CORONARY ARTERY DISEASE (CAD)

Rebecca W. Deduyo MD FPCP FACC

Internist/ Adult Cardiologist
Fatima University College of Medicine

- Leading cause of mortality and morbidity worldwide - Point B has wider lumen then Point A, w/c make it more
- In the US: dangerous
o More than 11M Americans have CAD - Wall is thicker
o Estimated cost of CAD treatment is $100B - Point of rupture cause thrombus for
annually occluding coronary segment
- Clinical course
o Extremely unpredictable Presentation of CAD
o Progression from early to establish disease - Acute coronary syndrome
is not linear - Sudden cardiac death
o Only 50% CAD patients will experience
angina, a large percentage proceed directly In Approximately Half of Patients,
to MI or sudden death without any overt the Initial Presentation of CAD is MI
signs and symptoms or Sudden Death

- Patients may cycle in and out of clinically defined Initial Presentation of CAD
phases (stable, unstable, MI) MEN 62%

THE TIGHT STENOSIS IS NOT THE ACTIVE LESION MI or

WOMEN 46% Sudden Death

0 10 20 30 40 50 60 70
Percent of Patients

Coronary artery at lesion prone location foam cells stick to

wall thicker lesion complicatedfissuring
hematomarupture blood clots circulate
Results in
- Coronary artery ACS
- Brainstroke
- Arterial occlusive disease

Angiogram x-ray visualization of the blood vessel by means

PROGRESSION OF ATHEROSCLEROSIS
of a contrast material, presence of dye to outline BV - Coronary artery at lesion prone location
- Outline lumen not measure the thickness of wall
o Adaptive thickening of the smooth muscle wall
- Atheroslcerosis disease in thickness of wall of BV
in the tunica intima
o With endothelial dysfunction, the macrophage
Right sight- in cardiac catheterization on angiogram where a
will engulf oxidized LDL and transform into a
catheter is inserted at the femoral artery and enters into the
foam cell leading to the thickness of the wall
coronary artery and through X-ray and technology the
diameter of the lumen is shown with the a labeled with A and - Type II lesion
B. A looks narrowed but is not the active lesion and B is wide. o Macrophage and foam cells begin to migrate
Looking at the angiogram you would think that there was
contributing to the thickening made by the
nothing wrong since it looks bigger but it is more dangerous
accumulation of the smooth muscle
proven by doing an intravascular ultrasound.
- Type III lesion
IVUS (Intravascular Ultrasound) o Pre-atheroma
- Involves usually the abdomen, reproductive o Small pools of extracellular lipid
system o Lumen still white
- Probe/Transducersound waves to machine o Extra cellular lipid
image created
- Probesmallerinserted to femoral artery ( - Type IV
bigger lumen)enter left side of heartcoronary o Atheroma
artery o Core of extracellular lipid
o Can use radial artery( smaller lumen)
- Advantages: Can outline wall of artery, measure - Type Va
thickness of tunica(intima, media) o Fibroatheroma
o Ruptures and lesions
A probe with the transducer is inserted into the blood vessel o Fibrous thickening
and is able to make an image of the blood vessel. The wall is
thicker. There is a point of rupture that causes release of - Type VI
blood clot or thrombus and is responsible for occluding the o Complicated lesion
corresponding segment of the coronary artery o Fissure & hematoma
o Thrombus
- Significant narrowing coronary artery o Point of rupture releases blood clot that
- Insufficient blood flow
obstructs or occludes
- Single vessel & multi-vessels
 More vessels obstructed, more
lesions
 Myocardium
Page 1 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

o Oxidized LDL → endothelial dysfunction

Atherosclerosis: A systemic Disease  Function of endothelium
• Systemic = widespread, not confined to just one organ o Barrier
• Coexistence of CAD, PAD, and ABI (acute brain infarct) in o Metabolic active organ that is capable of
1886 patients > 62 years in a long care facility selective permeability
• Pure CAD 21%  Tells you the % incidence based on risk factors
• Pure ABI 9%  Antioxidants prevent oxidation of LDL
• Pure PAD 8%  Statins cause stabilization of the plaque prevent
rupture releasing a blood clot
ABI = Atherothrombotic brain  Ascot trial
infarction or stroke o Atorvastatin & (Statin) shows significant
ABI
CAD 9% reduction in morbidity & mortality
8%
21%
PAD= Peripheral arterial disease o Rosavastatin in other trials
5% o Atorvastatin and rosavastatin shows
3%
9% dramatic benefical effect
 Helps against atherosclerosis
PAD o Vitamins
8%
 Vitamin C shows protection
 Vitamin E not shown to do
anything but good for skin
Key steps in the initiation of Atherosclerosis o Dark chocolate & red wine shows beneficial
• Risk Factors: Smoking, Hypertension,  LDL, DM, effects
Inflammatory cells  Endothelial Dysfunction o Coffee able to produce anti-oxidant effect
o Green tea shows anti-oxidant effect
• Endothelial Dysfunction causes to the following:
- Decrease NO and abnormal control of vascular
tonevasoconstriction

- Formation of Fatty Streaks:

1. The following leads to increased access to
subendothelial space  oxidation of LDL taken up by
macrophages  foam cells fatty streaks
a. Increase Permeability of endothelium allowing
the entrance of substance like free
i. Free Radicals—which oxidizes LDLs
ii. Cytokines and Cellular Adhesion Molecules
attracts monocytes (macrophages) 
engulfing the oxidized LDL

2. Platelet adherence and aggregation

•Fatty Streaks will lead the formation of a soft plaque
with thin fibrous cap
**Remember the Deadly Triad: Smoking, Hypertension,
and Dyslipidemia,
The plaque is the basic lesion of atherosclerosis. It is
dangerous because it may rupture.

PROTECTION OF BLOOD VESSELS

With regards to protection of vascular system with
antioxidantsVitamin C, Carnitine, Vitamin A
Preventative Anti-platelet therapyAspirin
Prevention of oxidation of LDLStatins
• Endothelial dysfunction →
o ↑ permeability of endothelium →
increased access to subendothelial
o ↓ NO & abnormal control of vascular tone
o Free radicals → Oxidized LDL → increased
access to subendothelial space
o Cytokines & cellular adhesion molecules →
attracts monocytes (macrophages) →
increased access to subendothelial
o Platelet adherence & aggregation → growth
factors → SMC (smooth muscle cell)
proliferation & migration → fatty streak →
soft plaque w/ thin fibrous cap
o Increased access to subendothelial→
oxidized LDL taken up by macrophages →
foam cells → fatty streak
Smoking, HPN, Increase LDL, DM, inflammatory cells,
HSCRP(high sensitive C-reactive protein marker of
inflammation)- major risk factor, one or more present in
one individual causes damage to endothelium
Endothelium
- Main lining of BV
- metabolic active organ, screen entrance of
obnoxious substance
Malfunctioning endothelium results to
A. increase permeability entrance of free radicals
oxidized LDL(free radicals) taken up by
macrophage foam cells fatty streak plaque
B. non-smooth BVAttracts platelet adherence and
aggregation growth factors producing
proliferation and migration of smooth muscle cell
fatty streak soft plaque with thin fibrous cap
use aspirin( protection)
Page 2 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

CORONARY ARTERY DISEASE

New drug: Aspirin + statin( lowers LDL) + ACE/ARB (CAD)

C. Decrease NO(vasodilatation of BV for integrity and

perfusion of organs)  cytokines and cellular Unstable plaque Stable plaque
adhesion molecules attracts monocytes
endothelial permeability
Acute/ catastrophic Gradual progression

The CAD Lifecycle

Vascular Injury
Risk Factors EVENT:
HTN HF
Consequences ARRHYTHMIA
Lipids MI
Endothelial Dysfunction Ischemia
Smoking
Angina
Diabetes RHYTHM OF ISCHEMIA
MI
Obesity
Plaque Unstable Angina
Age INCREASE PLATELET
SCD
AM AGGREGATION
INCREASE BP
&
INCREASE
DECREASE
Stable Unstable VASCULAR TONE FIBRINOLYTIC
Plaque Plaque ACTIVITY
PLAQUE
&
RUPTURE DECREASE BLOOD
FLOW HYPERCOAGULABLE
CV Events STATES

ISCHEMIA
THE CAD LIFECYCLE:
OCCLUSION
• Risk factors causes malfunctioning endothelium and
vascular
• Vascular Injury  Endothelial Dysfunction  Plaque MYOCARDIAL
SUDDEN
INFARCTION ANGINA PECTORIS
Formation  Stable or Unstable plaque  Cardiovascular DEATH

Events • DANGER!!! When there is elevated BP over systolic 200

- Stable plaque will last long and will not suddenly rupture
- Unstable plaque can rupture as if like a drainage pipe
with leak and can burst open at any time
• Consequences: Ischemiac chest pain  mild chronic chest
• Who are said to be in “Hypercoagulable States?”
pain of a Stable Angina Pectoris Moderate chest pain of
Unstable Angina Pectoris, Severe vasospastic pain of
Prinzmetal Variant Angina Pectoris, Sever chest pain of AMI,
or a patient not having chest pain but difficulty of breathing
in patient with CHF
Ventricular Arrythmia Sudden Cardiac Death
CORONARY ARTERY DISEASE (CAD)
mmHg  plaque rupture  occlusion  total/rear-
total/partial occlusion  Ranging from AP – SCD
• Diabetic Population, Smokers with polycythemia, and
Bed-ridden & elderly due to limitation of mobility 
decrease of blood flow.
• “Hypercoagulable” means there is an increase in
platelet aggregation resulting in thrombus formation 
occlusion  manifestation
• Hypertensive patient should be careful in high
altitude places

• Unstable Plaque  Acute/catastrophic events  SUDDEN
Heart Failure, arrhythmia or MI!
• Stable Plaque (benign in its course)  gradual progression
to events  Heart Failure, arrhythmias, and MI
- Arrhythmias: lead to sudden death because of the
irregularity of the rhythm
- Stable and Unstable Angina can both lead to catastrophic
events as stated above
- Goal is to stabilize the plaque to prolong the life of the
pt.
- Atherosclerosis is irreversible. It causes pathologic
damage that we cannot see until it is too late.
st
- Atherosclerosis starts in the 1 decade of life and
depends on the lifestyle and the risk factors of the
individual
• Ischemia- insufficient flow of blood to the myocardium. Still
some degree of myocardial profusion
• Infarction means there is an occlusion and therefore there
is a lack of blood supply
• Occlusion- complete cut off of blood flow. There can be MI
or sudden death
• Atherosclerosis of the coronary artery causes inadequate
blood supply to the heart
• The imbalance between the Oxygen supply and demand?
- The hypertrophied myocardium on account of a chronic
uncontrolled hypertension. The thicker the wall of
myocardium the more blood it requires. It cannot be
provided from a narrow coronary artery (which means
it’s partially obstructed by a blood clot) affected by
atherosclerotic changes
• Blood is essential for all organs. If the blood supply is cut off
there would be death of the myocardium necrosis
irreversible Fibrotic change to the myocardium
-  BP  plaque rupture  ischemia  MI
-  Vascular tone  Flow  ischemia  occlusion 
Angina
Page 3 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

-  Platelet aggregation/fibrinolytic activity/ MUSCULOSKELETAL PAIN  give analgesics/anti-

Hypercoaguable states (ex. Smoking,DM)  all of which inflammatory agents!!!
causes ischemia  Sudden death
ISCHEMIA
Symptomatic Events

ANGINA PECTORIS UNDERLYING MOST or ALL EVENTS

 STABLE: a relatively unchanging pattern of chest
discomfort described as tightness, heaviness, and SUPPLY DEMAND
aching. FLOW PRESSURE HR
FILLING TIME CONTRACTILITY
 Occurs during physical exertion O2 CAPACITY WALL TENSION
 Relieved by Rest and Nitrates (Nitroglycerine) • VOLUME

 Not pain more of discomfort last for few minutes • RESISTANCE

•DISTENSIBILITY
 Pain in chest for several hours  press the part +
pressure tenderness myocardial fascia syndrome, AN IMBALANCE ISCHEMIA

costochondritis (DOB is a psychological problem in

cases like this)
 DOB orthopnic, visible veins, (+)crackles Underlying most/all events
• Supply (coronary artery that gives you the blood)
 UNSTABLE ANGINA: Any change in the frequency, - Flow pressure
intensity, or duration of angina - Filling time
 Not related to exertion - O2 capacity

 VASOSPASTIC (Prinzmetal Variant Angina): • Demand (myocardium relies on blood supply from the
Nonexertional chest pain often occurring during rest or coronary artery)
at night. Angina in the absence of coronary - Heart Rate ex Exercise
atherosclerotic occlusion - Contractility
- Wall tension
Clinical Case: STABLE ANGINA. - Volume
A patient, who does not know he is hypertensive, had DM but - Resistance
he notices that every time he climbs the stairs he had to stop - Distensibility
a while because of chest discomfort and upon resting it
disappears. It happens every day. The degree of precipitating • ANY Imbalance  Ischemia (when there is an imbalance
factors and pain are the same. When the patient is rested, you always have ischemia)
the chest discomfort disappears.
Some patients may not be aware of the signs so it’s up to the • Drug therapy would be geared into reducing the demand in
physician to ask the right questions to lead to the diagnosis. order to set a balance
 In cases of unstable and vasospastic type of angina are
so painful and alarming that they are usually brought to • No drug that can improve the supply except for
the hospital because they are scared intervention therapy

How to determine the difference between Unstable and  SUPPLY

Prinzmetal Variant Angina— • Obstruction
• ECG changes - Fixed: because of the atherosclerosis
• Pathologically, with Prinzmetal Variant there are only - Spasm
spasms following dilatation of the blood vessel wall - Combination
causing pain that is so severe
• When spasms occur, the ECG will show transient ST- CLINICAL APPROACH TO PATIENTS WITH CHRONIC STABLE
segment elevation. After 24 hours, it will go back to ANGINA
normal.
• If after 24 h there is a progression of the ST-segment Diagnosis
depression = UNSTABLE ANGINA. - Clinical assessment (MOST IMPORTANT for Dx):
• If at the end of 24 h the ECG reading reveals Q-wave, (+) 1. Clinical Hx
serum cardiac biomarkers of troponin T & I and CK-MB 2. Clinical PE
Transmural MI - Non-invasive testing
• All will present the ST-Elevation except for stable 1. ECG
angina. Stable Angina will NOT! 2. 2-D echocardiography
3. Stress Testing
WHY IS ANGINA RELIEVED BY REST? 4. Stress Imaging Study
- B/c you bring the heart rate back to a normal heart rate, - Invasive testing
therefore less oxygen demand. 1. Angiography
2. Intravascular Ultrasound
IF THE PAIN UPON EXERTION IS TO THE RIGHT OR TO THE
LEFT THAT EVEN RADIATES: Risk stratification
- Apply pressure to the area to the Costochondral or even - Clinical assessment
directly to the ribs the patient complains about - Non-invasive testing
tenderness, pain upon applying pressure  - Coronary angiography

Page 4 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine
Treatment
- Pharmacologic
- Mechanical revascularization
Diagnosis of Chronic Stable Angina
• Clinical Assessment (Most important)
- Clinical Hx and PE
 Characterize the pain (Quality, Location, Provoking
factors, and Relieving factors)
 Classify: (typical or stable, atypical or unstable, non-
cardiac (ex. GERD or musculoskeletal discomfort is
always substernal --- behind the sternum))
 Risk factors: HPN(most common)
 PE: often normal, may reveal associated conditions
- Initial
 Hemoglobin, fasting glucose, and lipid panel
 (you can tell if the patient has DM with concomitant
hyperlipidemia)
 If Diabetic use hemoglobin A1C to check the glycemic
control for the past 3 months
- Laboratory tests
ECG/Chest X-ray
- Resting ECG abnormalitie (eg. Previous MI, LVH)
o Poorer prognosis
- Cardiomegaly on CXR, LV aneurysm or pulmonary venous
congestion poorer long-term prognosis
Non-invasive tests
- ECG (automatically done bc it’s the cheapest and most
accessible)/X-ray
 Ranges from normal ECG to evidence of a previous MI
because of the presence of a Q S pattern (when a Q
appears it is permanent, it will not disappear because
it signifies fibrosis
 Abnormalities ex Previous MI, LVH (in LVH ST-segment
depression should not be equated with ischemia
because it’s the same change you would see in LVH,
DO NOT do a stress test when a person has LVH and
ST-segment depression because you can not see a
positive one…you can also provoke an attack with LVH
because you increase oxygen demand
 Poor prognosis
 CXR: cardiomegaly on CXR, LV aneurysm, or
pulmonary venous congestion  poorer long term
prognosis
NONINVASIVE TESTS
A. Resting ECG
Recommended:
- Patients without an obvious non-cardiac cause of chest
pain
- During an episode of chest pain (most valuable)
 Normal rest ECG does not exclude severe CAD
 Resting ECG is normal in > 50% of patients
 ECG obtained during chest pain – abnormal in 50% of
patients with normal rest ECG
 It is a must to do it but RESTING ECG IS WILL NOT TELL
YOU THAT THERE IS NO CAD!!!
B. CXR
Recommended:
- Patients with signs or symptoms of CHF, VHD, pericardial
disease, aortic dissection/aneurysm.( But there are more
advanced diagnostic tools for Dx)
 Usefulness as a routine test not well established
 CXR often normal in patients with stable angina
pectoris
 Do not have to do CXR to tell if the heart is enlarged
because the PE should be enough to tell that the heart
is enlarged
 Valvular disease better with echocardiography
 Aortic aneurysm and aortic stenosis better with CT
scan
C. Exercise ECG (treadmill test)
- Recommended in patients with intermediate
probability of CD based on age, gender, and
symptoms including those with CRBBB (complete
right bundle branch block pattern) or <1 mm of ST
depression at rest (for it to be significant the ST
depression has to be > 2 mm within the two small
boxes
- True diagnostic value of the stress test lies in its
relatively high specific of 77% + 17% sensitivity is
68% + 16%
- Exercise testing less sensitive and specific on
women
D. Echocardiography is Recommeded in:
- Patients with systolic murmur (signifies turbulence
of flow across the valves) suggestive of AS (aortic
stenosis) ir HCM (hypertrophoiccardiomyography)
- When echocardiogram can be obtained during pain
or within 30 mins to evaluate extent of ischemia
you will be able to see wall motion abnomaility
- Patients with click/murmur to diagnose MVP (mitral
valve prolapse) (class IIB) usually seen in the young
- Most patients undergoing a diagnostic evaluation
for angina do not need an echo (only to rule out
other causes of chest pain)
• Stress imaging study: echocardiographic and nuclear
(thalium percent viability of myocardium)
- When to do stress imaging
1. CRBB, WPW (world parkinsons wide)
syndrome and other similar conduction,
abnormal, electronically placed ventricular
rhythm
2. Patients with >1mm ST segment
depression at rest including those with LVH
or on digitalis
3. Patients unable to exercise maximally (ex.
Obese, smokers, COPD etc)
- Patient with angina who have undergone prior
revascularization for localization of ischemia, myocardial
viability
- Stress imaging- not a routine diagnostic tool for patients
with a low or high pretest probability of disease
INVASIVE TEST
- Coronary angiography
- Intravascular ultrasound (IVUS)
- MRI
- Coronary angiography (most important test)
 Recommended in: Patients with known or possible
angina have survived sudden cardiac death
Page 5 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

 Uncertain diagnosis after non-invasive testing Adapted from Pepine CJ. Am J. Cardiol. 1998; 82 (suppl 104).
 Non-invasive testing not done due to disability, illness, From first decade of life
or morbidity o Foam cells
 Patients with an occupational requirement for o Fatty streak
diagnosis o Growth mainly by lipid accumulation
 Non-atherosclerotic causes for myocardial ischemia
 Suspected coronary artery spasm From third decade
 High pre-test probability of left main or 3V (vessel) CAD o Intermediate lesion
 ***most accurate diagnostic test for CAD*** o Atheroma
o Growth mainly by lipid accumulation
Goals of Treatment in Stable Angina
• Prevent MI and death = increase quality of life From fourth decade
• Reduce symptoms of angina and occurrence of ischemia  o Fibrous plaque( smooth muscle and collagen)
increase quality of life o Complicated lesion/rupture( thrombosis,
hematoma)
10 MOST IMPORTANT TREATMENT ELEMENTS OF STABLE
ANGINA MANAGEMENT ATHEROSCLEROSIS to ATHEROTHROMBOSIS

• ASPIRIN &ANTI-ANGINALS
- (nitrates reduce the workload of the heart by reducing the
pre-load and after load)

• BETA-BLOCKERS &BLOOD PRESSURE

- B-Blockers reduce the heart rate and improve ventricular
filling period) and Blood pressure (ACE inhibitors 
blocking the conversion of Angiotensin I to Angiotensin II)

• CHOLESTEROL &CIGARETTES Stable plaque

• DIET &DIABETES - Fibrous cap is thick
• EDUCATION &EXERCISE - Lipid core
- lumen
Atherothrombosis
Disrupted plaque
- Acute thrombosis occurring in the presence or pre-existing - Thick lipid core
atherosclerosis produces acute ischemic strokes, acute - Thin fibrous cap
ischemic strokes, acute ischemic syndromes of peripheral - (+) thrombus
arteries and acute coronary syndrome including unstable
angina, myocardial infarction (NSTEMI and STEMI) and Pathologic and Clinical Presentation of Acute Coronary
sudden death Syndromes

Burden of Acute Coronary Syndrome

- Significant public health problem both in industrialized and
developing countries

ACUTE CORONARY SYNDROME

- ST Elevation Myocardial Infarction (STEMI)
o 1,680,000 hospitalization for ACS in 2001
o 30% of ACS patients have STEMI
o 500,000 STEMI events per year in USA

ATHEROSCLEROSIS TIMELINE

UNSTABLE ANGINA and NSTEMI

(Imbalance between oxygen demand and supply)

Non- occlusive thrombus less severe ischemia and

myocardial damage unstable angina cardiac markers:
normal

Page 6 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

Vasospasm severe ischemia and myocardial damage - R wave gone or nearly gone
NSTEMI cardiac markers: elevated(Troponin I, Troponin T, - Significant Q wave
CKMB) - ST elevation may decrease
- T wave inversion beginning
Hx: severe localized chest or arm pain at rest or on minimal
exertion > 20mins crescendo pattern After 2 or 3 days
- Transmural infarction complete
PE: pulmonary edema new or worsening MR, S3, new or - No R wave
worsening rales - Deep Twave inversion
- Marked Q wave
ECG: transient ST segment changes (>0.05mv) new bundle - ST may be at baseline
branch block, sustained ventricular tachycardia
After several weeks or months
PATHOLOGIC and ECG changes in NSTEMI - Infracted tissue replaced by fibrous scar, sometimes
bulging (ventricular aneurysm)
First several days - Some R wave may return
- Some subendocardial muscle dies, lesion does not extend - T wave often less inverted
through the entire heart wall - Significant Q wave usually persists
- R wave persists but may diminish somewhat - ST elevation may persist if aneurysm _____
- Q wave not significant
- ST often returns to baseline STEMI ECG findings
- T-wave inversion may occur - At least 2mm ST segment elevation in two or more
precordial leads
After several weeks or months - ST segement elevation of at least 1 mm in two or more
- Lesion heals. Some subendocardial fibrosis may occur but leads
does not involve entire thickness of heart wall
- Q wave not significant Myocardial Ischemia, Injury and Infarction
- ST segment and T wave may or may not return to normal
- QRS Complexes in Infarction
ECG changes in Unstable Angina/NSTEMI o Normal QRS progression
- ST segment depression (30%) o Height of R wave is related to thickness of
- T-wave inversion (20%) viable myocardium
- Transient ST-segment elevation (5%)
Abnormal Q waves
- Duration: > 0.04sec
- Depth: > 25% of the height of R wave
ST ELEVATION MYOCARDIAL INFARCTION (STEMI)
Total occlusion Primary and Reciprocal ST changes in Acute Phase Infarction
Before Infarct In acute phase infarction
Pathological Diagnosis (Injury)
- Prolonged ischemia Lead facing infarct zone ST elevation typical
- Myocyte Death primary change
- Coagulation Necrosis Lead opposite infarct zone ST depressionTypical
- Myocytolysis reciprocal change

Clinical Diagnosis T wave changes in Myocardial Infarction

- History
o Accelerating Angina and rest pain(>30mins)
o Consistricting, crushing, compressing,
heaviness, choking
o Retrosternal radiating to ulnar aspect of left
arm
o Atypical presentation
- PE
o Soft S1, S3, S4, MR due to papillary muscle
dysfunction, pericardial friction rub
o Hypotension, tachycardia, bradycardia
- Deep symmetrical T wave inversion
- “Symmetry” refers to the equality of the angles of
downstroke and upstroke of the T wave
Evolution of ECG changes in Acute STEMI
a. Normal
b. Hours  ST elevation
c. Days  Qwaves, Small R, ST elevation
d. Weeks Q waves, Small R, ST isoelectric, Deep
T inversion
e. Months  Q waves, small R, ST isoelectric, T
wave upright

- ECG- ST Segment Elevation, Q waves Infarct, Location And ECG lead Involvement
- Cardiac Markers- Troponins (cTnT, cTnI), CK-MB mass,
Myoglobin Location of infarction Leads showing primary
changes
PATHOLOGIC and ECG changes in STEMI Typical changes
Anterior Infarction
First and second days Anteroseptal V1, V2, V3
- Transmural infarction nearly complete. Some ischemia and
Anterior V1-V3, V4-V6
injury may be present at borders
Page 7 of 8
CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine

Anterolateral V4-V6, I and AVL, possibly II  T-wave inversion or flattening or

Extensive Anterior V1- V6, I and AVL flattening in leads with dominant R
High Lateral AVL (plus high precordial waves
leads)
Inferior infarction Assess initial 12L ECG
Inferior II, III,AVF A. ST elevation or new LBBB/ ST elevation AMI
Inferolateral-Apical II, III, AVF, V5, V6 and - Treatment
sometimes also I and AVL o Start Adjunctive Treatment (within 24hrs of
Inferoseptal II, III, AVF, V1-V3 onset/ stable)
Other changes  B-blockers
Posterior infarction V1, V2( inverse of usual  Clopidogrel
changes elsewhere)  Heparin (UFH or LMWH)
 ACE inhibitors (or ARB)
Subendocardial Infarction Any lead (usually multiple
leads)
Time onset of symptoms
- >12 hours admit to monitored bed, assess risk status
ACS
- Most common proximate cause of sudden cardiac death
- <12 hours
- Chest pain
- ECG changes
Select reperfusion strategy
- Cardiac markers
Be aware of reperfusion goals:
- Door to balloon inflation(PCI) goal of 90 min
Case
- Door to needle (fibrinolysis) goal of 30 mins
- 55y/o man
- Continue adjunctive therapies and HMGCoA reductase
- Hypertensive, diabetic, smoker
inhibitor(statin)
- High cholesterol
- Severe substernal chest heaviness> 30 mins, “crushing”,
Cardiogenic shock or contraindications to fibrinolytics, PCI
“squeezing”
treatment of choice. PCI not available, use fibrinolytics
What do you do?
Primary PCI selected
a. Assess ABCs
- Experienced operators
b. Insert IV line
- High volume centers
c. Give oxygen per nasal cannula
- Cardiac surgical capability
d. Get a 12 lead ECG
Fibrinolytic therapy selected
Chest pain (Suggestive of ischemia)
- Altapase
- Streptokinase
A. Immediate assessment
- APSAC
- Vital sign, O2 saturation
- IV access
B. ST depression/ dynamic T-wave inversion (High risk
- 12 L ECG
UA/ non-STEMI)/ ST elevation or new LBBB/ ST-
- Brief history and PE
elevation AMI
- Cardiac Markers
C. Non-diagnostic ECG
- Electrolytes, coagulation and portable CXR
o ST depression 0.5-1mm
o T wave inversion or flattening in leads with
B. Immediate general treatment
dominant R waves
- Oxygen 4LPM
o Intermediate/low risk unstable angina
- ASA 160-325mg
- Nitroglycerin SL or spray
Absolute contraindications to beta blocker therapy
- Morphine
o Severe LV failure and pulmonary edema
- MONA Morphine, Oxygen, NTG, ASA
o Bradycardia(heart rate < 60bpm)
- Notify receiving hospital
o Hypotension( SBP < 100mm Hg)
o Signs of poor peripheral perfusion
C. Assess initial 12LECG
o Second or third-degree heart block
A. Assess the Initial ECG
B. 12L ECG is central to triage of ACS in the ER. Classify
patients as being 1 to 3 symptoms with 10 minutes
* Thanks to Esther Magkachi….
of arrival
a. STEMI
 ST-segment elevation 
 Or new or presumably new LBBB GOD bless!
b. High risk unstable (UNSTEMI)
 ST-segment depression
 Dynamic T-wave inversion
c. Intermediate/ low risk unstable angina
 Non-diagnostic ECG
 ST depression 0.5-1mm

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