Pathoma - Ischemic Heart Disease - Fundamentals Of Pathology

Front 1

What is ischemic heart disease?

Back 1

A group of syndromes related to myocardial ischemia

Front 2

IHD is usually due to?

Back 2

Atherosclerosis of coronary aa.

Front 3

What does stable angina mean?

Back 3

Chest pain that arises with exertion or emotional stress.

Front 4

Stable angina represents what injury to myocytes?

Back 4

Reversible injury

Front 5

How much of the lumen is stenosed in patients with stable angina?

Back 5

Stable angina occurs when there is atherosclerosis of coronary aa. with more than 70% stenosis

Front 6

How do patients with stable angina present?

Back 6

(1) Chest pain (which lasts less than 20 minutes) that radiates to jaw or left arm
(2) Diaphoresis
(3) Shortness of breath

Front 7

In stable angina, an EKG would show what?

Back 7

ST segment depression (subendocardial ischemia)

Front 8

How is the chest pain in stable angina relieved?

Back 8

Rest or nitroglycerin (decreases amount of blood returning to heart)

Front 9

Unstable angina is what? What is it due to?

Back 9

Chest pain that occurs at rest. It is due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery.

Front 10

Unstable angina represents what type of injury to myocytes?

Back 10

Reversible injury

Front 11

EKG in unstable angina would show what?

Back 11

ST-segment depression

Front 12

How can unstable angina be relieved?

Back 12

Nitroglycerin

Front 13

People with unstable angina is at high risk for what?

Back 13

MI. Unstable angina is sort of the dysplasia of cancer, only in the setting of IHD. Precursor to MI.

Front 14

What is Prinzmetal angina?

Back 14

Coronary artery vasospasm that causes chest pain. It leads to episodic chest pain unrelated to exertion.

Front 15

Prinzmetal angina represents what type of injury to myocytes?

Back 15

Reversible

Front 16

What is shown on an EKG in prinzmetal angina?

Back 16

EKG shows ST-segment elevation due to transmural ischemia

Front 17

How is prinzmetal angina relieved?

Back 17

(1) Nitroglycerin
(2) Calcium channel blockers

Front 18

What ischemic heart disease syndromes do you know?

Back 18

(1) Angina pectoris
(2) Chronic ischemid heart disease
(3) SCD
(4) AMI

Front 19

What happens in MI?

Back 19

Necrosis of cardiac myocytes

Front 20

How does MI classically occur?

Back 20

Due to rupture of atherosclerotic plaque with thrombosis and complete occlusion of coronary artery.

Front 21

What is similar in unstable angina and MI?

Back 21

Both are due to rupture of atherosclerotic plaque with thrombosis, however, unstable angina (as opposed to MI) has an incomplete occlusion of a coronary artery.

Front 22

Mention causes of MI.

Back 22

(1) Rupture of atherosclerotic plaque with thrombosis
(2) Coronary artery vasospasm (Prinzmetal or cocaine)
(3) Emboli
(4) Vasculitis (Kawasaki)

Front 23

How do patients with MI present?

Back 23

(1) Severe, crushing chest pain that last longer than 20 minutes and radiates to left arm and jaw.
(2) Diaphoresis
(3) Dyspnea (congestion, edema)
(4) Symptoms NOT relieved by nitroglycerin

Front 24

The heart can withstand an ischemic state for _________ before irreversible injury occurs.

Back 24

20 minutes

Front 25

MI usually involves what part of the heart?

Back 25

Left ventricle. RV and atria are generally spared.

Front 26

What artery is most commonly involved in MI?

Back 26

LAD

Front 27

What is infarcted in LAD occlusion?

Back 27

Anterior wall of the ventricle, apex, anterior third of interventricular septum

Front 28

Second most commonly involved artery?

Back 28

Right coronary artery

Front 29

Occlusion of right coronary artery results in infarction of what areas of heart muscle?

Back 29

Posterior wall of left ventricle, posterior portion of interventricular septum

Front 30

The third most commonly involved artery in CAD? What is infarcted?

Back 30

Left circumflex artery; lateral wall

Front 31

___________________ (transmural/subendocardial) infarction is the most common type of MI.

Back 31

transmural

Front 32

What happens in the initial phase of MI? EKG?

Back 32

Subendocardial necrosis involving less than 50% of the myocardial thickness. EKG show ST-segment depression.

Front 33

If initial phase of MI continues, what happens? EKG?

Back 33

Continued or severe ischemia leads to transmural necrosis involving most of the myocardial wall (transmural infarction); EKG shows ST-segment elevation.

Front 34

The presence of cardiac enzymes in the blood would tell you that the heart has undergone ____________________.

Back 34

irreversible injury to myocytes

Front 35

Most sensitive and specific marker for MI? How does it rise and change with time?

Back 35

Troponin I

(1) Rises 2-4 hours after infarction
(2) Peaks at 24 hours
(3) Returns to normal by 7-10 days

Front 36

Another useful marker outside of troponin I. What is it useful for? How does it rise and change with time?

Back 36

CK-MB. Useful for detecting REINFARCTION. You couldn't prove reinfarction lets say five days after the initial infarction just by using troponin I.

(1) Rises 4-6 hours after infarction
(2) Peaks at 24 hours
(3) Returns to normal by 72 hours

Front 37

Treatment for MI?

Back 37

(1) Aspirin and heparin (limit additional thrombosis)
(2) Supplemental oxygen
(3) Nitrates
(4) Beta blocker
(5) ACE inhibitor

Front 38

Definitive treatment for MI?

Back 38

Fibrinolysis or angioplasty.

Percutaneous angioplasty with stent treatment is shown to have a lower 30-day mortality than thrombolytic therapy.

Front 39

Reperfusion to the heart results in two complications.

Back 39

(1) Contraction band necrosis (calcium is returned back to the dead tissue)
(2) Reperfusion injury

Front 40

What sequence of events microscopically would you predict would happen in the cardiac myocytes after complete occlusion of an artery.

Back 40

1. Coagulative necrosis (pyknosis, karyorrhexis, karyolysis)
2. Inflammation follows necrosis (neutrophils)
3. Macrophages now arrive
4. Healing; granulation tissue
5. Fibrosis (scar)

Front 41

A memory help for you to remember when microscopic events in the heart occur after an MI.

Back 41

1 day
- For the first day we see coagulative necrosis. After first day and up to a week we get inflammation. Begins w/neutrophils then macrophages.

1 week
- After one week you're gonna get granulation tissue.

1 month
- It takes one month for granulation tissue to become scar.

Front 42

What gross and microscopic changes do you observe in the heart less than 4 hours after an infarction?

Back 42

Nothing

Front 43

What is a complication of MI during the first four hours? (four hours from infarction)

Back 43

(1) Cardiogenic shock
(2) Congestive heart failure (blood backs up)
(3) Arrhythmia

Front 44

When do arrhythmias as a complication of MI usually occur?

Back 44

0-24 hours after an MI. Dmg to conducting system is going to become evident in the first 24 hours after cells are dying. After that, it becomes less likely to occur.

Front 45

A heart muscle biopsy shows coagulative necrosis but no neutrophils or inflammatory cells. How long time after infarction could this be?

Back 45

4-24 hours

Front 46

What gross changes are seen 4-24 hours after an infarction of the heart?

Back 46

Dark discoloration

Front 47

When do we see neutrophils in the heart muscle after infarction?

Back 47

from day 1 to day 3, after coagulative necrosis

Front 48

When do we see macrophages in the heart muscle after infarction?

Back 48

from day 4 to day 7

Front 49

What is the gross changes in a heart between 1 day after infarction up to a week?

Back 49

Yellow pallor due to inflammatory cells.

Front 50

When do we see fibrinous pericarditis as a complication of MI? How does it happen?

Back 50

In the inflammatory phase involving neutrophils, 1-3 days after an infarction.

Transmural inflammation can make the exudate get into the pericardium.

Front 51

In what MI do we see fibrinous pericarditis, subendocardial or transmural infarction?

Back 51

transmural

Front 52

When do we see ventricular free wall rupture as a complication of infarction of heart muscle? Why at this time is the wall at risk for this?

Back 52

The phase when macrophages enter, 4-7 days after an infarction. They eat away all the dead necrotic debree.

It is at risk because that is the time the wall is at its weakest.

Front 53

During days 4-7 (macrophages), rupture can occur. How might it occur?

Back 53

(1) Rupture of free wall creating cardiac tamponade.
(2) Rupture of interventricular septum (L-->R shunt)
(3) Rupture of papillary muscle with mitral insufficiency

Front 54

The papillary muscle is fed by the ___________________.

Back 54

right coronary artery

Front 55

The scaffold or base for scar formation is called ______________.

Back 55

granulation tissue

Front 56

What would you see microscopically 1-3 weeks after infarction of heart muscle?

Back 56

Granulation tissue with plump fibroblasts, collagen and blood vessels.

Front 57

How does the heart look grossly 1-3 weeks after an infarction?

Back 57

Red border emerges as granulation tissue enters from edge of infarct (they come from normal tissue around the necrotic focus and grow into it)

Front 58

Microscopic and gross changes to the heart months after an infarct?

Back 58

Microscopy would show fibrosis. Fibrosis looks white (white scar).

Front 59

When could we see an aneurysm as a complication of infarction of heart muscle?

Back 59

Months after an infarct. A scar is not as robust as normal healthy myocardial wall. The wall is now weakened, increasing risk for aneurysm.

Front 60

When can we see the risk for mural thrombus in the chamber of the heart associated with infarction of heart muscle?

Back 60

Months later. The nidus for this thrombus would be an aneurysm which could form at the same time.

Front 61

What is Dressler syndrome?

Back 61

A syndrome that can occur as complication some time (6-8 weeks) after an infarction. The idea is that transmural infarction can exposure previously hidden myocardial antigens to the immune system, this could then lead to Ab against myocardial antigens. It is an autoimmune pericarditis.

Front 62

How old is it?

Back 62

4 hours to 24 hours (coagulative necrosis)

Front 63

How old is it?

Back 63

4-24 hours - coagulation necrosis

Front 64

How old is it?

Back 64

Inflammation, so day 1 to day 3.

Front 65

How long after an MI could we observe this complication?

Back 65

1-3 days after given that a transmural infarction occurred, this is fibrinous pericarditis.

Front 66

When might this happen?

Back 66

Day 4 to day 7

Front 67

The type of collagen present in a scar of a myocardium would be __________.

Back 67

type I

Front 68

What is sudden cardiac death? How does it occur?

Back 68

Unexpected death due to cardiac disease. It occurs without symptoms or less than 1 hour after symptoms arise.

Front 69

Sudden cardiac death is usually due to what?

Back 69

Fatal ventricular arrhythmia.

Front 70

Most common etiology of sudden cardiac death?

Back 70

Acute ischemia. 90% have preexisting severe atherosclerosis.

Front 71

Other than acute ischemia, what are some causes of sudden cardiac death?

Back 71

(1) Mitral valve prolapse
(2) Cardiomyopathy
(3) Cocaine abuse

Front 72

What is chronic ischemic heart disease? How does it progress?

Back 72

Poor myocardial function due to chronic ischemic damage (with or without infarction). Progresses to CHF.

Front 73

Rupture of a ventricular aneurysm is __________ (common/uncommon).

Back 73

Rupture is uncommon.
• Scar tissue has good tensile strength,