NSTEMI DrHafiz

NON-ST ELEVATION MI
BBH, Bangalore
Ahmad Hafiz
Nov 2011

ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention

ACUTE CORONARY SYNDROME SPECTRUM

STEMI

NSTEMI
Acute
Coronary
Syndrome Minimal
Myocardial
Necrosis
Ischemic Heart
Disease Unstable
Angina

Coronary
Stable Angina
Artery Disease


WHAT IS NSTEMI?
 Unstable angina = angina pectoris
with at least one of three features:
1. it occurs at rest (or with minimal
exertion) usually lasting more
than 20 minutes (if not
interrupted by nitroglycerin)
2. it is severe and described as
frank pain and of new onset
(i.e., within 1 month); and
3. it occurs with a crescendo
pattern (i.e., more severe,
prolonged, or frequent than
previously). With or without
ischemic ECG changes

 NSTEMI = UA with evidence of
myocardial necrosis on the basis of
the release of cardiac markers


PATHOPHYSIOLOGY

 UA/NSTEMI is caused by
reduction in oxygen supply
and/or increased myocardial
oxygen demand
superimposed on an
atherosclerotic coronary
plaque with varying
degrees of obstruction

1. Plaque rupture or
erosion with
superimposed non-
occlusive thrombus
2. Dynamic obstruction
3. Progressive mechanical
obstruction
4. Secondary unstable
angina related to
increased myocardial
oxygen demand and/or
decreased supply

Increasing
age
Male
Personality
gender

Family
Alcohol
history

RISK
FACTORS
Obesity Smoking

Physical
Hypertension
activity

Hyper-
Diabetes
cholesterol-
mellitus
emia


CLINICAL PRESENTATION
 SYMPTOMS:
 chest discomfort
 epigastric discomfort
 shortness of breath
 nausea and vomiting
 excessive sweating
 palpitation, anxiety, sense of
impending doom, and feeling of
being acutely ill


PHYSICAL EXAMINATION
 Resembling that of stable
angina
 Large NSTEMI may resemble
that of large STEMI e.g.
diaphoresis, pale cool skin,
sinus tachycardia, S3 or S4,
basilar rales and sometimes
hypotension
 Signs of co-morbidities e.g.
peripheral or cerebrovascular
diseases
 Autonomic disturbances e.g.
pallor, sweating
 Complications e.g. arrhythmia
or heart failure


ECG CHANGES
1. ST depression (70-80%)
2. T wave inversion (10-20%)
3. Both ST depression and T
wave inversion
4. Post MI NSTEMI - ECG
changes variable (Ironically,
even a residual ST elevation
may be present)
5. Normal ECG


CARDIAC MARKERS

TROPONIN-T
 Peak – 12 hours
 Troponin is released during MI from the cytosolic
pool of the myocytes
 Its subsequent release is prolonged with
degradation of actin and myosin filaments
 Differential diagnosis of troponin elevation
includes acute infarction, severe pulmonary
embolism causing acute right heart overload,
heart failure, myocarditis
 Troponins can also calculate infarct size but the
peak must be measured in the 3rd day. released
in 2–4 hours and persists for up to 7 days.

BNP
 B-type natriuretic peptide is a cardiac
neurohormone released upon ventricular myocyte
stretch as proBNP, which is
enzymatically cleaved to the N-terminal proBNP
(NT-proBNP) and, subsequently, to BNP. The
usefulness of assessing this neurohormone was
first shown for the diagnosis and evaluation of
HF.

GLYCOGEN PHOSPHORYLASE
ISOENZYME BB
 Peak – 7 hours
 Glycogen phosphorylase isoenzyme BB (abbreviation:
GPBB) is an isoenzyme of glycogen phosphorylase
 Glycogen phosphorylase exists in 3 isoforms. One of
these Isoforms is GP-BB. This isoform exists in heart
and brain tissue
 Because of the blood-brain barrier GP-BB can be
seen as heart muscle specific. During the process of
ischemia, GP-BB is converted into a soluble form and
is released into the blood. This isoform of the enzyme
exists in cardiac (heart) and brain tissue. GP-BB is
one of the "new cardiac markers" which are discussed
to improve early diagnosis in acute coronary
syndrome. A rapid rise in blood levels can be seen in
myocardial infarction and unstable angina. GP-BB
elevated 1–3 hours after process of ischemia.

MYOGLOBIN (MB)
 Myoglobin is used less than the other markers
 Myoglobin is the primary oxygen-carrying
pigment of muscle tissue
 It is high when muscle tissue is damaged but it
lacks specificity. It has the advantage of
responding very rapidly, rising and falling earlier
than CK-MB or troponin. It also has been used in
assessing reperfusion after thrombolysis

CK-MB
 Peak – 10-24 hours
 CK-MB resides in the cytosol and facilitates high
energy phosphates into and out of mitochondria
 It is distributed in a large number of tissues even
in the skeletal muscle
 Since it has a short duration, it cannot be used
for late diagnosis of acute MI but can be used to
suggest infarct extension if levels rise again
 This is usually back to normal within 2–3 days.

MANAGEMENT GUIDELINE
Suspicion
Early management
-Emergency management
-Hospital phase management
-Pharmacotherapy

Late Management
-Risk stratification
-Life style modification
-Secondary prevention drug therapy

ALGORITHM FOR EVALUATION AND
MANAGEMENT OF PATIENTS SUSPECTED OF
HAVING ACS


EMERGENCY MANAGEMENT
ABC, Pulse Oximeter, Attach ECG monitor and record 12-lead ECG,

High flow O2 by face mask

IV access [bloods for CBC, U&E, glucose, lipids, cardiac enzymes]

Brief assessment

History of CVS disease, risk factors for IHD
Examination: pulse, BP, JVP, cardiac murmurs, scar from previous cardiac surgery

Aspirin 300 mg or Clopidogrel 75mg

Morphine 5-10 mg IV + metoclopramide 1 mg IV

GTN sublingually

Thrombolysis management

Beta blockers + ACEI

ACUTE REPERFUSION THERAPY
1. Thrombolysis
2. PCI
3. CABG

Aim :
•Restore coronary patency
•Preserves left ventricular
function
•Improves survival rate and
reduced mortality rate.


THROMBOLYSIS
 Indication:
 Ischaemic chest pain > 30 minutes
duration
 Less than 12 hours from the onset of pain
 ECG changes:
 new ST elevation of at least 2 mm in two
consecutive chest leads;
 or ST elevation of at least 1 mm in two

consecutive limb leads;
 or a new left bundle branch block.

Fibrinolysis
Streptokinase
 Dosage : 1.5 million units in 100 ml saline

 Route of administration : IV infusion over 1 hour

 Mode of action : Catalyze the conversion of
plasminogen to active plasmin which further lyse
the clots.
 Side effects :
-Allergic manifestations
-Hypotension
-Systemic bleeding

Note: production of circulating neutralizing antibodies following therapy
may cause subsequent infusion with streptokinase ineffective

Alteplase
Tissue plasminogen activators

MOA : specifically bound to fibrin-bound plasminogen

Route of administration:
IV infusion over 90 minutes duration First 30 mins Bolus dose 15mg

Side effects : Followed by 0.75mg/kg
less compared to streptokinase
- risk of intracranial bleeding Next 60 mins 0.5mg/kg
(not > 35mg)
Other drugs:
Tenecteplase –longer plasma half life

Reteplase - given as double bolus instead of infusion

FULL THERAPEUTIC ANTICOAGULATION
 Use either an infusion of unfractionated
heparin or low molecular weight heparin(e.g.,
enoxaparin sodium).
 In the context where pathology is not readily
available, low molecular weight heparin is often
easier to use

enoxaparin
sodium 1 mg/kg
subcutaneously
twice daily

ADJUNCTIVE THERAPY
 Consider intravenous beta-blocker (metoprolol 5
mg IV slow bolus at 0 min, 5 min and 10 min to
give a total dose of 15 mg) then oral therapy (2).
 IV beta-blockers decreases mortality when given
early in acute myocardial infarction though the
evidence is less clear in the reperfusion therapy
setting;
 it is more commonly used in the United States and
parts of Europe and is routine therapy in
Scandinavia.
 ACE-inhibitors: when started within 24 hours
reduce morbidity and mortality.

CONTRAINDICATIONS TO THROMBOLYTIC
THERAPY

 Active internal bleeding
 Previous history of subarachnoid or
intracerebral bleeding
 Uncontrolled hypertension

 Recent surgery (less than 1 month)

 Recent trauma

 High probability of active peptic ulcer

 Pregnancy


PRIMARY PERCUTANEOUS CORONARY
INTERVENTION

Primary percutaneous intervention is more effective
than thrombolysis for treatment of AMI.
Death, non fatal reinfarction and stroke reduced
from 14% with thrombolytic therapy to 8% with
primary PCI

Keeley EC, et al. Lancet 2003;361:13-20

 Treatment of choice to prevent reinfarction

 Avoid hemostatic problems encounter with
thrombolytic therapy

 Preferred in case of presence of cardiogenic
shock, bleeding risk, symptoms of more
than 2-3h

Disadvantage

Expensive in terms of facilities and personnel,
limited availability.


CORONARY ARTERY BYPASS GRAFTING
(CABG)
 surgical procedure performed
to relieve angina and reduce
the risk of death
from coronary artery disease.

 Arteries or veins from
elsewhere in the patient's
body are grafted to
the coronary arteries to
bypass atherosclerotic
narrowing and improve
the blood supply to
the coronary
circulation supplying
the myocardium.


HOSPITAL PHASE MANAGEMENT
 Coronary care units- provide intensive care. Duration of stay
depends on the condition of patient.

 Activity – advise bed rest for first 12 hours, as increase workload
to the heart may cause increase size of the infarct.

 Diet – clear liquids for first 4-12 hours due to risk of emesis and
aspiration. Diet should contain 50% complex carbohydrate and low
fat contents.

 Bowels – prevention of constipation by giving high fiber diet,
laxative can be prescribed.

 Sedation – Diazepam, oxazepam or lorazepam is given for sedation
to enforced inactivity with tranquility.


LATE MANAGEMENT
 Risk stratification and investigation

1. Left ventricular functions
 Assess by physical findings i.e tachycardia,3rd heart
sounds, crackles at lung bases
 Echocardiography and radionuclide imaging to assess LV
ejection fraction.
2. Arrhythmias
 Presence of ventricular arrhythmias during convalescence
phase may benefit from specific anti arrhythmic therapy
such as implantable cardiac defibrillator.

3. Early post MI ischemia is managed like unstable
angina

If no spontaneous ischemia, assess by exercise testing
to look for residual ischemia
-Good exercise tolerance – 1-4% chance of adverse
event in 12 months

-Low exercise tolerance – consider revascularization
by CABG

4. Other risk factors include age >75,diabetic patient,
prolonged sinus tachycardia, hypotension and silent
ischemia


SECONDARY PREVENTION
 Long term drug therapy with low dose aspirin,
clopidogrel, beta blockers and ACEI

 Cessation of smoking

 Control of hypertension and hyperlipidemia

 Regular exercise

 Diet – diet high in fibers, fruit, oily fish, low in
saturated fat, weight control

 Returning to work after 4-6 weeks

REFERENCE
 2011 ACC/AHA Guidelines for the Management
of Patients With Unstable Angina/Non–ST-
Elevation Myocardial Infarction
http://content.onlinejacc.org/cgi/content/short/57/19/
e215
 Harrison's Principles of
Internal Medicine, 17e
 Davidson’s Principles & Practice of Medicine, 20e

 wikipedia

 Medscape
http://emedicine.medscape.com/article/811905-
overview#aw2aab6b3

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