ACUTE CORONARY

SYNDROME
A BREIF REVIEW

Dr. R.NIRANJAN REDDY MD.,DM

Definition of Atherosclerosis & ACS

Etiology and pathogenesis
UA, NSTEMI, and STEMI
Patient approach & Risk stratification
Management

ATHEROSCLEROSIS DEFINITION

Atherosclerosis
A progressive inflammatory disorder of the

arterial wall that is characterised by focal lipid

rich deposits of atheroma that remain clinically
silent
until they become large enough to impair tissue
perfusion , or
until ulceration and disruption of the lesion
result in thrombotic occlusion or distal
embolisation of the vessel.

AHA CLASSIFICATION OF ATHEROSCLEROSIS

DEFINITIONS

CAD is a continuum of disease.

Stable angina -> unstable angina -> AMI -> sudden cardiac

death

Acute coronary syndrome

encompasses Unstable angina,

NSTEMI, STEMI
Stable angina transient episodic chest pain due to

myocardial ischaemia,comes during exertion, reproducible ,

frequency constant over time, usually relieved with rest or NTG.

Canadian Cardiovascular Association

Classification of Angina
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

Definition Of ACS
A constellation of symptoms related to

obstruction of coronary arteries with chest pain

being the most common symptom in addition to
nausea , vomiting, diaphoresis etc.
Chest pain related to ACS is often
radiating to the left arm or angle of the jaw
pressure-like in character
associated with nausea and sweating.
Chest pain is often categorized into typical and
atypical angina.

UNSTABLE ANGINA
Angina pectoris (or equivalent type of ischemic

discomfort) with at least one of three features:

(1) occurring at rest (or minimal exertion) and
usually lasting >20 minutes (if not interrupted by
the administration of a nitrate or an analgesic);
(2) being severe and usually described as frank
pain; or
(3) occurring with a crescendo pattern (i.e., pain
that awakens the patient from sleep or that is
more severe, prolonged, or frequent than
previously).

UNSTABLE ANGINA
65% of patients with unstable angina have

evidence of myocardial necrosis -NSTEMI

Elevated cardiac serum markers, such as

cardiac-specific troponin T or I and creatine

kinase isoenzyme (CK)MB,
ECG normal or ST depression(>0.5mm), T

wave changes

ACUTE MYOCARDIAL INFARCTION

ACC DEFINITION rise and fall in cardiac enzymes with one or

more of the following:

Ischaemic type chest pain/symptoms
ECG changes ST changes, pathological Q waves
Coronary artery intervention data
Pathological findings of an acute MI

STEMI = SYMPTOMS + ST ELEVATION ON ECG +

ELEVATED CARDIAC ENZYMES

NSTEMI

= UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES + NO ST ELEVATIONS BUT
ST DEPRESSIONS (or) T INVERSIONS

Classification of MI
Type 1spontaneous MI related to ischaemia due to a

primary coronary event such as plaque fissuring,

erosion or rupture, or dissection
Type 2myocardial infarction secondary to ischaemia
due either to increased oxygen demand or to decreased
supply (e.g. coronary spasm or embolism, anaemia,
arrhythmias, hypertension, or hypotension)
Type 3sudden unexpected cardiac death, including
cardiac arrest, with symptoms suggestive of myocardial
ischemia, accompanied by new ST elevation, or new left
bundle branch block, or definite new thrombus by
coronary angiography (death before blood samples
obtained) or in the lag phase of cardiac biomarkers
Type 4MI associated with PCI
Type 5MI associated with CABG

STEMI: ECG
Hyper acute T waves, ST elevations followed by T

wave inversions, Q waves.,

Clinically significant ST segment elevations:

> than 1 mm (0.1 mV) in at least two contiguous limb leads

or 2 mm (0.2 mV) in two contiguous precordial leads (V2
and V3)Note: LBBB and pacemakers can interfere with
diagnosis of MI on EKG

NSTEMI:
ST depressions (0.5 mm at least) or T wave

inversions ( 1.0 mm at least) without Q waves in 2

contiguous leads with prominent R wave or R/S
ratio >1.
Associated with rise in Troponin or CK-MB levels
Isolated T wave inversions:
can correlate with increased risk for MI
may represent Wellens syndrome:
critical LAD stenosis
>2mm inversions in anterior precordial leads

UA/NSTEMI Pathophysiology
Plaque rupture or erosion with

superimposed nonocclusive thrombus - most

common cause of UA/NSTEMI
Dynamic obstruction due to
a. spasm of an epicardial coronary artery, as in
Prinzmetal angina or variant angina
b. constriction of the small, intramural muscular
coronary arteries, that is, the coronary resistance
vessels
c. local vasoconstrictors, such as thromboxane
A2, released from platelets;
d. dysfunction of the coronary endothelium
e. adrenergic stimuli including cold and cocaine.

Severe coronary luminal narrowing -

Progressive coronary atherosclerosis or

post percutaneous coronary intervention
restenosis;
Secondary unstable angina - severe

myocardial ischemia related to increased

myocardial oxygen demand or decreased oxygen
supply (e.g., tachycardia, fever, hypotension, or
anemia).

Individual patients may have several of these

processes coexisting as the cause of UA/NSTEMI.

Pathophysiology of ACS

APPROACH TO THE PATIENT WITH

ACUTE ONSET CHESTPAIN

Identifying those with chest pain suggestive of IHD/ACS.

Thorough history required
Character of pain , Onset and duration, Location and radiation,

Aggravating and relieving factors, Autonomic symptoms

Failure to recognise symptoms other than chest pain -> approx

2 hr delay in seeking medical attention

Identifying ischaemic cardiac pain: the

balance of evidence.

TOOLS USED IN RISK STRATIFICATION

HISTORY

ECG

BIOCHEMICAL MARKERS

2D ECHO

ELECTROCARDIOGR
APHY
ECG should be obtained within 10 minutes after

presentation in patients with ongoing chest

discomfort ,
Helps in identifying patients who might benefit
from immediate reperfusion therapy (mechanical
or pharmacologic)
The ECG provides critical information for both
diagnosis and prognosis.
New persistent or transient ST-segment
abnormalities (0.05 mV) that develop during a
symptomatic episode at rest and resolve when
the symptoms resolve strongly suggest acute
ischemia and severe coronary disease.

Nonspecific ST-segment and T wave

abnormalities -- defined as lesser amounts of

ST-segment deviation or T wave inversion of
0.2 mV or less, and are less helpful for risk
stratification.
A completely normal ECG does not exclude
the possibility of ACS;
the risk of acute MI is about 4% among
patients with a history of coronary artery
disease and 2% among patients with no such
history.
Patients with a normal or near-normal ECG
have a better prognosis than patients with
clearly abnormal ECGs at presentation.

Diffuse ST-segment elevation and PR-segment depression

suggest pericarditis.
Right axis deviation, right bundle branch block, T wave
inversions in leads V1 to V4, and an S wave in lead I and
Q wave and T wave inversion in lead III suggest
pulmonary embolism (S I Q3 T3 PATTERN).
The availability of a prior ECG improves diagnostic
accuracy and reduces the rate of admission for patients
with abnormal baseline tracings.
Serial electrocardiographic tracings improve the
clinicians ability to diagnose acute MI, particularly if
combined with serial measurement of cardiac
biomarkers.
Posterior leads can be useful for identifying ischemia in
the territory supplied by the left circumflex coronary
artery, which is otherwise relatively silent
electrocardiographically.

Thrombolysis In Myocardial Ischemia (TIMI) risk score for unstable

angina or nonST elevation myocardial infarction (UA/NSTEMI).

TIMI risk score for UA/NSTEMI to predict the

benefit of an early invasive strategy.

The TIMI risk score was

applied in the Treat
Angina with Aggrastat
and determine Cost of
Therapy with an Invasive
or Conservative Strategy
(TACTICS)TIMI 18 trial.
As shown, 75% of
patients had a risk score
of 3 or higher, and a
significant benefit of an
invasive strategy was
observed in these
patients

ACUTE IWMI

ECG in ACS- NSTEMI

CHEST RADIOGRAPHY.
A chest X-RAY typically obtained in all patients

presenting with chest pain.

It is usually nondiagnostic in patients with ACS,
but can show pulmonary edema caused by
ischemia-induced diastolic or systolic
dysfunction.
It is more useful for diagnosing or suggesting
-- may show a widened mediastinum or aortic
knob in aortic dissection.
-- The chest radiograph is usually normal in
pulmonary embolism,
-- but can show atelectasis, an elevated
hemidiaphragm, a pleural effusion or, more
rarely, Hamptons hump or Westermarks sign.
-- can reveal pneumonia or pneumothorax.

BIOCHEMICAL MARKERS OF
MYOCARDIAL NECROSIS
CREATINE KINASE MB ISOENZYME.
Major limitation to CK-MB as a diagnostic biomarker

is its relative lack of specificity

CK exist in 3 Isoenzyme forms (MM, BB, and MB).
Brain and kidney -- BB isoenzyme
Skeletal muscle -- MM, but also contains some
MB (1% to 3%)
Cardiac muscle --- both MM and MB isoenzymes.
The MB isoenzymes of CK can also be present in
small quantities in the small intestine, tongue,
diaphragm, uterus, and prostate.
Strenuous exercise, particularly in trained longdistance runners or professional athletes, can cause
elevation of both total CK and CK-MB.

Use of the CK-MB relative index (the ratio of CK-MB to

total CK) partially addresses this limitation for skeletal

muscle as a source.
CK-MB - increased from skeletal muscle in patients
with conditions that cause chronic muscle destruction
and regeneration, such as muscular dystrophy, highperformance athletics (e.g., marathon running), or
rhabdomyolysis or muscular trauma.
One advantage of CK-MB--shorter half-life in the
circulation
Useful for gauging the timing of an MI
A normal CK-MB with an elevated troponin level could
represent a small MI or an MI that occurred several
days ago
For diagnosing reinfarction in a patient who has had
an MI in the past week.

TROPONINS
Different genes encode troponins I and T in cardiac

muscle, slow skeletal muscle, and fast skeletal muscle

Assays for cardiac troponins are more specific than the

assay for CK-MB for myocardial injury

Cardiac troponin is the preferred diagnostic biomarker.

The high specificity of cardiac troponins for

myocardium make false-positive elevations (i.e., an

elevated cardiac troponin in the absence of myocardial
injury) exceedingly rare.

Elevations in the absence of other

clinical data consistent with an ACS

usually represent true myocardial damage from
causes other than atherosclerotic coronary artery
disease.
Such damage may occur with
Myocarditis, myocardial contusion, or
cardioversion or defibrillation,
Left ventricular strain from congestive
heart failure , hypertensive crisis, or
extreme exercise,
Right ventricular strain from pulmonary
embolus, or other causes of acute
pulmonary hypertension.
Patients with renal disease, severe

With serial sampling up to 12 hours after

presentation , cardiac troponins offer a

sensitivity higher than 95% and a
specificity of 90%.
When using only a single sample at presentation,
performance has been substantially worse, with a
sensitivity of only 70% to 75%.
Sensitive assays - offer a lower limit of
detection, (approx. 0.001 to 0.01 ng/mL) and
acceptable imprecision at low levels that, are now
below the 99th percentile in a normal reference
population (typically 0.01 to 0.07 ng/mL), thereby
improving the ability to detect myocardial injury.
Using such assays, the sensitivity for detecting
myocardial infarction using a single sample at
presentation is approximately 90%, the specificity

UNSTABLE ANGINA /NSTEMI TREATMENT

Oral Antiplatelet Therapy

Aspirin Initial dose of 325 mg nonenteric

formulation followed by 75162 mg/d of an enteric or

a nonenteric formulation
Clopidogrel Loading dose of 300-600 mg followed
by 75 mg/d
Prasugrel Pre-PCI: Loading dose 60 mg followed
by 10 mg/d
Intravenous Antiplatelet Therapy
Abciximab 0.25 mg/kg bolus followed by infusion
of 0.125 g/kg per min (maximum 10 g/min) for 12 to
24 h
Eptifibatide 180 g/kg bolus followed by infusion of
2.0 g/kg per min for 72 to 96 h
Tirofiban 0.4 g/kg per min for 30 min followed by
infusion of 0.1 g/kg per min for 48 to 96 h

Heparins :
Unfractionated Heparin (UFH) -

Bolus 60
70 U/kg (maximum 5000 U) IV followed by
infusion of 1215 U/kg per h (initial maximum
1000 U/h) titrated to a PTT 5070 s
Enoxaparin - 1 mg/kg SC every 12 h; the first
dose may be preceded by a 30-mg IV bolus; renal
adjustment to 1 mg/kg once daily if creatine Cl <
30 cc/min
Fondaparinux - 2.5 mg SC OD
Bivalirudin - Initial bolus intravenous bolus of
0.1 mg/kg and an infusion of 0.25 mg/kg per
hour. Before PCI, an additional intravenous bolus
of 0.5 mg/kg was administered, and the infusion
was increased to 1.75 mg/kg per hour.

Class I Recommendations for Use

of an Early Invasive Strategy (PCI)
Class I (Level of Evidence: A)indications
Recurrent angina at rest/low-level activity

despite Rx
Elevated TnT or TnI
New ST-segment depression
Angina/ischemia with CHF symptoms, rales, MR
Positive stress test
EF < 0.40
Decreased BP
Sustained VT
PCI< 6 months, prior CABG
High-risk score

STEMI Management
Initial management for STEMI:
Cardiac monitor
Supplemental O2
Nitrates
Beta blocker
Morphine
Clopidogrel
Aspirin
Good IV access
Call cardiologist immediately after seeing ECG OF
MI

Major components of time delay between onset of infarction

and restoration of flow in the infarct-related artery.

Importance of time to
reperfusion in patients
receiving
fibrinolytic
The data from
22 trials of
therapy
for
STEMI.
fibrinolytic therapy were

pooled and the findings

stratified by the six time
categories shown in the
figure.

Because the
lifesaving effect of
fibrinolysis is
maximal in the first
hour from onset of
symptoms, this has
been referred to as
the golden hour
for pharmacologic
reperfusion.

The kinetics of release of CK-MB and cardiac troponin in patients

who do not undergo reperfusion are shown in the solid blue and
pink curves as multiples of the upper reference limit (URL).

TIMI risk score for STEMI predicting 30-day mortality.

Classic shock paradigm is shown in pink. The influence of

the inflammatory response syndrome initiated by a large MI
is illustrated in black coloured arrows

Emergency management of complicated STEMI.

Conclusions
ACS is the major cause of mortality
Care full history about chest pain onset, characteristics ,

associated symptoms , and risk stratification using history

and ECG ,Bio markers is needed for identifying high risk
patients who need early invasive strategy
Chest pain protocol implemention and avoiding time
delays in transport, trying to achieve ideal door to
needle and door to balloon time are essential in
reducing the area of infarct and preventing complications
Carefull serial monitoring of vitals and serial ECG are
essential things in managent of ACS patients
Main risk factors Diabetes , HTN, Hyperlipidemia ,
smoking , alchohol , obesity are to be managed
effectively as primary and secondary prevention measures.

THANK YOU ALL

ALL

THANK

YOU