3. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
5. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
6. 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
7.
8. Increasing
age
Male
Personality
gender
Family
Alcohol
history
RISK
FACTORS
Obesity Smoking
Physical
Hypertension
activity
Hyper-
Diabetes
cholesterol-
mellitus
emia
9.
10. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
11. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
12. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
16. 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.
17. 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.
18. 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.
19. 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
20. 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.
23. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
24. ACUTE REPERFUSION THERAPY
1. Thrombolysis
2. PCI
3. CABG
Aim :
•Restore coronary patency
•Preserves left ventricular
function
•Improves survival rate and
reduced mortality rate.
25. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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.
26.
27. 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
28. 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
29. 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
30. 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.
31. 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
32. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
33.
34. 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.
35. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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.
36. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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.
37. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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.
38. 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
39. ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >
Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
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
40. 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