Download coronary artery disease

By Dr. Zahoor
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1.
Introduction to Coronary Artery Disease (CAD)
2.
Acute Coronary Syndrome (ACS) – Unstable
Angina, Non ST Elevation MI, ST Elevation MI Pathophysiology
3.
Acute Coronary Syndrome – Presentation,
Investigation and Treatment
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Why myocardial ischemia occurs?
 Myocardial ischemia occurs when there is
imbalance between the supply of Oxygen and
myocardial demand.
 Coronary blood flow may be reduced due to
- Atheroma
- Thrombosis
- Spasm
- Embolus
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Other causes of decreased blood flow of
Oxygenated blood to the myocardium
- Anemia
- Hypotension
- Carboxyhaemoglobulinaemia
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Increased demand of Oxygen may occur
- Thyriotoxicosis
- Myocardial Hypertrophy in hypertension
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Coronary Artery Disease is the largest cause
of death in many parts of the World

In UK, in 2009, one in five male and one in
eight female death were due to CAD
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Sudden death is prominent feature of CAD
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Note – It is recommended that adults should
do 30 minutes of moderate activity e.g. brisk
walking , cycling on 5 days of the week
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Acute Coronary Syndrome includes
- Unstable angina (UA)
- Non ST-elevation myocardial infarction
(NSTEMI)
- ST-elevation myocardial infarction (STEMI)
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Process of coronary Atherosclerosis
 Coronary Atherosclerosis is inflammatory
process, characterized by accumulation of
lipid, macrophages and smooth muscle cell in
intima of large and medium size epicardial
coronary arteries
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Why there is initial endothelial injury or dysfunction
which triggers atherogenesis in coronary artery?
 It may be due to
- mechanical stress from hypertension
- biochemical abnormality e.g. increased LDL,
Diabetes mellitus
- Smoking – free radicals
- Infection – Chalmydophila pneumoniae
- Genetic factors
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Process of Atherosclerosis
 When there is endothelial dysfunction, there
is accumulation of lipoprotein which are
taken by macrophage to produce foam cell
 There is smooth muscle cell proliferation
 Collagen is produced by smooth muscle cell
and it leads to formation of fibro lipid plaque
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Plaque may grow slowly
Plaque may be stable or unstable
Stable plaque causes stable angina
Unstable plaque may rupture and forms
thrombosis and obstruction
Unstable plaque causes ACS (UA, NSTEMI,
STEMI)
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In ACS, there is rupture or erosion of the
fibrous cap of plaque in the coronary artery
This leads to platelet aggregation and
adhesion
This causes localized thrombosis,
vasoconstriction due to release of serotonin
and Thromboxone – A2 by platelet
There in increased risk of rupture of plaque
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Presentation
 Chest pain may occur at rest or minimal
exertion and lasts for more than 20 minutes
 It is not relieved by sublingual GTN
 There is ischemia with no myocardial
damage
 ECG may show ST-depression and T-wave
inversion
 Cardiac enzymes – Troponin T and I are
normal
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Chest pain lasts for more than 20 minutes, it
is not relieved by sublingual GTN
 ECG shows ST-depression and T-wave
inversion
 Cardiac enzymes Troponin T and I are raised,
CK-MB raised
Why enzymes are raised in NSTEMI?
 Because there is partial thickness myocardial
infarction
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Chest pain is severe last for 30 minutes or
more , it is not relieved by sublingual GTN
ECG shows ST-elevation
Cardiac enzymes Troponin I and T, CK-MB are
raised as cardiac myocyte die due to coronary
artery thrombosis
Full thickness myocardial infarction causes ST
elevation, and later Q wave appear.
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Important Points
 Some patient may present with atypical features
like
- Pain epigastric region, indigestion, pleuritic
chest pain, dyspnoea
- 12 lead ECG may be normal
- ST – depression and T-wave inversion are
highly suggestive of ACS, when associated with
anginal chest pain
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Important Points
- In STEMI – ST elevation or left bundle branch
block (LBBB) may occur
- Cardiac Troponin I and T are highly sensitive and
specific
- CK-MB signifies cardiac myocyte death but
CK-MB increase also occurs with skeletal muscle
damage which has limited its accuracy
- Myoglobin – useful for rapid diagnosis of ACS as
levels increase early in MI, but test is not specific
as Myoglobin is present in skeletal muscle also
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Unstable
Angina
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes
NSTEMI
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
STEMI
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
ST depression +/T wave inversion on
ECG
Elevated cardiac
enzymes
Elevated cardiac
enzymes
More severe
symptoms
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Investigation and treatment of NSTEMI and UA
 High risk patient should have early coronary
angiography and intervention in less than 72
hours
Who are high risk patient?
 Patients who are likely to progress to MI
 Patient with persistent or recurrent angina with
ST changes ≥ 2mm or deep negative T-wave
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High Risk Patient (cont)
 Clinical Signs of heart failure or hemodynamic
instability
 Life threatening arrhythmia (VF, VT)
 Patient with high risk score
- increased Troponin
- dynamic ST and T-wave changes
- diabetes mellitus
- PCI within 6 months
- previous CABG
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Low Risk Patient
 They should be managed with
- oral aspirin
- plavix (Clopidogrel)
- β blockers
- Nitrates
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Who are low risk patients?
 Patient with angina
- No reoccurrence of chest pain during
observation
- No signs of heart failure
- No dynamic ST changes
- Normal ECG or minor T-wave changes
- No increase in Troponin I and T
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Oxygen 35-50%
Antiplatelet drugs – Aspirin and Plavix
Antithrombin – low molecular weight heparin
Glycoprotein IIB/IIIA inhibitors – Abciximab
Analgesia – Diamorphine or morphine
Coronary vasodilator – GTN
Plaque stabilization – Statins e.g. Lipitor,
Zocor
They are HMG – CoA reductase inhibitors
- ACE inhibitors e.g. Lisinopril
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Mechanism of action
 Aspirin – blocks formation of thromboxane
A2 (TXA2), therefore, prevents platelet
aggregation
 Plavix (Clopidrogrel) – inhibits ADP, therefore,
prevents platelet aggregation
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MI occurs when cardiac myocyte die due to
prolong myocardial ischemia
 Diagnosis of STEMI
1. Clinical History
- chest pain more than 30minutes and does not
respond to sublingual GTN
- pain may radiate to left arm, neck, jaw or
epigastric region
- Patient may be pale, sweating
- There may be bradycardia or tachycardia,
hypotension
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Diagnosis of STEMI (cont)
2. ECG
 ECG shows ST elevation in leads facing the
infarction
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ECG acute antrolateral MI
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Acute
Inferior MI
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ECG evolution
of STEMI
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Diagnosis of STEMI (cont)
3. Biochemical markers
 Increased Troponin I and T, increased CK-MB
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Other test
- Full blood count, serum electrolytes,
glucose, lipid profile
- Transthoracic Echo cardiography (TTE) – to
see for wall motion abnormalities
NOTE – Bradycardia and Heart block is
common with Inferior MI .
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Time is Muscle so urgent management is
required
 Oxygen – nasal cannula 2-4l/min
 I/V access
 12 lead ECG
 Aspirin – 150 to 300 mg chewed
 Plavix – 300 mg orally
 I/V Diamorphine or morphine 2.5 to 5mg plus
antiemetic metoclopramide 10mg
 Beta blocker if no contra indication
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PCI within 90 minutes when patient presented in
12 hours of STEMI, PCI should be done where
facilities are available
 If PCI not available, thrombolysis is done
 Fibrinolysis within 6 hours of STEMI or LBBB
prevented 30 death in every 1000 patient treated
 Fibrinolysis within 7-12 hours prevented 20
deaths in every 1000 patient
 After 12 hours limited benefit, increase risk of
stroke in older patient
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Heart failure
Myocardial rupture
VSD
Mitral regurgitation
Papillary muscle dysfunction
Cardiac arrhythmias – VT and ventricular
fibrillation (can cause sudden death)
Atrial fibrillation
Conduction disturbance are common with
inferior MI as right coronary artery usually
supplies SA and AV node
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After recovery, patient should be encouraged
to participate in exercise program
Diet – Omega 3 fatty acid from fish
Physical activity 20-30 minutes/day
Stop smoking
Decrease weight if over weight
Control hypertension
Control diabetes mellitus (Hb A1C < 7%)
Alcohol consumption in safe limits
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Aspirin 75 – 100mg/day
Plavix 75mg/day for one year
Beta blocker – maintain heart rate < 60 bpm
ACE Inhibitors or ARB
Statins – Lipitor or Zocor
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