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Cardiovascular > SM 127 Ischemic Heart Disease: Pathology > Flashcards

SM 127 Ischemic Heart Disease: Pathology Flashcards

1
Q

When is a myocardial infarct most likely to rupture?

A

Between 3-7 days after onset of ischemia, due to replacement of dead cardiomyocytes with fibroblasts

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2
Q

Why are women less likely to develop IHD?

A

Protective effects of Estrogen; wears off in PMP women

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3
Q

What time frame is an early MI?

A

Early MI is < 6 hours after the onset of ischemia

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4
Q

Where do thrombi form on stents?

A

Thrombi form directly on the implanted stent, ironically causing the same issue the stent is trying to fix

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5
Q

What is LDH?

A

Lactate Dehdyrogenase is an enzyme found in heart, skeletal muscle and liver, erythrycoytes, and kidney

Commonly elevated in MI but also other diseases in many organs

Peaks in 3 days, several isozymes L1-L5

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6
Q

Why is cardioplegia able to avoid reperfusion injury?

A

Inhibits ischemic injury by reducing the oxygen needs of the heart via asystole

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7
Q

Why does cardiac surgery involve myocardial injury?

A

Cardiac surgery requires a bloodless field, achieved by clamping the Aorta

Aortic clamping leads to ischemic injury, unclamping leads to reperfusion injury

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8
Q

How is MI diagnosed in lab?

A

Cardiac enzymes are used to diagnose an MI, but elevations in enzyme levels are not specific for any mechanism of injury

Need to correlate with ECG and clinical findings

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9
Q

What encompasses coagulative necrosis in an MI?

A

Muscle fibers stain more intensely red and their nuclei under go pyknosis, between 6-12 hours

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10
Q

Compare and contrast transmural to subendocardial MI?

A

Transmural MI involves most or all of the ventricular wall, usually due to a fixed lesion with severe occlusion of a coronary artery due to a thrombi

Subendocardial MI involves the inner half of the ventricular wall, and is not associated with intraluminal thrombosis; due to high sensitivity of subendocardium to ischemia

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11
Q

What causes Ischemic Heart Disease?

A

A mismatch between oxygen supply and demand

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12
Q

What factors reduce coronary blood flow?

A 
Decreased aortic diastolic pressure
Increased IV pressure and myocardial contraction
Coronary artery stenosis
Aortic valve stenosis/regurgitation
Increased right atrial pressure
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13
Q

How does cardiac tamponade follow MI?

A

Transmural infarcts during the period of time 3-7 days after an MI are very likely due to fibroblasts not yet fully replacing dead cardiomyocytes, making the dead portion of the heart susceptible to rupture

If the ruptured portion of the heart is on any face of the LV that faces the outside of the heart (not the IV septum), blood can escape and fill the pericardial sac, resulting in cardiac tamponade and SCD

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14
Q

Why can reperfusion be dangerous following a period of ischemia?

A

Injury may be reversible or irreversible, and although eventual reperfusion is necessarycan lead to myocardial stunning and irreversible cell damage

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15
Q

Why are occlusions early in arteries more dangerous?

A

More dependent tissue downstream at higher portions of an artery, leading to greater effect/ischemia in earlier occlusions

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16
Q

What is the LD1/LD2 ratio?

A

Ratio of LD1 (heart LDH) to LD2 (reticuloendothelial LDH)

Reversal of LD1/LD2 ratio indicates MI

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17
Q

Infarcts of the LAD affect what areas?

A

Anterior LV free wall and anterior Septum

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18
Q

What are “stunned” myocytes?

A

Myocytes that are not contracting due to lack of oxygen supply but have not yet undergone irreversible damage or cell death

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19
Q

What are the risk factors for IHD?

A

HASLIPIDS

Heredity
Age
Sex (M > F)
Lipidemia
Increased Weight (Obesity)
Pressure (Hypertension)
Inactivity
Diabetes
Smoking
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20
Q

How do coronary stents give rise to plaques?

A

Insertion of a foreign object promotes plaque formation, as does vessel stretch caused by stent insertion which can tear the vessel itself and predispose clot formation

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21
Q

When does coagulative necrosis occur in an MI?

A

Changes begin around 6-12 hours following onset of ischemia

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22
Q

Why do venous grafts form thrombi if atherosclerosis is restricted to arteries?

A

Venous grafts link arteries using transplanted veins, and the transplated venous vessel is subjected to high pressures, “arteriolizing” them and predisposing atherosclerosis

23
Q

What is Troponin?

A

A contractile protein of the myofibril with highly specific cardiac isoforms; frequently assess Troponin I and L

Peaks in 12-16 hours

24
Q

What is cardioplegia?

A

Stopping cardiac activity, often given as a solution that avoid ischemic injury through hypothermia and asystole

25
Q

What findings can be found in an early MI?

A

Mitochondrial changes can be observed with EM

“Wavy” muscle fibers due to stunned myocytes not contracting and instead being pulled around by other contracting myocytes

26
Q

What factors effect infarction size and location?

A

Duration of occlusion, size of artery and vascular bed effected, extent of collaterals, extent of spasm

27
Q

What portion of the cardiac wall is most susceptible to injury?

A

The subendocardium

28
Q

When do cardiac myocytes lose their nuclei and cross-striations?

A

Between 12-24 hours, and the infarct becomes infiltrated with neutrophils

29
Q

What does the Right Coronary Artery supply?

A

Anterior right ventricle
Posterior 1/3 of the IV Septum
Posterior surface of the right and left ventricle

30
Q

Are there anastomoses between the three major coronary arteries?

A

Yes, but they are poorly developed

31
Q

Infarcts of the Right Coronary affect what areas?

A

Posterior LV free wall, posterior Septum

32
Q

What is vascular remodelling and why does it not protect against most MI?

A

Following occlusion, vascular bed remodels to compensate for loss of blood flow; slow process that cannot respond to rapid onset MI

33
Q

Compare and contrast: Hypoxia, Anoxia, Ischemia?

A 
Hypoxia = reduced Oxygen supply with normal perfusion
Anoxia = absence of oxygen despite normal perfusion
Ischemia = oxygen deprivation due to reduced perfusion
34
Q

How can an aneurysm lead to MI?

A

Aneurysms allow for blood to pool in the thin ballooned out portion of an artery, which can result in thrombi formation that blocks a coronary vessel leading to MI

35
Q

What plaques are most likely to cause an MI?

A

MI is frequently due to thrombosis of a coronary artery, with the thrombi dislodging from a ruptured atheromatous plaque

Plaques that are contained with a thin fibrous cap or in high pressure change areas are more likely to rupture

36
Q

How do scars form following an MI?

A

Fibroblasts invade 3-7 days after ischemia ensues and replace dead cardiomycotes, forming a thin but stable scar that may form an aneurysm

37
Q

What are the presentations of Ischemic Heart Disease?

A

Chest Pain
Myocardial Infarction
Chronic Ischemic Heart Disease = scarring and heart failure
Sudden Cardiac Death

38
Q

What does hypertrophy of the heart indicate?

A

Increased systemic oxygen demand

39
Q

Outline the pathogenesis of Ischemic Heart Disease?

A

Stenosing atherosclerosis of coronary arteries
Platelet aggregation and formation of intraluminal thrombi
Coronary vasospasm
Nonatherogenic coronary disease
Hemodynamic derangements

40
Q

What is myoglobin?

A

Protein found in striated muscle, in circulation after damage to skeletal or cardiac muscle

Peaks 6-8 hours after MI

False positives due to skeletal muscle injury and renal failure

41
Q

Why is oxygen delivery dependent on coronary flow?

A

The heart extracts nearly all oxygen from blood at baseline, so increased flow is the only way to increase oxygen delivery

42
Q

Define Sudden Cardiac Death

A

Death within 1 hour of symptoms, often times the first manifestation of IHD

43
Q

Infarcts of the Left Circumflex affect what areas?

A

Later LV free wall

44
Q

What does the Left Circumflex supply?

A

Lateral left ventricle

45
Q

What is the MB fraction?

A

The fraction of total CK that is from heart muscle, rises and normalizes sooner than total CK

46
Q

How can cardiac ischemia lead to hemorrhage?

A

After 1 hour of cardiac ischemia, microvascular injury occurs

Once vessels are injured and “leaky”, reperfusion results in blood escaping the vessels and hemorrhaging

47
Q

What attributes of a plaque set the risk for life threatening outcomes?

A

Composition and vulnerability of a plaque to rupture matter more than volume or severity of stenosis in progression to MI

Lipid rich and soft plaques are more likely to rupture than collagen rich and hard plaques, generating thrombi that block coronary arteries and lead to MI

48
Q

What are the most common sites of thrombosis in the coronary circulation?

A

LAD, Right Coronary, Left Circumflex in a 3:2:1 ratio

49
Q

What is contraction band necrosis?

A

Common in MI, due to thickened increased Calcium permeability causing influx and a thickened Z line

50
Q

How is CK used to detect MI?

A

Creatine Kinase is found in the heart, skeletal muscle, and brain

CK is commonly elevated in MI, but can also be elevated in muslce trauma and delirium

Peaks 24 hours after MI and returns to normal after 4 days

51
Q

Where are coronary arteries normally found, and what pathologies can be associated with them?

A

Coronary arteries normally found on epicardium

May be found in the walls of muscle as well, which predisposes occlusion during contraction leading to SCD

52
Q

What is the preferred marker for MI and why?

A

Troponin T and I, the contractile proteins of myofibril with specific cardiac isoforms not present in healthy individuals

53
Q

What are the complications following MI?

A

SCACFDP

Sudden Cardiac Death
Congestive Heart Failure
Aneurysm with Mural Thrombus
Cardiac Arrythmia
Free wall rupture into cardiac tamponade
Dressler's syndrome
Papillary muscle dysfunction
54
Q

What does the Left Anterior Descending artery supply?

A

Anterior surface of and right ventricles
Anterior 2/3 of IV septum
Apex

Cardiovascular (25 decks)

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