elevated cardiac enzyme • Extracardiac vascular Dz    
s in a rising and falling pat • ST depression 0.5-1.0 mm or
tern
inverted-T of ≥1 mm    
• Low-level Tn elevation that is
"flat" and does not rise or fall

Hurst’s the heart 13th edition


TIMI risk score
• All cause mortality, new o
r recurrent MI, urgent rev
ascularization at 14 days
GRACE risk sco
re
Recommendation for invasive evaluatio
n (CAG) and revascularization

Urgent • Refractory angina with associated heart failure,


life-threatening ventricular arrhythmia or
(<2h) hemodynamic instability

Early • Grace score > 140 (in-hospital death >3%)


• Relevant rise or fall in troponin

(<24h) • Dynamic ST or T wave change (symptomatic or


silent

Invasive • Recurrent symptom


• Other high risk : DM, eGFR < 60, LVEF <40%,

strategy early post MI angina, recent PCI, prior CABG,


GRACE score 109-140
NSTE-ACS management
Antiplatelet • ASA 300 mg  75-100 mg daily
(both of) • Clopidogrel : 300 mg loading 75 mg daily dose

Anticoagula • Fondaparinux 2.5 mg sc OD (least bleeding) C/I if cr


nt <20mL/min
• Enoxaparin 1mg/kg twice daily ( OD if CrCl <30)
3-8 days • UFH : bolus 60 IU/kg (max 5000 IU)  12 IU/kg/hr titrate to
(Any of) keep aPTT 50-70ms (1.5-2.5 ratio) max 1000 IU/h

• NTG, MO, O2
• Beta-blocker
Other • ACE-I / ARB
• Statin

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