1DDX: NOVEMBER 15TH, 2006

Coronary Artery Disease

Beginning of Myocardial Infarction

(There were 3 cases covered, but I couldn’t copy them all down, and couldn’t get them from Dr.
Pachkovskaja… Here’s what I could get!)

1Case #2:
A 66-year old man complains of chest pain and shortness of breath for 2 days. His current problems
began abruptly after a “cold” 2 days ago. He noted shaking chills and a cough productive of rust-
coloured sputum. The chest pain is right-sided, sharp, and much worse with deep breathing and
coughing. The medical history is significant for... (I didn’t get the rest…) See notes from November
17th: we saw this case again.

DDX:
Pneumonia
Bronchitis

Case #3:
A 42-year-old registered nurse is seen because of pain in the chest. She describes a “pain in my
heart” and points to a 1cm2 area above the left breast. The pain is intensified by deep breathing,
coughing and twisting motions. It has lasted continuously for 2 days. Findings from complete
physical examination are normal.

DDX:
Angina (unstable)
Fractured rib
Musculoskeketal problem.

Dyslipidemia: in slide that we were shown, evidence of lipid deposits around eyes (xanthelasma: not
100% signs of dyslipidemia, may happen just because of aging). In severe cases of dyslipidemia:
deposits on knees, hands.

Handout: Diseases of the Cardio-Vascular System #2

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Clinical features of coronary artery disease (CAD)

ANGINA PECTORIS
• chest pain due to underlying CAD.
• Pain in chest could be due to other factors, look out for these. Aortic dissection, pneumonia.
These are not angina.

3 types of angina:
Have to know how patient presents (pain) to know how to manage case.

1. STABLE ANGINA: FIXED atherosclerotic plaque.

What are characteristics of pain?
• Pain on exertion, emotions, relieved by rest. Relieved within 3-5 minutes of rest.
• Pain is described as “squeezing, tightening, pressure-like, vice-like”, “feeling of heaviness, heavy

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 feeling”, “burning”. Pain is in centre of chest, behind sternum (sub/retrosternal)
• Clenched fist over sternum as pt. describing pain is characteristic.
• Predictable.
• May be precipitated by :
o Temperature extremes (eg. Cold weather—because cold constricts. Causes
vasospasm).
o Also possible after meal: blood shunted to digestive system.
o Walking into wind -> vasoconstriction -> angina
• Increasing in intensity, begins with low intensity, within 2-3 minutes, increases in intensity. Within
several minutes of rest, pain is relieved. If it takes more than 10 minutes to relieve pain from rest,
IT IS NOT ANGINA.
• Pain for more than 25 minutes? May lead to MI.

Location and radiation of pain:

• Classic presentation: pain radiates to left arm, shoulder blade, between scapulae, down L arm to
fingers, patient may experience tingling sensation. Pain may radiate to jaw, but never extends
beyond auricle. May radiate to xyphoid process, to upper part of abdomen.
• Location that pain radiates to will depend on the part of the heart that is affected by angina.
• Also relieved immediately by nitroglycerin if it is angina (another characteristic feature).

If you take ECG during angina episode, will note ST segment depression (below baseline)

DDX:
Musculoskeletal / pleural origin of pain: can point with finger at the location of the pain.

2. UNSTABLE ANGINA:
• MEDICAL EMERGENCY! Underlying pathology: Ulceration, rupture, fissure forms on plaque.
Activates formation of thrombus. Can form embolus: more dangerous. Not fixed.
• Any changes in presentation of pain... consider that angina may have become unstable. It may
have been pain on exertion before, but now, it is shortness of breath. Look for changes in
previous description of pain. Does it now last longer? Does the patient need more nitroglycerin to
relieve pain? These changes alert you that something has changed, the condition has evolved.
• Unstable angina may develop from stable angina, or may be unstable from the onset.

Characteristics of pain:
• Unstable angina: responsible for 75,000 hospital admissions annually in Canada. 7000 will
develop MI in hospital.

• If you have a patient with unstable angina in your office, call 911: emergency.

• Patient usually presents w/ more than 1 problem. Maybe they come to you for eczema, but has
episode in your office. Take nitroglycerin and it doesn’t work. Take another right away, doesn’t
work? Start thinking about emergency. Call ambulance: unstable angina is 1 step before MI. We
have to know this and be able to recognize it. Time is crucial. May be unstable angina for first
few minutes, but may move from ischemia to damage to necrosis in matter of minutes.

• With unstable angina, patient may present with dyspnea alone (especially in women, patients with
diabetes). May not present with classic chest pain.

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• ECG may show ST depression OR elevation from baseline.

• ECG changes will resolve when pain goes away. In MI, the changes will last much longer on
ECG.
In unstable angina, cardiac enzymes stay the same: no damage yet. (DDX from MI)

Hallmark of MI: ECG changes, cardiac enzyme changes (indicating necrosis)

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3. VARIANT ANGINA (PRINZMETAL’S)

Spasm: occurs at rest d/t coronary artery spasm.
No anatomical lesions in Variant Angina. Will not see narrowing of arteries d/t plaques, lipid
deposition. May see narrowing d/t spasm during spasm, but it will stop when episode subsides.
Mechanism is unknown.

This type of angina is responsible for sympathetic death: after delivery of bad news. Causes
vasospasm due to activation of sympathetic nervous system. Feeling of fear, shock, tension, and
panic. Acute spasm can cause sudden death.

ECG during episode of pain: shows ST elevation (Hallmark)

Very hard to diagnose CAD because the ECG will be normal unless they are having an episode of
angina.

ECG:
Depressed ST segment is due to moderate ischemia anoxia
Elevation: due to severe ischemia and anoxia

Diagnosis of Angina (all forms):

• **Patient history!!*** Most important. All tests, examinations may be normal, but if the patient
gives a description of pain, this is most important.
• *Risk factors! See “global risk assessment” for men and women: Scores risk factors for men and
women. Total points, see what risk percentage is within 10 years.
• Other side: desirable levels of HDL, LDL. Set targets for patient.
• PCD: may not see anything abnormal.

Rule out:
1. Pulmonary embolism, dissecting aortic aneurysm, MI.
2. MSK problem. Have to palpate the chest: look for fractures, muscles, masses. May be able to
reproduce the pain if it is from MSK source. Eg. Inflammation of costochondral joints (Titzes
syndrome). Pain, description may mirror presentation of MI, but you can reproduce it by palpation
and rule out MI. Remember that pt. may present with 2 pathologies... could have MI + MSK problem)

CONFIRMATION OF ANGINA DIAGNOSIS

Chest x-ray
Echocardiography
Resting ECG (normal DOES NOT RULE OUT CAD!) Normal ST is on baseline.

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Page 6

Holter monitor:
• Records electrical activity for 24-48 hours (or longer) of pt. heart. Has to keep diary of pain,
activities. Compared with electrical activity of heart. Correlation between patient’s report of
symptoms and the actual activity of the heart.
• This is an excellent tool: inexpensive, relatively unobtrusive, and can rule out CAD. May be other
symptoms that are causing the chest pain. Is it anxiety? If there is no change in the heart activity,
it is probably not the heart causing the problem.

Stress test:
• Goal of stress test? Provoke imbalance between coronary supply and demand. Make patient
exercise. If coronary arteries are not involved in pathology, you will see normal increase in HR,
and normal delivery of blood to heart through coronary arteries.
• But: if patient has CAD, with increase exercise, there is a threshold that the patient will reach,
ECG changes will occur (ST depression), BP will drop or increase above predicted value, will see
increases in heart rate, maybe arrhythmias
• Treadmill: monitored by doctor/nurse, all equipment for monitoring potential MI is there.
• When should stress test be stopped? Chest pain, arrhythmia, extreme tiredness.

Analysis of results of stress test: image of myocardium a few hours afterwards.

May see cold spot (scar tissue). Will not pick up thallium (not tested on this)

ST elevation: especially in early morning hours d/t catecholamines

ST depression: (look for pictures of this online to illustrate it for yourself.)

Coronary angiography and cardiac catheterization (won’t be asked for details on exam)
CA: radiographic material is injected to get image. Can see interrupted blood flow.

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TREATMENT OF ANGINA:
• Treat pain: nitroglycerine
• Pharmacologic treatment: keep mechanism of pathology in mind. Have to re-establish balance
between myocardial demand/myocardial blood supply. See handout on “drug therapy for angina
pectoris”. See the mechanism of action for nitrates, beta-blockers, calcium channel blockers

In patient with unstable angina, regular exercise is contraindicated (unless it becomes stable angina).
But if their angina is unstable, it is a medical emergency, and they should be in the hospital until it
becomes stable again.

Percutaneous transluminal angioplasty (PCTA)

Percustaneous means: “through the skin”
First done in Switzerland in 1977. Alternative to bypass surgery for some patients. Not all patients
are candidates for this. Must have a SINGLE narrow segment in 1 coronary artery (2 may be
possible). Removes or obstructs atherosclerotic plaque.
Do angiography (x-ray of coronary artery). If there is obstruction, may consider angioplasty.
Goal: increase diameter of obstructed lumen, increase blood supply.
Uses balloon catheter to introduce stent into coronary artery. Passed up through femoral artery.
Balloon is inflated, compresses the plaque against the artery wall. Stent keeps the vessel open
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permanently.

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Bypass surgery:
• Began in 1960's. Purpose: to increase circulation/nourishment to heart muscle.

2 approaches:
• saphenous vein: superficial vein from the leg that we can survive without. Still have good venous
drainage in leg. May remove both veins, depending on how many bypasses need to be done.
Attach vein to aorta and to artery, below the blockage, to bypass the blockage.
• 2nd approach: internal mammary artery bypass (arteries behind breastbone) Left is especially
suited (size and location), joins aorta (left clavicular artery?) To coronary artery below obstruction.

See last page of 2nd note package for chart of drug class, examples, actions. Don’t memorize drugs,
but know the major group of drugs and their mechanism of action.

Review:
What other systems can give chest pain?
Respiratory disease: pleural pain, pulmonary embolism
GI: acid reflux, hiatus hernia, cholecystitis
Rib fracture, pulled muscle, diseases of cervical vertebrae
Herpes zoster: may complain of chest pain. Will find dermatomal pain in this condition
Neurological diseases
Depression, anxiety

Handout: Diseases of the Cardio-Vascular System #3

MI: refers to ischemic necrosis. Heart attack.

Thrombus is responsible for 85% of cases. Thrombus originates from ruptured or growing plaque.
Virchov’s triad: Stasis (very slow blood flow d/t obstruction downstream), hypercoagulability (d/t
stasis?), injury (to vessel wall): these predispose patient to MI.

In rare cases, MI may not be due to thrombus, but rather, to coronary spasm (with cocaine use).

It is a process. There are stages in the development of MI:

• Ischemia (reversible stage!) At foundation of CAD/MI. Timely dx and management/monitoring will
save their life.
• Injury (still reversible)
• Necrosis (not so reversible)

CLASSIC CLINICAL SYMPTOMS OF MI

How is it different from CAD?
• DDX Feature: This pain does not subside with rest. Lasts much longer than anginal pain (15-30
minutes)
• Location: like CAD, it is also substernal. Same thing.
• Same radiation of pain
• **occurs at rest: different from stable angina

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• DDX Feature: Unresponsive to nitroglycerin. (Unstable angina may also be unresponsive to
nitroglycerin: may be indistinguishable from MI without bloodwork, ECG.)

ATYPICAL PRESENTATION:
Elderly, diabetics, may not have chest pain, just shortness of breath, extreme fatigue. May have
abdominal pain, indigestion.
• These symptoms (SOB) presented in 42-year old man, no risk factors, died of transmural MI.
• Another patient: sore throat: 35 years old. No risk factors, sports coach, normal pulse, BR. His
father died of stroke. Just before stress test, took ECG: found that he had transmural MI. That
morning, he had been running around the hospital, exercising for 2 hours. His only symptom was
a sore throat.

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