Coronary Artery Disease

Pendrik Tandean
Division Cardiology of Internal Medicine
Department
And
Cardiology Department, Medical Faculty of
Hasanuddin University, Makassar

Coronary Artery Disease

Occluded of the coronary artery
Partial
Total
1 coronary artery and branches
Blood flow

5/98

Left Coronary Artery

Right Coronary Artery

Global Burden of Cardiovascular

Disease

In 2002 : CVD contributed to

approximately a third of all global
deaths (17 million). 80% of burden is
in low and middle income countries.
By 2020 : CHD and Stroke will
become the leading cause of death
and disability worldwide. Mortality
for CVD will increase to 20 million.

Worldwide Statistics
Each year:
> 4 million patients are admitted
with unstable angina and acute MI
> 900,000 patients undergo PTCA
with or without stent

Risk Factors for cardiovascular

disease

Modifiable :
- Smoking
- Dyslipidemia (Raised LDL-C, Low
HDL-C, Raised triglycerides)
- Raised Blood pressure
- Diabetes melitus
- Obesity

Risk factors for cardiovascular

disease

Non-Modifiable :
- Personal History of CVD
- Family History of CVD
- Age
- Gender

Family History
Premature CHD
Men (first degree) < 55 years.
Women (first degree) <65 years.

Supply = Demand

Myocardial ischaemia
Ischemic heart disease

Clinical Manifestation

Stable Angina Pectoris

Acute coronary syndromes include
ST-elevation MI (STEMI)
Non ST-elevation MI ( NSTEMI)
Unstable Angina

Ischemic heart disease

Acut coronary
syndrome

Stable angina
pectoris

Congestive heart failure

ST elevation:
NO
Non ST elevation
myocardial infarction

Unstable angina

Conduction
disturbances
Sudden death

ST elevation:
YES

Myocardial infarction
Myocardial infarction (Q)
(non Q)

STABLE ANGINA PECTORIS

Stable angina is a clinical syndrome

characterized by discomfort in the
chest, jaw, shoulder, back or arms,
typically elicited by exertion or
emotional stress and relieved by
rest or nitroglycerin. Less typically,
discomfort may occur in the
epigastric area.

Diagnosis of stable angina

Clinical assesment
Laboratory test
Specific cardiac investigations

History

Features of the history important in

risk stratification include current
smoking, increasing age, prior MI,
symptoms of heart failure, and the
pattern of occurance(recent onset
or progressive), and severity of
angina, particularly if unresponsive
to therapy.

Physical examination

Patient with (suspected) angina

pectoris should be focused on
identification or exclusion of causal
or associated conditions or
precipitating factors and on risk
stratification.

Indications of exercise test

1. Evaluation of pts with
chest pain (pretest
probability of CAD
between 10-90%)
2. Evaluation of pts with
stress provoked
symptoms
3. Prognostic evaluation
of pts with known CAD
4. Evaluation of
antiischemic therapy
(drugs and/or

Non invasive diagnostic

tests
Exercise perfusion scintigraphy
Exercise echocardiography
CT angiography
MRI

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina I.
Test

For Diagnosis

For Prognosis

Class of
Indication

Level of
Evidence

Class of
Indication

Level of
Evidence

Full blood count, creatinine

Fasting glucose

Fasting lipid profile

IIb

IIb

Initial evaluation

During episode of angina

IIb

IIb

Laboratory tests

hs CRP, homocysteine, Ip(a), apoA, apoB

ECG

Routine periodic ECG on successive visits

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina II.

Test

For Diagnosis
Class of
Indication

Level of
Evidence

IIa

IIa

For Prognosis
Class of
Indication

Level of
Evidence

Ambulatory ECG monitoring

Suspected arrhythmia
Suspected vasopastic angina
In suspected angina with normal exercise
test
Chest X-ray
Suspected heart failure, or abnormal
cardiac auscultation
Suspected significant pulmonary disease

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina III.

Test
Echocardiogram
Suspected heart failure, abnormal
auscultation, abnormal ECG, Q waves,
BBB, marked ST changes
Previous MI
Hypertension or Diabetes Mellitus
Intermediate or low risk patient not due to
have alternative assessment of LV function

For Diagnosis

For Prognosis

Class of
Indication

Level of
Evidence

Class of
Indication

Level of
Evidence

B/C

IIa

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina IV.

Test
Exercise ECG
First line for initial evaluation, unless unable
to exercise/ECG not evaluable
Patients with known CAD and significant
deterioration in symptoms
Routine periodic testing once angina
controlled

For Diagnosis

For Prognosis

Class of
Indication

Level of
Evidence

Class of
Indication

Level of
Evidence

IIb

IIb

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina V.

Test
Exercise imaging technique
(echo or radionuclide)
Initial evaluation in patients with
uninterpretable ECG
Patients with non-conclusive exercise test
(but adequate exercise tolerance)
For Angina post revascularization
To identify location of ischaemia in planning
revascularization
Assesment of functional severity of
intermediate lesions on arteriography

For Diagnosis

For Prognosis

Class of
Indication

Level of
Evidence

Class of
Indication

Level of
Evidence

IIa

IIa

IIa

IIa

Summary of recommendations for routine non-invasive

investigations in evaluation of stable angina VI.

Test
Pharmacological stress imaging
technique
Patients unable to exercise
Patients with non-conclusive exercise test
due to poor exercise tolerance
To evaluate myocardial viability
Other indications as for exercise imaging
where local facilities favour
pharmacological rather than exercise stress
Non-invasive CT arteriography
Patients with low probability of disease and
non-conclusive or positive stress test

For Diagnosis

For Prognosis

Class of
Indication

Level of
Evidence

Class of
Indication

Level of
Evidence

IIa

IIa

IIa

IIb

TREATMENT

Aims of treatment.
A. Improve prognosis by
preventing myocardial infarction
and death
B. Minimize or abolish symptoms.

Non-pharmacological

Advice should be given for the

management of an acute attack, i.e. to
rest, at least briefly, from the activity
that provoked the angina and the use of
sublingual nitrate for acute relief of
symptoms.
Need to seek medical advice if angina
persist >10-20 minutes after rest and/or
is not relieved by sublingual nitrates.

Non-Pharmalogical

Stop cigarette smoking

Mediterranean diet, with vegetables,
fruit, fish and poultry being the
mainstays.
Weight reduction diet --- Overweight
Alcohol in moderation may be
beneficial, but excessive
consumption is harmful

Non-Pharmacological

Fish oil rich in omega-3 fatty acids (n-3

polyunsaturated fatty acids) are
recommended at least once weekly
Physical activity within the patients
limitation should be encouraged.
Concomitant disorders such as diabetes
and hypertension should be managed
appropriately.
Sexual intercouse may trigger angina.
Nitroglycerine prior to intercourse may
be helpful.

Pharmacological therapy

Antitrombotic drugs. Antiplatelet

therapy to prevent coronary trombosis
is indicated. Low dose aspirin (75-100
mg) is the drug of choise in most cases.
Aspirin allergic --- clopidogrel
Aspirin + clopidogrel --- post stenting or
after ACS
History of GI bleeding --- aspirin +
proton pum inhibitor

Pharmacological therapy

Anticoagulant drugs (warfarin or

thrombin inhibitors), which are
combined with aspirin in certain
high risk patients, such as post MI,
are not indicated in the general
stable angina pectoris without a
separate indication such as atrial
fibrillation for example.

Pharmacological therapy

Lipid lowering drugs

ACE inhibitors
Beta-blockers
Antianginal drugs : beta-blockers,
calcium antagonist and organic
nitrates

Acute Coronary Syndrome

PATOGENESIS

Fixed Coronary Obstruction

(Chronic Ischemic Heart Disease)

Unstable Plaque

Occlusive Thrombus

Acute Coronary Syndrome

Ischemic Discomfort
Unstable Symptoms

No ST-segment
elevation

Unstable
angina

History
Physical Exam

ST-segment
elevation

Non-Q
AMI

Q-Wave
AMI

ECG

Acute
Reperfusion

Unstable Angina

angina at rest (> 20 minutes)

new-onset (< 2 months) exertional
angina (at least CCSC III in severity)
recent (< 2 months) acceleration of
angina (increase in severity of at
least one CCSC class to at least
CCSC class III)
Canadian Cardiovascular Society Classification
Agency for Health Care Policy Research - 1994

CANADIAN CARDIOVASCULAR
SOCIETY FUNCTIONAL
CLASSIFICATION

CLASS I No angina with ordinary

activity. Angina with strenuous, rapid or
prolonged exertion.
CLASS II Slight limitation of ordinary
activity ; angina when walking up stairs
briskly, or walking on a cold or windy day.
CLASS III Marked limitation ; angina
when walking at normal pace up flight of
stairs, or walking 1-2 blocks distance.
CLASS IV Angina on minimal exertion or
at rest.

Clinical Features of MI

Crushing, heavy substernal chest

pain radiating to the neck and
medial aspect of the left arm
Pain may be atypical (like a
burning), localized (only in the
jaw), or absent
Stable angina is usually caused
by exercise or anxiety, is shortlived, and is relieved by rest
and/or NTG
Unstable angina occurs at rest
and lasts longernew pain,
altered stable angina pattern,
nausea/sweating, and radiation to
new sites also suggests unstable
angina

Clinical features, cont

Myocardial infarction signs/symptoms

Abrupt onset of severe, prolonged pain

Autonomic symptoms (sweating, nausea)
Dyspnea
Anxiety
Tachycardia or bradycardia, depending on
site of MI
Hypotension
Gallop heart rhythm

Determining/confirming an
MI

Serial EKGs

Angina

T wave inversion
ST depression
Conduction defects (eg-bundle branch blocks)

MI

Subendocardial (doesnt go all the way thru the muscle)

Transmural (goes all the way thru the muscle)

ST depression
T wave inversion
Presence of Q wave
Elevated ST segment

Cardiac enzymes

Myocardial necrosis releases cardiac enzymes into the

plasmaCTT and CK-MB peak within 24 hoursLDH-1 peaks
at ~3-4 days out
Increased cardiac troponin T (CTT) at 12 hrs makes diagnosis
Increased LDH-1suggests late presentation MI
Doubling of baseline CK-MB confirms MI

Electrocardiogram

A normal ECG does not exclude ACS

High probability include ST segment
elevation in two contiguous leads or
presence of q waves
Intermediate probability ST
depression
T wave inversions are less specific

Ischemia & Infarction

Indications of an acute infarction
Usually no ECG changes are seen in the first few minutes after occlusion
Appearance of tall narrow T-waves or ST-segment elevation
5 to 30 minutes post occlusion
A few hours later, the T-waves invert (ischemia)
in an MI, the T-wave inversion is symmetrical an may persist for years
inverted T-waves without other indications are not diagnostic of an MI
ST-segment elevation indication of injury (although it may be reversible)
ST-elevation may also indicate transmural ischemia
usually the first definite sign of an infarction
may or may not be accompanied by T-wave inversion
1mm or more in limb leads or 2mm or more in precordial leads
differentiate between early repolarization or J-point elevation
the larger the ischemic area, the greater the ST displacement
ST elevation persisting for more than a few hours may indicate ventricular aneurysm
ST depression may be seen in reciprocal leads.

ST segment Elevation

http://www.emedu.org/

ST segment Elevation

http://www.emedu.org/

ST SEGMENT ELEVATION

ST segment depression

http://www.emedu.org/

Cardiac Biomarkers

Cardiac biomarkers are protein

molecules released into the blood
stream from damaged heart muscle
Since ECG can be inconclusive ,
biomarkers are frequently used to
evaluate for myocardial injury
These biomarkers have a
characteristic rise and fall pattern

Troponin T and I

These isoforms are very specific

for cardiac injury
Preferred markers for detecting
myocardial cell injury
Rise 2-6 hours after injury
Peak in 12-16 hours
Stay elevated for 5-14 days

Creatine Kinase (MB)

Time sequence after myocardial

infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days

Ischemia & Infarction

Biomarkers in an MI:

Multiples of the AMI cutoff Limit

50

Myoglobin

20

Cardiac Troponin
CK-MB

10

Cardiac Troponin after unstable angina

5
2

AMI decision limit

Upper normal limit

0

Days after MI Onset

Determining MI, cont

Echocardiography

May show dyskinesia of muscle,

mural thrombus, perforations,
aneurysms, papillary muscle rupture,
and valve lesions

Nuclear scans

Technetium pyrophosphate

Concentrates in area of damage

Thallium scans

Show cold spots in non-perfused

myocardium and demonstrate areas of
reversible ischemia

Echocardiography

Use 2-dimentional and M mode

echocardiography when evaluating
overall ventricular function and
wall motion abnormalities
Echocardiography can also identify
complications of MI ( eg. Valvular or
pericardial effusion, VSD)

Coronary Angiography

Dadkhah

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