Path: Ischemic Heart Disease

Question 1

What is the difference between myocardial ischemia and myocardial infarction?

Answer 1

Ischemia is hypoxia and accumulation of waste metabolites.

Infarction is tissue death due to ischemia.

Question 2

What is the main cause of Ischemic Heart Disease (IHD)?

Answer 2

Insufficient coronary perfusion relative to myocardial demand:

Chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries

Variable degrees of superimposed acute plaque change, thrombosis, and vasospasm

Question 3

How much coronary occlusion usually occurs before patients develop stable angina?

Answer 3

75%

Question 4

How much coronary artery occlusion occurs to develop unstable angina or even infarction?

Answer 4

90%

Question 5

Describe the atherosclerotic plaque changes that occur in:

1. Stable angina
2. unstable angina
3. Myocardial Infarction
4. Sudden Cardiac Death

Answer 5

1. Undisrupted plaque growth
2. Plaque is disrupted and ruptures leading to partially occlusive thrombus formation
3. Infarct results from disruption of plaque and complete occlusion by a thrombus leading to tissue death.
4. Sudden death occurs from complete occlusion of vessels by thrombus leading to ventricular arrhythmia.

Question 6

What is the difference between hypoxemia and ischemia?

Answer 6

Hypoxemia – failure to deliver adequately oxygenated blood to tissues

Ischemia – hypoxemia along with the inadequate removal of metabolites

Question 7

Describe a Transmural MI.

Answer 7

Necrosis of all the layers of the ventricles caused by complete occlusion of ONE coronary vessel.

Question 8

Describe a Subendocardial MI.

Answer 8

Necrosis of the inner 1/3-1/2 of the ventricle wall due to incomplete occlusion of multiple vessels. This accompanies vasospasm.

This tissue is not as well perfused as the outer layers of the heart and partial occlusion has drastic effects.

Question 9

Major cause of MI in a younger population (late teens, early twenties).

Answer 9

Cocaine Use

Question 10

Describe the 4 steps of evolution of an MI.

Answer 10

1. Sudden change in atherosclerotic plaque exposing subendothelial collagen.
2. Platelets adhere to collagen thinking it’s an injury leading to plug and thrombus formation
3. Platelets secrete mediators leading to vasospasm of coronary vessels
4. Tissue Factor activates coagulation pathway increasing the size of the thrombus

Question 11

At what time during the pathology of an MI is it possible to not see anything on gross examination of the heart?

Answer 11

30min - 4 hrs. post MI

Question 12

At what time during the pathology of an MI are necrosis, hemorrhage, and edema visualized on microscopy?

Answer 12

4-12 hours post MI

Question 13

At what time during the pathology of an MI is a yellow tan center viewed grossly and Neutrophil invasion viewed on microscopy?

Answer 13

1-3 days post MI

Question 14

At what time during the pathology of an MI is a hyperemic border with yellow-tan softening noticed on gross exam?

Answer 14

3-7 days post MI

Question 15

At what time during the pathology of an MI is granulation tissue formed?

Answer 15

7-10 days post MI

Question 16

At what time during the pathology of an MI does a gray-white scar and collagen deposition finally develop?

Answer 16

2-8 weeks

Question 17

Reperfusion of myocardial tissue may limit the extent of necrosis, but how can it also cause further injury?

Answer 17

Reperfusion not only brings nutrients and washes away waste, it also brings inflammatory mediators and WBCs that secrete free radicals that can damage tissue. This leads to swelling of the vasculature and can lead to ischemia.

Question 18

What is the characteristic seen on biopsy of reperfusion injury and when do you biopsy?

Answer 18

Contraction Band Necrosis

This is seen on biopsy. You only biopsy on patients that have had a heart transplant. This is because they have had their nerve innervation cut and won’t feel MI or angina and this is the only way to make a Dx.

Question 19

`How can contractile dysfunction be diagnosed on X-ray?

Answer 19

Kerley B lines. The dysfunction leads to pulmonary edema.

Question 20

When does a myocardial rupture occur post MI?

Answer 20

3-7 days post MI. The necrosis results in a weakened wall that can rupture.

Question 21

Type of necrosis that occurs in pericarditis.

Answer 21

Fibrinoid Necrosis

Question 22

What is the difference between extension and expansion?

Answer 22

Extension: New necrosis adjacent to an existing infarct

Expansion: Stretching, thinning and dilation of the infarcted region of myocardium (no new tissue involved in necrosis)

Question 23

Cause and danger of a mural thrombus.

Answer 23

Some contraction abnormality that leads to blood stasis and/or injury to ventricular endothelium that leads to clot formation.

This clot can break free and lead to pulmonary embolus or stroke.

Question 24

What is a complication of ventricular aneurysm and how does it form?

Answer 24

Mural Thrombus:
Bulging of the entire wall (transmural) of the ventricle causes thinning of it and scar tissue formation. This prevents the wall from contracting and blood stasis results in clot formation.

Rupture does not occur due to rigid scar tissue.

Question 25

Common complication due to papillary muscle dysfunction.

Answer 25

Mitral Valve regurgitation or prolapse.

Question 26

Increased ventricular wall is a risk for sudden cardiac death. What ventricular wall thickness is considered normal?

Answer 26

Should be 0.5 centimeters or less

measured 2cm below the valves