L42 Ischemic Heart Disease

Question 1

What is the leading cause of mortality worldwide?

Answer 1

Cardiovascular disease (25% of US deaths)

Question 2

What happens in heart failure (also known as congestive heart failure)?

Answer 2

The heart is unable to pump blood sufficiently to meet the needs of the tissue

Question 3

What are the two types of heart failure?

Answer 3

Diastolic (inability of the heart chamber to relax, expand, and adequately fill during diastole; ventricle is unable to fill with blood)

Systolic (inadequate myocardial contractile function; the ventricle is unable to eject blood)

Question 4

In which type of heart failure does the ejection fraction decrease?

Answer 4

Systolic heart failure

Question 5

What increases in heart failure?

Answer 5

End diastolic ventricular volume, end diastolic pressures, venous pressure

Question 6

What happens in right sided heart failure?

Answer 6

Engorgement of the systemic and portal venous circulation

Question 7

What happens in left sided heart failure?

Answer 7

Damming of blood in the pulmonary circulation and diminished peripheral blood flow

Question 8

What are some causes of left sided heart failure?

Answer 8

Ischemia, hypertension, aortic and mitral valve diseases, and non-ischemic myocardial diseases

Question 9

What are the causes of right sided heart failure?

Answer 9

Left sided heart failure, cor pulmonale

Question 10

What are some signs and symptoms of right sided heart failure?

Answer 10

Edema, dark purple legs (blood pooling), ascites, hepato/splenomegaly

Question 11

What are some signs and symptoms of left sided heart failure?

Answer 11

Dyspnea, orthopnea, no edema, no ascites

Question 12

What causes ischemic heart disease?

Answer 12

Decreased perfusion (coronary blood flow) and increased myocardial demand

Question 13

What are four syndromes caused by ischemic heart disease?

Answer 13

1. Angina pectoris
2. Acute myocardial infarction
3. Chronic ischemic heart disease/heart failure
4. Sudden cardiac death

Question 14

What are the three types of angina pectoris?

Answer 14

1. Stable
2. Unstable
3. Prinzmetal

Question 15

Describe stable angina pectoris.

Answer 15

Result of chronic stenosing coronary atherosclerosis; leads to increased cardiac demand and workload needs unmet

Question 16

Describe the lumenal obstruction in stable angina pectoris.

Answer 16

> 75% reduction of lumen area

Question 17

What are the symptoms of stable angina pectoris?

Answer 17

Substernal chest pressure during physical activity and emotional excitement that is relieved with rest

Question 18

Describe unstable angina pectoris (aka crescendo agina, pre-infarction angina)

Answer 18

Caused by atherosclerotic plaque disruption; atheroma cap is breached, exposing the core, leading to platelet activation and aggregation; vasospasm may also occur. Eventually, there is a partially occluding thrombus formed.

Question 19

Describe the lumenal obstruction of unstable angina pectoris.

Answer 19

50-75% (less than stable)

Question 20

What are the symptoms of unstable angina pectoris?

Answer 20

Anginal symptoms, but they occur frequently with less effort/at rest for a longer duration

Question 21

What types of plaques are vulnerable?

Answer 21

Lipid rich atheromas with thin fibrous caps and lots of inflammation

Question 22

Describe Prinzmetal variant angina.

Answer 22

Caused by a coronary artery spasm unrelated to physical activity, heart rate, and blood pressure

Question 23

Describe the pathogenesis of myocardial infarction.

Answer 23

Plaques are disrupted. Platelets adhere/aggregate/activate. Vasospasms occur. Coagulation is activated. Ultimately, an occlusive thrombus forms.

(There are other possible mechanisms).

Question 24

Describe the development of acute coronary syndromes.

Answer 24

Atherosclerosis causes a fixed coronary obstruction (typical angina). This plaque can be disrupted/healed, leading to severe fixed coronary obstruction (chronic ischemic heart disease) or to thrombus formation.

Question 25

What are the acute coronary syndromes?

Answer 25

Unstable angina, acute myocardial infarction

Question 26

When does reversible ischemia become irreversible and progress to coagulative necrosis?

Answer 26

After 30 minutes

Question 27

What is the difference between a transmural and nontransmural infarction?

Answer 27

Transmural: entire thickness of the wall is infarcted Non-transmural: only a portion of the myocardium is infarcted

Question 28

When a coronary artery is obstructed, which part of the heart infarcts first?

Answer 28

The part of the heart furthest from it (except a thin portion of the lumenal myocardium that is spared)

Question 29

Describe the morphology of the myocardium after 0.5-4 hours.

Answer 29

No gross or light microscopic changes

Question 30

Describe the morphology of the myocardium after 4-12 hours.

Answer 30

Beginning of coagulative necrosis, hemorrhage (eosinophilia of cytoplasm, loss of some nuclei, some hemorrhage)

Question 31

Describe the morphology of the myocardium after 12-24 hours.

Answer 31

Gross: dark mottling (hemorrhage) Histology: Ongoing coagulative necrosis, pyknosis of nuclei (very pink fibers, RBCs)

Question 32

Describe the morphology of the myocardium after 1-3 days.

Answer 32

Gross: mottled myocardium Histology: loss of nuclei and myocytes, neutrophil infiltrate

Question 33

Describe the morphology of the myocardium after 3-7 days.

Answer 33

Myocyte disintegration, dying neutrophils, phagocytosis of dead cells

Question 34

Describe the morphology of the myocardium after 7-10 days.

Answer 34

Well-developed phagocytosis and early granulation tissue

Question 35

Describe the morphology of the myocardium after 10-14 days.

Answer 35

Granulation tissue

Question 36

Describe the morphology of the myocardium after 2-8 weeks.

Answer 36

Scar formation

Question 37

What are the symptoms of MI?

Answer 37

Crushing substernal chest pain, dyspnea, diaphoresis, tachycardia, pulmonary congestion, edema

Question 38

What laboratory evaluations can be done to look for an MI?

Answer 38

Myoglobin (first), creatinine kinase (second), and troponin (third) all increase

Question 39

What is a triphenyletrozolium chloride stain used for?

Answer 39

Stains LDH red (yellow when it isn't there); this enzyme is depleted in MI

Question 40

How can MI's be treated?

Answer 40

1. Aspirin/anti-platelet agents (counteract thrombus formation) 2. Heparin (counteract coagulation cascade) 3. Thrombolytic therapy (counteract thrombus formation) 4. Beta blockers (slow heart rate/contractility, decrease demand of heart) 5. ACE inhibitors (decrease remodeling) 6. Nitrates (vasodilation) 7. Oxygen (decrease demand)

Question 41

What is the goal of therapy in the setting of an MI?

Answer 41

Myocardial salvage

Question 42

What is reperfusion injury?

Answer 42

Restoration of blood flow leads to local myocardial damage (free radical production, hypercontracture due to increased intracellular calcium, leukocyte aggregation, and mitochondrial dysfunction)

Question 43

What are 5 serious MI complications?

Answer 43

1. Cardiogenic shock 2. Arrhythmia 3. Rupture 4. Acute pericarditis 5. Ventricular aneurysm

Question 44

What happens in cardiogenic shock?

Answer 44

Severe pump failure in 10-15% of patients who have very large infarctions

Question 45

Why does arrhythmia occur in the setting of an MI?

Answer 45

Myocardial irritability, conduction disturbances

Question 46

When does myocardial rupture typically happen after MI?

Answer 46

After 3-7 days

Question 47

Where can the myocardial rupture occur?

Answer 47

Free wall (leading to hemopericardium or cardiac tamponade), ventricular septum, or papillary muscle

Question 48

Ventricular aneurysm is a late complication of MI. What is a complication of the aneurysm?

Answer 48

Mural thrombus

Question 49

What is remodeling?

Answer 49

Alteration in the structure of the heart in response to hemodynamic load and/or cardiac injury in association with neurohormonal activation

Question 50

Describe the process of remodeling.

Answer 50

Hypertension (pressure overload), valvular disease (pressure/volume overload), and MI (regional dysfunction with volume overload) all increase cardiac work. This increases wall stress. Cells stretch and hypertrophy and/or dilate.

Question 51

What is the mechanism of sudden cardiac death in ischemic heart disease?

Answer 51

Lethal arrhythmia caused by myocardial irritability from ischemia or fibrosis

Question 52

What are the effects of hypertension/left-sided hypertensive heart disease?

Answer 52

Hypertrophy of the left ventricle (can even be caused by mild BP elevation)

Question 53

Compare a normal heart weight/LV wall thickness to that of someone with systemic hypertension and aortic stenosis.

Answer 53

Normal: 250-350 gm, 1.5cm thick HTN: 500+ gm, 2+cm thick Aortic stenosis: 800 gm

Question 54

What can happen to someone with left-sided hypertensive heart disease?

Answer 54

1. Asymptomatic 2. CHF 3. Arrhythmias/A Fib

Question 55

What causes cor pulmonale (pulmonary hypertensive heart disease)?

Answer 55

Pulmonary HTN (caused by COPD, pulmonary fibrosis, chronic pulmonary thromboembolism, primary pulmonary HTN, increased resistance)