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- 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%
0 10 20 30 40 50 60 70
Percent of Patients
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
• Unstable Plaque Acute/catastrophic events SUDDEN • Ischemia- insufficient flow of blood to the myocardium. Still
Heart Failure, arrhythmia or MI! some degree of myocardial profusion
• Infarction means there is an occlusion and therefore there
• Stable Plaque (benign in its course) gradual progression is a lack of blood supply
to events Heart Failure, arrhythmias, and MI • Occlusion- complete cut off of blood flow. There can be MI
- Arrhythmias: lead to sudden death because of the
or sudden death
irregularity of the rhythm • Atherosclerosis of the coronary artery causes inadequate
- Stable and Unstable Angina can both lead to catastrophic
blood supply to the heart
events as stated above • The imbalance between the Oxygen supply and demand?
- Goal is to stabilize the plaque to prolong the life of the
- The hypertrophied myocardium on account of a chronic
pt. uncontrolled hypertension. The thicker the wall of
- Atherosclerosis is irreversible. It causes pathologic
myocardium the more blood it requires. It cannot be
damage that we cannot see until it is too late. provided from a narrow coronary artery (which means
st
- Atherosclerosis starts in the 1 decade of life and
it’s partially obstructed by a blood clot) affected by
depends on the lifestyle and the risk factors of the atherosclerotic changes
individual • 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
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CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine
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
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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)
ATHEROSCLEROSIS TIMELINE
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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 depressionTypical
- Myocytolysis reciprocal change
- 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
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CORONARY ARTERY DISEASE (CAD)
Rebecca W. Deduyo MD FPCP FACC
Internist/ Adult Cardiologist
Fatima University College of Medicine
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