m INTRODUCTION ²

EPIDEMIOLOGY/PREVALENCE/DEFINITION

m PATHOPHYSIOLOGY OF ACUTE CORONARY

SYNDROMES

m APPROACH TO SUSPECTED ACUTE

CORONARY SYNDROME ² GUIDELINE
UPDATE

m TREATMENT/MANAGEMENT UPDATE
m Coronary Artery Disease ² leading
cause of morbidity & mortality in
industrialized nations.
m Although decrease in cardiovascular
mortality  still major cause of
morbidity & burden of disease.
m HIGH RISK POPULATION FOR CAD/ACS:
INDIAN

m Increasing due to
Lifestyle/socioeconomic changes,
urbanization

m In US ² 2004 ² 1.56 million admissions for

ACS ² 669 000 for unstable angina, 896
000 for MI
m CAD is a continuum of disease

m Angina -> unstable angina -> AMI ->

sudden cardiac death

m Acute coronary syndrome encompasses

unstable angina, NSTEMI, STEMI

m Stable angina ² transient episodic chest

pain d/t myocardial ischemia,
reproducible, frequency constant over
time. usually relieved with rest/GTN.
CLASS 1 NO PAIN WITH ORDINARY PHYSICAL
ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL

ACTIVITY ±PAIN OCCURS WITH
WALKING, CLIMBING
STAIRS,STRESS
CLASS 3 SEVERE LIMITATION OF DAILY
ACTIVITY ± PAIN OCCURS ON
MINIMAL EXERTION
CLASS 4 UNABLE TO CONDUCT ANY
ACTIVITY WITHOUT PAIN, PAIN AT
REST
m Pain occurring at rest ² duration > 20min
m New onset angina ² ~ Class 2 severity
m Worsening of chest pain ² increase by at
least 1 class, increases in frequency,
duration
m Angina becoming resistance to drugs
that previously gave good control.

ECG ² normal, ST depression(>0.5mm), T

wave changes
m ECC/ACC DEFN ²rise and fall in cardiac enzymes
with one or more of the following:
m Ischemic type chest pain/symptoms
m ECG changes ² ST changes, pathological Q waves
m Coronary artery intervention data
m Pathological findings of an acute MI

m NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES
m STEMI = ST ELEVATION ON ECG + SYMPTOMS
m5 -17% suffer an MI within a week
after admission.
m 3 -15% die within a year.
m Distruption of coronary
artery plaque -> platelet
activation/aggregation
/activation of
coagulation cascade ->
endothelial
vasoconstriction -
>intraluminal
thrombus/embolisation -
> obstruction -> ACS
m Severity determines
characteristics of clinical
presentation
m Identifying those with chest pain suggestive
of IHD/ACS.
m Thorough history :
m Character of pain
m Onset and duration
m Location and radiation
m Aggravating and relieving factors
m Autonomic symptoms
CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF
ANGINA
TYPE OF PAIN DULL SHARP/STABBING
PRESSURE/CRUSHING
PAIN
DURATION 2-5 MIN, <20 MIN SECONDSTO
HOURS/CONTINUOUS
ONSET GRADUAL RAPID

LOCATION/CHEST WALL SUBSTERNAL, NOT LATERAL CHEST

TENDERNESS TENDER TO PALP. WALL/TENDER TO PALP.
REPRODUCIBALITY WITH WITH
EXERTION/ACTIVITY BREATHING/MOVING
AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT
m RISK FACTORS FOR DEVELOPING ATYPICAL
PAIN:
m Diabetes, females, non white patients,
elderly, dementia, no prior history of MI
m ATYPICAL SYMPTOMS:
m GIT symptoms
m Syncope
m SOB
m Pleuritic/positional pain
m Chest wall tenderness
m No chest pain/symptoms
m MI without chest pain -> increased risk
of death (23% vs 9%)
m More complications ²
hypotension,heart failure, stroke
m Delayed ED presentation, delayed
intervention
m Provides prognostic information

m Determines treatment and level of intervention ->

low risk patients ²early discharge, high risk ->
admission to high care

m Helps decongest the ED and make available

medical resources to more needy patients

m Risk stratification should be ongoing ² at admission,

6-8 hrs, 24hrs, discharge
m HISTORY

m ECG

m BIOCHEMICAL MARKERS
m First point of entry into ACS algorithm

m Neither 100% sensitive or 100% specific for AMI

m Single ECG for AMI ² sensitivity of 60%, specificity

90%

m Represents single point in time ²needs to be read in

context

m Normal ECG does not exclude ACS ² 1-6% proven

to have AMI, 4% unstable angina
m Initial 12 lead ECG ² goal door to ECG time
10min, read by experienced doctor
m If ECG not diagnostic/high suspicion of ACS
² serial ECGs initially 15 -30 min intervals

m ECG adjuncts ² leads V7 ²V9, RV 4

m Continuous 12 lead ECG monitoring

reasonable alternative to serial ECGs
IDEAL MARKER:
m High concentration in myocardium
m Myocardium specific
m Released early in injury
m Proportionate to injury
m Non expensive testing

m Troponins
m CKMB
m Myoglobin
m Other markers
m Troponin T vs I ²
m both equivalent in diagnostic and
prognostic abilities ( except in renal failure ²
Trop T less sensitive)

m Elevation ~ 2hrs to 12hrs

m ~30 ² 40% of ACS patients without ST

elevation ² had normal CKMB but elevated
troponins on presentation
m Rapid release within 2 hours

m Not cardiac specific

m Rule out for NSTEMI rather than rule in.

CKMB
Used in conjunction with troponins
Useful in diagnosing re-infarction
HEART FATTY ACID BINDING PROTEIN (HF ABP)
m Identifies AMI <4hrs after onset
m Protein involved in myocardial lipid
synthesis, but also expressed outside heart
m Therefore may be sensitive but not specific
for injury
m Possible role in multi-marker strategy
m Cardiac MRI
m Multidetector CT for coronary
calcification
m Coronary CT angiography
m Undergoing clinical evaluation
m Cardiac biomarkers measured in all
patients with suspicion of ACS
m Troponin preferred marker
m If troponin negative within 6 hours of onset,
repeat 8-12hours later
m Remeasuring of positive biomarkers to
determine infarct size/necrosis
m Patients presenting within 6 hours of
symptom onset ² myoglobin in
conjunction with troponin measured
(Class 2b B)
m 2hr delta CKMB/Delta troponin
considered in <6hr presentation
m BNP level ² for global risk assessment
m Class 3 ² AST/LDH/CK without CKMB
m 2007 ACS/AHA GUIDELINES:
m Risk stratification models useful in decision making with regard
to treatment options ( Class 2a B)
m TIMI vs GRACE vs PURSUIT

m PURSUIT & GRACE risk scores allow better discrimination of in

hospital and 1 year mortality in patients compared to TIMI.
(à
 
    à

m What·s   

2007ACS/AHA GUIDELINES:
Rapid catergorisation of patient

Possible ACS, non diagnostic ECG/biomarkers ²

observed in facility with cardiac monitoring

Alternative to in patient treatment: for those with 12hr

ECG/markers negative ² stress ECG in 72hrs

Giving precautionary treatment for those for OPD

stress
m Early invasive strategy for refractory
angina, hemodynamic instability
m Early invasive strategy for stabilised
patients with elevated risk for clinical
events.
m Recurrent angina, ischaemia at rest or
minimal activity
m Elevated troponins
m New ST depression
m Signs of heart failure/worsening mitral
regurg.
m Ventricular tachycardia
m Prior CABG
m PCI in last 6 months
m High TIMI/GRACE scores
m LVEF < 40%
m Invasive strategy -not recommended in
patients with multiple co morbidities, low risk
patients, patients not consenting.
m GENERAL:

m IV B Blockers downgraded from Class 1 to 2a

recommendation. (COMMIT Trial)

m Oral B Blockers in first 24hrs still Class 1 ² but not used in signs of
heart failure, cardiogenic shock and reactive airway
disease.(LOE B)

m MORPHINE downgraded from Class 1 to 2a ² findings from

CRUSADE Registry
m ANTIPLATELET THERAPY:
CLASS 1 RECOMMENDATION
m Aspirin to all patients as soon as possible and
continued (if no C/I)
m Initial dose 162 -325mg
m Maintenance 75 -162mg
m No added benefit from higher doses except post
stenting

m Clopidogrel for those allergic to aspirin or major GI

bleeding (LOE A)

m For initial invasive strategy ² aspirin + clopidogrel or

IV glycoprotein 2b/3a therapy
m Anticoagulant therapy should be added as
soon as possible
m For patients undergoing angiography/PCI ²
enoxaparin/UFH of Bivalirudin/ fondaparinux

m For conservative strategy: enaxaparin, UFH,

fondaparinux

m For patients with increased risk of bleeding

with conservative strategy ² fondaparinux
m STRESS TEST should be performed for those
managed conservatively.
m If stress test positive/ high risk ² needs
diagnostic angiography

m If classed as low risk ²

m need to continue aspirin indefinitely
m Clopidogrel for at least 1 month, ideally up
to 1 year
m MORPHINE: titrated doses

m NSAIDS/COX 2 INHIBITORS: those on it should

have it discontinued ( increased risk of
mortality, re infarction, heart failure,
myocardial rupture)

m NSAIDS should not be administered in

hospital for MI
m Oral Beta Blockers should be initiated
in first24rs, if no contra-indications
(heart failure, risk of cardiogenic
shock)
m Patients with early contraindications ->
re- evaluated later for possible use
m Role of IV B blockers ² used in
hypertensive patients with STEMI
m Increase use of prehospital 12 lead ECG
emphasised.

m In PCI capable hospital ² door to PCI time

90 min

m In non PCI capable hospital ² door to

needle time 30 min or timeout transfer to
PCI capable hospital.
AVAILABLE FIBRINOLYTICS:
m STREPTOKINASE ² 1.5mu infusion over
30min (1hour ²ACLS)
m rtPA ² accelerated infusion over 1.5hrs
m - 15mg IV bolus, 0.75mg/kg over
30 min, 0.5mg/kg over 1hr
m ANISTREPLASE ² 30 U IV over 5 min
m TENECTEPLASE ² 30 TO 50 MG
m RETEPLASE ² 10 U IV bolus,10U IV after
30 min
m INCREASED FOCUS ON SECONDARY PREVENTION:

m SMOKING CESSATION

m DIET MODIFICATION/WT CONTROL

m BP CONTROL

m LIPID MANAGEMENT

m EXERCISE

m DIABETES MANAGEMENT
m Despite good reperfusion strategies approx.
1/3 of patients worldwide miss out.
m Attributed to ² delayed presentation,
atypical presentation, complicated disease
presentation, older age

m SYMPTOMS OF INFARCT BUT NO

ESTABILISHED ECG CHANGES - keep in mind
aortic dissection, GIT disease, other chest
pathology
m With increase burden of CVD, and lack of health resources
risk stratification becomes important.

m Emphasis should also be placed on primary &secondary

prevention of ACS.

m Early intervention helps prevent complications, decreases

morbidity & mortality

m The way forward ² fully equipped CHEST PAIN OBSERVATION

UNIT