Acute coronary syndrome

SHAMMITHA.S

Unstable angina/NSTEMI

UA
-New onset(< 2 months) angina.
- That is severe (angina with mild exertion) and or frequent(> 3
episodes/day).
- accelerating angina previously chronic stable angina which
becomes more frequent, severe,prolonged, or precipitated by less
exertion than before.
- angina at rest (>20min).
- development of unstable symptoms carries a 10-20% risk of
progression to AMI .

Definition(ACS)

Acute coronary syndrome (ACS) is the name given to several syndromes which are caused
by the sudden formation of blood clots (thrombosis) within a coronary artery.
These blood clots are generally caused by rupture of a plaque in the wall of the artery. The
clots produce partial or complete blockage of the artery, leading to ischemia (insufficient
blood flow to the heart muscle).
The type of ACS syndrome that occurs depends on the degree of blockage produced by the
clot, and how long the clot persists.
When ACS is diagnosed, further stratification into categories of ST-elevation myocardial
infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina
[SPECTRUM] guides therapeutic decision-making.

Clinical feature n diagnosis..

Symptoms
-chest pain/discomfort,usually retrosternal, central or in the left chest, may radiate to jaw or
down upper limb. -may be crushing or burning in nature.
-severity of pain is variable
-may be difficult to differentiate between symptoms of STEMI and UA/NSTEMI.
-some patients may present with acute left venricular failure
-atypical presentations include unexplained fatigue,sortness of breath,epigastric discomfort,
nausea,vomiting
Physical examination
-to identify precipitating factors and consequences of UA/NSTEMI
Investigations
-ECG during episodes of chest pain is especially valuable. Repeat ECG may be necessary to
make a diagnosis. Features sugessting UA/NSTEMI are:
-ST segment depression
-T wave inversion

Continued..

troponin,cardiac enzymes( CKMB,AST,LDH)

Echocardiography
CXR,FBC,PT,PTT,LFT, creatinine,BUSE, glucose and lipid profile.

Differentiating UA from NSTEMI

-If ischaemia is severe enough to cause myocardial damage,detectable

quantities of a marker of myocardial injury, most commonly troponin
I, troponin T and creatine kinase MB( CK-MB) will be released.
-If no elevated biochemical marker is detected the patient is said to
have UA.
-NSTEMI is diagnosed if an elevated biochemical marker is present.

Management of ACS
Beta-blocker contraindicated
Yes

No
Aspirin + Clopidrogel +
Heparin + IV nitrate +
statin + beta-blocker

Aspirin + Clopidrogel
+Heparin + IV nitrate +
Statin +Ca antagonist
Control in 24 hours

Yes
No

Risk factor ++
Exercise stress ECG

Consider coronary
angiography

Positive

Negative
Medical Therapy
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Continued.

General measures

admit CCU for observations. monitor cardiac rhythm for 24-48hour. Patient are encouraged
to report any recurrence of pain.
Bed rest, sedation and analgesics should be administered as in AMI.
IV morphine is recommended for patients with or recurrent symptoms despite anti ischaemic
therapy.
BP every 15-30 min for a few hr, then every 1-2 hr.
IV line for drug administration.
Oxygen via nasal prongs.
Serial ECG and cardiac enzymes to detect AMI and silent recurrent ischaemia
Other coronary risk factors (e.g. diabetes mellitus, hypercholesterolaemia) and precipitating
factors( e.g. anaemia) should be treated.

Anti thrombotic therapy

2)Anti thrombotic therapy
a)Anti platelet
-choice of agents :- cyclo-oxygenase inhibitors:

(aspirin)
-adenosine diphosphate
receptors antagonists:
( clopidogrel,ticlopidine)

Continued..
b)Anticoagulants
-IV unfractionated heparin (UFH) decreases incidence
of MI in patients with UA.
c)Platelet glycoprotein IIb/IIIa receptor antagonists
-Abciximab(reopro)
-Epitofibatide(intergrilin)
-tirofiban(aggrastat)

Continued..
3)Beta blocker.
Propranolol or metoprolol
4)Nitrates
Sublingual nitroglycerine
IV nitroglycerin

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Continued..

5)Calcium channel blockers

Nifedipine,verapamil,dilitiazem
6)Statin therapy
7)Angiotensin converting enzyme inhibitor(ACEi)
and angiotensin receptor blockers(ARB)
8)Correct precipitating factors
9)Invasive therapy; urgent cardiac catheterization

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Acute myocardial infarction( STEMI)

A)RISK FACTORS.
Abnormal serum lipids (elevated total cholesterol, high LDL cholesterol, low HDL
cholesterol, smoking, hypertension, family history of premature CAD, age male>55, female>
65, DM
B) ANATOMICAL COLLERATIONS.
VESSELS OCCLUDED
-left ant desc.artery
-left circumflex artery
-right coronary artery

area of infarction
ant wall on the left vent. (LV), ant part of the
septum (affect intraventricular conduction).
lateral or inf. walls of the LV & post wall of
LV.
post and inf. Surface of the LV, post part of
the septum, RV.AV node 90% cases
SA node 60% cases

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Clinical features..
-pain:- retrosternal,>20mins, radiation to the
arms, neck and jaw.
-severe and crushing in nature not relieved
by GTN.
SYMPTOMS
-Sweating, nausea,vomiting,dyspnoea,weakness,
restlessness and anxiety
-25% are asymp.&detected by ECG
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INVESTIGATIONS
1)ECG..-provides valuable information on the size, extent, age of the MI and some
anatomical correlations of vessels occluded.
a)
STEMI( Q wave infarction)
ECG changes
onset
duration
ST elevation
within mins or hours
days or weeks
T inversion
immediate or hours
several months
Q wave
hours or days
remain indefinitely
b) NSTEMI (non Q wave infarction)
- Changes are prolonged ST depression and T inversions
- NSTEMI generally results frm incomplete occlusion or spontaneous lysis of
thrombus and is associated with higher incidence of reinfarction and recurrent
ischaemia.

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Continued..

Localization on infarction area.

Infarct site
Ant
-small
-extensive
Anteroseptal
Anterolateral
Lateral
Inf.
Post.
Subendocardial (non Q)

lead showing main changes

V3-V4
V2-V5
V1-V3
V4-V6,I,AVL
I,AVL,V5-V6
II.III,AVF
VI-V2( reciprocal ST DEPRESSION), tall R waves in V1V2, ST elevation in post leads(V7-V9)
Any lead
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2) Cardiac enzymes
Ck: creatine kinase

AST:aspartate aminotransferase

LDH-lactic dehydrogenase

HBD-hydroxybutyrate dehydrogenase
Enzymes are measured in the first 3 days following a suspected MI.
TROPONIN T
-cardiac specific protein
- undetactable in healthy people
-appears in circulation as early as 2.5 hours after onset of chest pain and remains
elevated for > 7 days post-infract
- can be measured using rapid assay kit

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Continued
Troponin I
- Not detectable in healthy individuals.
- highly specific and sensitive for myocardial
tissue injury.

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Continued

MI is diagnosed with troponin T( cTnT) or

(cTnI) level above the 99th percentile at least
once within 24 hrs of index clinical event.
Small infarct may be missed just by
measuring CK-MB. Troponins should be
measured for patients suspected to have
STEMI with (-) serial CK-MB
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Continued

3) other diagnostic techniques

a)Radionuclide studies
Pyrophosphate scan-useful when the ECG is
unhelpful due to preexisting abnormalities or
when patient presents late and cardiac
enzymes are no longer elevated or unreliable
(test is only optimal 2-7 days after AMI)
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CONTINUED
b)ECHOCARDIOGRAPHY
Images the cardiac structures, pericardium, and aorta
allowing identification of regional wall motion
abnormalities, valvular abnormalities as well as
global, left and right ventricular function
c)Coronary angiography
Interventional treatment is indicated then its
performed. In the peri -infarct period, thrombus is
known to appear and vanish with spontaneous
reperfusion.
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continued

d)General investigations
FBC,BUSE, blood sugar, cholesterol( within
24 hours or 3 months after MI) CXR, serum
creatinine, coagulation profile.

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Management STEMI..

Clinical features, ECG +/- biochemical markers

suggestive of STEMI

Rapid examination to exclude hypotension and acute pulmonary oedema

ECG monitoring
Aspirin and clopidogrel
Statin
Analgesia
Sedation
Others

Reperfusion therapy

Thrombolysis if no
contraindication

Primary PCI if available

Beta-blocker if no contraindication

Not for reperfusion therapy

e.g>12hrs,contraindicated for
thrombolysis but primary PCI not
available

ACE inihibitor especially anterior MI,CCF,EF<40% or HPT

Monitoring and treatment of

complications

Nitroglycerin IV if chest pain or pulmonary oedema

Rehabilitation & sec.prevention

IV heparin if indicated

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THANK
YOU
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