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A Dr(Brig) YD Singh
MBBS, MD (Medicine), FIACM, DIT
Professor (Medicine) & Head
Unit of Medicine, FOM,
AIMST University
 Introduction: ACS
Cardiovascular Disease (CVD) is one of
the main causes of mortality and
morbidity in Malaysia
The estimated incidence of Acute
Coronary Syndrome is 141 per 100,000
population per year
Inpatient mortality rate is approximately
7% (CPG 2011)

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 ACS
A clinical spectrum of ischemic heart
disease and depending upon the
degree and acuteness of coronary
occlusion, it can present as
– Unstable angina (UA)
– Non-ST elevation myocardial infarction
(NSTEMI)
– ST elevation myocardial infarction (STEMI)
These changes may be dynamic.
– A patient presenting with UA may progress
to NSTEMI or even STEMI
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 Spectrum of Coronary Artery Disease

SUB CLINICAL CLINICAL

Stable ACS
Angina

UA STEMI

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 Risk Factors in ACS
Non Modifiable
– Age >
– Sex = Males 10 years earlier that females
– Family H/O premature IHD ( age < 50 yrs)
Modifiable
– Hypertension
– Diabetes mellitus
– Chronic Kidney Disease (CKD)
– Hyperlipidaemia
– Obesity (Central)
– Smoking
– Sedentary life style (Lack of exercise)
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 Pathogenesis ACS
ACS is caused by secondary reduction
in myocardial blood flow due to
– Disruption of atherosclerotic plaques
– Platelet aggregation or thrombus
formation at site of atherosclerotic lesion
– Coronary arterial spasm

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 Vulnerable Plaque

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 Thrombus Formation in ACS
Atherosclerotic plaque formation occurs
through repetitive injury to vessel wall
usually at point of bifurcation of vessels
– When plaque ruptures, potent thrombogenic
substances are exposed to platelets
– These platelets respond by adhesion,
activation, and aggregation thus initiating
thrombus formation in the coronary vessels

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 Ischaemia / Infarction in ACS
Extent of O2 deprivation and thus clinical
presentation of ACS depend on limitation
of O2 delivery by thrombus adhering to
fixed, fissured, or eroded plaques
– Severity and duration of imbalance between
supply and demand determine whether
damage is reversible ( <20 min) or permanent
with myocardial necrosis (>20 min)

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Unstable angina : Classification

1.New onset severe angina (no rest

pain) (Stable to unstable)
2. Angina at rest within past month but
not within preceding 48 hours
– (Angina at rest = subacute)
3. Angina at rest within 48 hours
– (Angina at rest, acute)

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Unstable angina : Classification
It may be further classified according to
clinical circumstances into either:
A) Secondary = Develops in presence
of extracardiac disease
B) Primary = Develops in absence of
extracardiac disease
C) Post-infarct = Develops within 2
weeks of an acute MI

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 Important facts about AMI
(STEMI + NSTEMI)
50% of the patients die before reaching
hospital
50% of deaths within 1 hour of the event
(Ventricular fibrillation)
50% of the patients have non diagnostic
initial ECG (repeat 8 hourly or earlier)

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 NSTEMI
In Non ST elevation MI, Clinical picture
is similar to unstable angina but cardiac
biomarkers are RAISED
In ECG ST-T changes usually present
– ST depression & T inversion
In UA ECG changes usually NOT
present
– If present then are TRANSIENTr
– Cardiac biomarkers are NOT raised

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 STEMI
Diagnosed by RISE and FALL of Cardiac
enzymes + any ONE of followings:
– Clinical history consistent with chest pain of
cardiac ischaemic origin >30 minutes
– ST elevation / new LBBB in ECG
– Imaging evidence of new loss of viable
myocardium or new wall motion abnormality
– Evidence of intra-coronary thrombus by
angiography or autopsy

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 Cardiac Biomarkers in ACS
Cardiac troponins (troponin T or I) are the
recommended biomarkers
– Highly specific & sensitive for myocardial
injury and/or necrosis (infarction)
– Also provide prognostic information
– Correlation between level of troponin &
cardiac mortality / other adverse cardiac
events
Troponin level may not be elevated if test
is done early (<6 hours)
– Should be repeated after 6 hours
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 Cardiac Biomarkers in ACS
Non coronary causes of High Troponins
– Acute Myocarditis
– Acute Pulmonary embolism
– Dissecting aortic aneurysm
– Acute Heart Failure
– Septic shock
– Severe Renal Dysfunction

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 Time course of elevation of serum
Cardiac biomarkers in ACS

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 Presentations of ACS
Chest Pain / discomfort
– Typically vice like, pressing, heaviness, crushing type
– Lasting > 30 minutes (ACS)
– Onset at rest, usually No relief with NTG
– Retrosternal = May radiate to Left /Right /both arms
Lower jaw, Epigastrium
– Associated with
Shortness of breath, cold sweats, palpitation
Cardiac Failure / LVF/ Acute Pulmonary Oedema
Cardiac arrhythmias
Asymptomatic
– Diabetes = due to autonomic neuropathy
Sudden death
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 Cardiac Pain Distribution

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 Physical Examination (1)

Corneal arcus – “ring” around the

periphery of cornea
 Xanthelasma – intracellular lipid
deposits near lower lids
 Arterial – decrease ankle/brachial index
(<.9)
Decreased peripheral pulses
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 Xanthelasma

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 Physical Examination (2)

Bradycardic rhythms are more common

with Inferior wall MI
– in the setting of anterior wall MI,
bradycardia or heart block is very poor
prognostic sign
Extremes of blood pressures are
associated with worse prognosis

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 Physical Examination (3)
 S1 and S2 are often diminished due to
poor myocardial contractility
 S3 is present in 15-20% of pts with AMI
implies a failing myocardium
 S4 is common in pts with long standing
HTN or myocardial dysfunction
 Presence of new systolic murmur is an
ominous sign
signifies papillary muscle dysfunction, flail
leaflet of mitral valve, or VSD
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 EVOLUTION OF ACUTE MI

E F

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 Echocardiography in ACS

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 Coronary Angiography in ACS

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 Nuclear Scan in AMI

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 Acute MI
Impact of Modern Critical Care on Mortality
Short-Term Mortality (%)
40
Defibrillation
30 Hemodynamic
30 Monitoring
-Blockers Aspirin
20
Thrombolysis
15 PTCA
10
6.5
0
Pre-CCU CCU Reperfusion
Era Era Era
Adapted from Antman, Braunwald In:Braunwald ed. Heart Disease p 1184.
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 Management in the Emergency
Department
Provide facilities for defibrillation
Immediate measures:
– High flow oxygen
– IV access
– ECG monitoring
– 12 lead ECG
– IV Analgesic (Inj Morphine 3mg IV repeated
5-15 min interval )

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 Treatment Measures in ST
elevation MI or BBB
General treatment Measures:
– Asprin, 300 mg (Chew & swallow stat)
– Clopidogrel 300 mg stat oral
– Nitroglycerine sublingual: test for Prinzemetal
angina, reversible spasm, anti-ischemic,
antihypertensive effects
– Oxygen: probably indicated in first 2-3 hrs in
all, continue if SpO2 <90%
– Adequate Analgesia: small doses of Morphine
(2-4mg) as needed
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 Reperfusion therapy

PCI
Balloon Angioplasty

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 Reperfusion therapy
Goal

Re-establish
Limit Infarct
Infarct Vessel  Mortality
Size
Patency

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 SIMPLIFIED FLOW CHART INFORMATION

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 Drug Eluting Stent By PCI

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 Thrombolysis
Streptokinase :
– 1.5 million units in 100ml saline over 30-60
mins
Tissue Plasminogen Activator (rt-PA):
– Accelerated dose :15 mg bolus+50mg in 30
min +35 mg in 30 min =100mg in 1 hr

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 Thrombolytic therapy
No benefit in UA/ NSTEMI unlike in
STEMI where it is the cornerstone of
therapy

In UA / NSTEMI thrombolytic therapy is

harmful as thrombin generated during
thrombolysis can convert subtotal
occlusion in UA to total occlusion

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 Thrombolysis in Acute MI
Relative Contraindications

 Uncontrolled HTN (BP > 180/110) on presentation

 History prior CVA beyond 1 yr
 Anticoagulant Rx with INR > 2-3; bleeding diathesis
 Recent trauma (within 2-4 wks)
 Noncompressible vascular punctures
 Recent internal bleeding (within 2-4 wks)
 Pregnancy
 Active peptic ulcer
 Prior exposure (5 day - 2 yr) for SK or APSAC

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 Thrombolysis in Acute MI
Absolute Contraindications

 Previous hemorrhagic stroke

 CVA within previous yr
 Intracranial neoplasm or AVM
 Active internal bleeding (not menses)
 Suspected aortic dissection

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 Acute MI
PTCA vs Lysis
Death
Death ++ MI
MI (%)
(%)
20
20
Thrombolysis
PTCA
15
15

10
10

55

p<0.0001
00
00 22 44 66
Months
Months from
from Randomization
Randomization

11 RCTs (2725 patients) PCAT Collaborative Group, 2001

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 Aspirin in Acute MI
ISIS-2
35 Day Mortality (%)
20

15
13.2
10 10.7 10.4
8
5
4300 4295 4300 4292
0
Placebo ASA SK SK + ASA

ISIS-2 Collaborative Group, Lancet 1988;2:349.

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 Cardiac Risk Factors
Management
Stop smoking
Treat hyperlipidaemia – Statin
Treat Diabetes Mellitus aggressively
Weight reduction
Regular exercise
– (120-150 Min/ 5-6 days a week)
Cut down on alcohol
Hypertension control
Healthy diet
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 Heparin in Acute MI

• Intravenous heparin recommended with t-PA

(initial bolus 5000 U, infusion 1000 U/hr, adjust for
weight < 50 kg)
• No clear data for benefit with streptokinase and
increased bleeding
• Discontinue after 24 hrs, except for:
 atrial fibrillation
 recurrent ischemia
 anteroapical MI for CVA prophylaxis

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 Beta blockers in Acute MI
•Reduces subsequent MI / Recurrent Ischaemia
•Decreases HR , BP, myocardial O2 demand
•Metoprolol : 5mg IV 5min apart, 3doses
50mg BD PO
•Atenolol : 10 mg IV stat ; 50mg daily PO
•Esmolol: 0.5mg/kg IV bolus;
0.05mg/kg/min infusion
•Contraindication : Bradycardia, AV block,
Hypotension, Pul
oedema,
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Br Asthma
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 Ace Inhibitors / ARBs in Acute MI
• Long term benefit

• Reduces recurrent MI, need for

revascularization

• Benefits due to improvement in

endothelial functions, plaque
stabilization, anti-inflammatory, anti-
thrombotic and vasodilatory properties

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 Complications of Acute MI

Extension / Ischemia Arrhythmia

Pericarditis

Expansion / Aneurysm Acute MI RV Infarct

Mechanical Heart Failure Mural Thrombus

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 Late Management of Myocardial
Infarction
Risk stratification
Lifestyle Modification:
– Stop smoking
– Regular exercise
– Diet (weight control, lipid lowering)
Secondary Prevention drug therapy:
– Antiplatelety drug(aspirin 0r clopidogrel
– Beta blocker Ace Inhibitor
– Statin
– Additional therapy for control of DM, HTN
Rehabilitation

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