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CVB by Minnie (Madeleine) > SM 127a/128a - Ischemic Heart Disease Pathogenesis and Pathology > Flashcards

SM 127a/128a - Ischemic Heart Disease Pathogenesis and Pathology Flashcards

1
Q

Which anti-ischemic agents work to decrease O2 demand and increase O2 supply?

A

Nitrates

Ca2+ channel blockers

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2
Q

What is hypoxia?

Common causes?

A

Decreased oxygen supply to a tissue with normal perfusion

Cyanotic congenital heart disease, anemia, CO poisoning

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3
Q

Describe the morphology of the heart 1 week - 1 month after infarction

A
  • Necrotic muscle is resorbed
  • Fibrous tissue becomes a myocardial scar
    • Thin, strong
    • Low risk of rupture
    • Prone to aneurysm
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4
Q

What is the gold standard for diagnosing ischemic heart disease?

Why isn’t it always performed?

A

Coronary angiography

  • Catherization
  • Inject radiographic dye for contrast

It is not used all the time because it is invasive

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5
Q

Describe the morphology of a later (6-12 hour) myocardial infarction

A
  • Contraction band necrosis
  • Coagulative necrosis (cell outlines but no centers)
    • Muscle fibers are eosinophilic (red)
    • Pyknosis of nuclei
      • Shrinkage and darkening
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6
Q

Thrombosis in ____________ would cause infarction in the Lateral LV wall

A

Left Circumflex Artery

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7
Q

How would increased intraventricular pressure affect coronary blood flow?

A

Increased intraventricular pressure would decrease coronary blood flow

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8
Q

Describe Class II Angina

A

Slight limitation of ordinary activity

Angina with…

  • Walking or climbing stairs rapidly
  • Walking uphill
  • Exertion after meals
  • Cold weather
  • Emotional stress
  • The first few hours after awakening
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9
Q

Describe the characteristics of a subendothelial MI

A
  • Ischemic necrosis in the inner 1/3-1/2 of the ventricular wall
  • NOT associated with intraluminal thrombosis
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10
Q

What are the indications for myocardial revascularization?

A
  • Failure of pharmacologic therapy
    • Progression of symptoms
  • Intolerable side effects of pharmacologic therapy
  • Compelling anatomy
  • Severe cardiac dysfunction
    • Ejection fraction < 40%
  • Low threshold for ischemia
    • Ex: at rest, or more severe classification
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11
Q

How do renin/angiotensin inhibitors work to treat ischemic heart disease?

A

Renin/Angiotensin agents…

  • Decrease blood pressure -> reduce chance of thrombotic event
  • Inhibit progression of atherosclerosis -> Increase vascular integrity (prevent rupture)

This reduces the risk of clot formation that could completely occlude a coronary artery

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12
Q

After MI, when is the heart most vulnerable to rupture? Why?

(When is its mechanical integrity weakest?)

A
  • 3-7 days after infarct
    • Dead muscle is replaced by macrophages and reparative cells
    • Everything is soft and inflammed
    • Repair has not yet begun
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13
Q

What 4 clinical syndromes may result from ischemic heart disease?

A
  • Angina pectoris
  • Myocardial infarction
  • Chronic ischemic heart disease
  • Sudden cardiac death
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14
Q

Describe the timeline of ATP loss due to cardiac ischemia

A
  • <2 min: Noticible decrease in contractility
  • 10 min: 50% ATP loss
  • 40 min: 90% ATP loss
  • 1 hour: Myovascular injury
    • Reperfusion at this point leads to hemorrhage
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15
Q

Which angina class is described as:

“Ordinary activity does not cause angina - Angina with strenuous, rapid, or prolonged exertion only”

A

Angina Class I

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16
Q

What is CABG?

A

Coronary Artery Bypass Surgery: Surgical intervention for ischemic heart disease

  • Arterial and/or venous conduits are places in the mid to distal coronary arteries
    • The stenosis is proximal to the conduit
    • Leave occlusion in place; make new paths around it
  • This increases blood flow to the ischemic myocardium
  • Vein remodels and becomes revascularized
  • Use in more severe cases or if multiple occlusions exist
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17
Q

After MI, when would you begin to see infiltration by neutrophils?

A

12-24 hours

(peak 3 days after infarct)

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18
Q

List the 4 major causes of myocardial infarction

A
  • Thrombosis of a coronary artery (leading cause)
    • Usually due to ulceration or rupture of an atheromatous plaque
  • Infarct without thrombosis
    • Lysis of thrombus or arterial spasm (rare)
  • Thromboembolism
  • Arteritis or dissection (rare)
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19
Q

Describe the mechanism of action of Ranolazine

A

Ranolazine closes the late inward Na+ gate

  • Less Na+ in = less Na+/Ca2+ exchange
    • Prevents Ca2+ overload that leads to arrythmia
  • Does not alter HR or BP
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20
Q

What are the pros and cons of PTCA as treatment for ischemic heart disease?

A
  • Pros
    • It is effective!
  • Cons
    • Metal may induce re-occlusion due to proliferation of endothelium in response to inflammation
    • It must damage the vessel in order to expand the lumen
      • This can cause rupture or hemorrhage
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21
Q

When would you expect total creatine kinase to rise, peak, and return to normal after MI?

What about the MB subform of creatine kinase?

A
  • Total Creatine Kinase
    • Rise after 4-6 hours
    • Peak 24h
    • Return to normal after 3-4 days
  • MB subform
    • Peak <24h
    • Return to normal after 2 days
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22
Q

What 3 cell types would you expect to find in an ischemic myocardium?

A
  • Necrotic myocytes
  • Interstitial hemorrhage
  • Reversibly injured “stunned” myocytes
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23
Q

What is anoxia?

A

Complete lack of oxygen supply to a dissue despite normal perfusion

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24
Q

What is atypical angina?

A

Angina in an atypical location, or not related to typical provoking factors

More common in women, diabetic patients

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25
Q

Desribe the mechanism of action of Nitrates

A

Nitrates increase cGMP to promote myocardial relaxation and aterial dilation to decrease O2 demand and increase O2 supply

  • Venodilation
    • -> Decreased myocardial wall tension
      • -> Increaesd myocardial blood flow
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26
Q

Which coronary is the most common site for thrombosis?

A

Left anterior descending artery (40%)

Right coronary artery (27%)

Left circumflex artery (11%)

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27
Q

What structures of the heart are supplied by the right coronary artery (RCA)?

A
  • Anterior right ventricle
  • Posterior 1/3 fo the IV septum
  • Posterior right ventricle
  • Part of the posterior left ventricle
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28
Q

Which anti-ischemic agent prevents arrhythmia and does not alter blood pressure or heart rate?

A

Ranolazines

(works by closing late inward Na+ gate -> reduces Na+/Ca2+ exchange -> prevents Ca2+ overload)

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29
Q

Describe the mechanism of action of Ca2+ channel blockers in treating ischemia

A

Ca2+ channel blockers decrease Ca2+ entry into myocardial and atrial smooth muscle

  • Decreases oxygen demand
    • Decrease HR
    • Decrease blood pressure
    • Decreaes contractility
  • Increases oxygen supply
    • Increase ventricular relaxation
    • Increase dilation of coronary arteries
    • Prevents coronary arterial spasm
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30
Q

When would you expect myoglobin to rise, peak, and return to normal after MI?

A
  • Rise 2h after infarction
  • Peak 6-8 h
  • Return to normal after 20-36
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31
Q

When would you expect lactate dehydrogenase to rise, peak, and return to normal after MI?

A
  • Rise begins at 24h
  • Peak after 3 days
  • Return to normal after 8-9 days
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32
Q

How would reduced aortic diastolic pressure affect coronary blood flow?

A

Reduced aortic diastolic pressure would reduce coronary blood flow

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33
Q

What is ischemia?

A

O2 deprivation + inadequate removal of metabolites due to reduced perfusion

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34
Q

Describe the morphology of an early (1-6 hour) myocardial infarction

A
  • No gross or light microscope findings
  • Electronic microscope reveals…
    • Wavy “lasagna noodle” muscle fibers
    • Leakage of myocardial enzymes (can be detected with dye)
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35
Q

After myocardial infarction, rupture of which walls would most likely lead to cardiac tamponade?

When is this likely to occur?

A

Free walls

  • Anteror, lateral, or posterior walls of LV

Most likely to happen 3-7 days after infarction, when the heart is most vulnerable

  • Everything is soft and inflammed
  • Repair has not yet begun
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36
Q

When would you expect Troponin to rise, peak, and return to normal after MI?

A
  • Rise in 4-6h
  • Peak 12-16 h
  • Return to normal after 10+ days
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37
Q

What are the goals of treatment for angina pectoris?

A
  • Symptom control to increase quality of life
  • Prevention of life-threatening complications
    • MI, death
  • Prevention of disease progression
38
Q

Which enzyme assay to diagnose MI rises most quickly after infarction?

A

Myoglobin

39
Q

What pathology are myocardial scars prone to?

A

Aneurysm

40
Q

How do lipid lowering agents (statins) work to treat ischemic heart disease?

A
  • Inhibit progression of atherosclerotic lesions
    • Prevent further coronary artery occlusion
    • Reduce the risk of plaque rupture -> thrombosis -> complete occlusion
  • Promotre regression of atherosclerotic lesions
41
Q

After MI, how when would you begin to see coagulative necrosis?

A

6-12 hours

42
Q

Describe the mechanism of action of beta-blockers

A

Beta blockers are competitive antagonists of epinephrine/norepinephrine

  • They block beta 1 receptors in the heart
    • Decrease pulse
    • Decrease arterial blood pressure
    • Decrease myocardial contractility
    • This decreases myocardial O2 demand
      • Prevents exercise-incuced increase in contractility
43
Q

In a myoglobin assay to diagnose MI, what might cause a false positive?

A

Renal failure

Skeletal muscle injury

44
Q

What are the two major types of anti-ischemic Ca2+ channel blockers?

How are they different?

A
  • Dihydrophyridines
    • Arterial vasodilators
    • Side effect = Pedal edema
  • Non-Dihydropyridines
    • Decrease HR
    • Less effect on blood pressure
    • Side effect = bradycardia, heart failure
    • Do not prescribe with other medications that lower HR (beta blokers), or in patients with LV dysfunction
45
Q

Describe Class III Angina

A

Marked limitations of ordinary physical activity

Angina on…

  • Walking 1 or 2 blocks on level ground
  • Climbing 1 flight of stairs at a normal pace under normal conditions
46
Q

What structures of the heart are supplied by the Left Anterior Descending Artery (LAD)?

A
  • Anterior surface of the left ventricle
  • Partial anterior surface of the right ventricle
  • Anterior 2/3 of the IV septum
  • Apex
47
Q

Describe the morphology of an MI 3-7 after the initial infarct

A
  • Dead muscle is replaced by macrophages and reparative cells
    • Proliferating fibroblasts and capillaries
  • Low mechanical integrity
    • Most prone to rupture, especially after transmural MI​
    • Everything is soft and inflammed
    • Repair has not yet begun
    • Rupture -> Cardiac tamponade -> Death
48
Q

How would decreased right atrial pressure affect coronary blood flow?

A

Decreased right atrial pressure would increase coronary blood flow

49
Q

Thrombosis in the Left Anterior Descending artery would cause infarction which sections of the myocardium?

A
  • Anterior LV wall
  • Anterior interventricular septum
50
Q

Which anti-ischemic agents work to decrease O2 demand (without changing O2 supply)?

A

Beta blockers

51
Q

Why does hypertension increase one’s risk of myocardial infarction?

A

High blood pressure puts additional stress on the fibrous caps of any existing atherosclerotic plaques

  • This increases the chance of plaque rupture
    • Plaque rupture -> thrombosis

Thrombosis of a coronary artery = leading cause of MI

52
Q

Which angina class is described as:

“Marked limitations of ordinary physical activity - Angina on walking 1 or 2 blocks on level ground or 1 flight of stairs at a normal pace under normal conditions”

A

Class III Angina

53
Q

Describe the characteristics of a transmural MI

A
  • Ischemic necrosis affecting nearly all of the ventricular wall thickness
  • Severe fixed atheromas + intraluminal thrombosis
  • Develops from endocardium -> outward
    • Subendocardial myocardium is the first affected, because it is at the most distal end of the coronary artery
54
Q

What are anginal equivalents?

A

Symptoms of myocardial ischemia other than angina

  • Dyspnea
  • Nausea
  • Fatigue
  • Faintness

More common in women, elderly people, diabetics

55
Q

Which angina class is described as:

“Slight limitation of ordinary activity - Angina with walking or climbing stairs rapidly, walking uphill, or exertion after meals, in cold weather, under emotional stress, or only during the first few hours after awakening”

A

Class II Angina

56
Q

What enzymes can be used to diagnose MI?

Which are most commonly used?

A
  • Troponin T (most commonly used)
  • Troponin I
  • Troponin L (new)
  • Creatine kinase
    • Total or MB (specific for cardiac muscle)
  • Lactate dehydrogenase
  • Myoglobin (not commonly used)
57
Q

What is PTCA?

A

Percutaneous transluminal coronary angioplasty: surgical intervention for ischemic heart disease

  • Dilate coronary artery
  • Insert a metal stent
    • May be drug-eluting
58
Q

What are the major side effects of Nitrates in treating ischemic heart disease?

A

Lightheadedness

Headache

Tolderance develops (don’t take the medication at night, allows for re-set)

59
Q

Which angina class is described as:

“Inability to carry on any physical activity without discomfort, or angina at rest”

A

Class IV Angina

60
Q

What are the major classes of pharmacologic intervention for ischemic heart disease?

List major drug types in each class

A
  • Anti-Ischemic agents
    • Nitrates
    • Beta-blockers
    • Ca2+ Channel blockers
    • Ranolazine
  • Antiplatelet agents
  • Anti-hypertension medication
    • Renin/angiotensin inhibitors
  • Lipid lowering agents
61
Q

How do antiplatelet agents work to treat ischemic heart disease?

A

Decreaseing platelet aggregation prevents thrombotic events that could cause complete occlusion of a narrow artery

62
Q

What causes the majority of all myocardial infarctions?

A

Thrombosis of a coronary artery

Forms at the site of an ulcerated or ruptured atheromatous plaque

63
Q

Thrombosis in ____________ would cause infarction in the anterior LV wall and/or the anterior interventricular septum

A

Left Anterior Descending artery

64
Q

In a lactate dehydrogenase assay to diagnose MI, what might cause a false positive?

A

Lactate dehydrogenase is found in many different muscle types

  • Heart muscle
  • Skeletal muscle
  • Liver
  • RBC
  • Kidney
  • Neoplasms
65
Q

Which isoenzymes of lactate dehydrogenase are relevant to MI?

A

LD1: Heart, RBC, renal

LD2: Reticuloendothelial

Reversal lf LD1 : LD2 implies MI

66
Q

Describe Class I Angina

A

“Ordinary activity does not cause angina - Angina with strenuous, rapid, or prolonged exertion only”

67
Q

What is angina pectoris?

A

Pain or discomfort in the chest or adjacent areas caused by insufficient blood flow to the heart

  • May be stable or unstable
  • 4 clinical types
  1. Chronic, stable angina
  2. Atypical angina
  3. Anginal equivalents & silent ischemia
  4. Other
68
Q

What are the 2 types of myocardial infarction?

A

Transmural

Subendothelial

69
Q

Which patients should not recieve non-dihydropyridine Ca2+ channel blockers as treatment for ischemic heart disease?

A

Patients with LV dysfunction

Patients taking another medication that lowers heart rate

(non-dihydropyridine Ca2+ channel blockers lower HR)

70
Q

Which structures of the heart are supplied by the left circumflex artery?

A
  • Lateral left ventricle
71
Q

When is CABG used over PTCA?

A

In more severe cases, or if multiple occlusions exist

72
Q

How would increased myocardial contraction affect coronary blood flow?

A

Increased myocardial contraction would decrease coronary blood flow

73
Q

What would happen to perfusion if there was no difference between the aortic diastolic pressure and the right atrial pressure?

A

Perfusion would cease

74
Q

Thrombosis in ____________ would cause infarction in the posterior LV wall and/or the posterior 1/3 of the interventricular septum

A

​Right Coronary Artery

75
Q

Describe the morphology of a 12-24 hour myocardial infarction

A
  • Infiltration by neutrophils (peak in 3 days)
    • Sign of inflammation
  • Muscle cells lose nuclei and cross-striations
76
Q

How can reperfusion injury after surgery be prevented?

A
  • Use cardioplegic solution
    • Selective perfusion agent that helpts ot prevent reperfustion injury
  • Hypothermia during surgery
    • Decrease the O2 needs of the heart to reduce imbalance between demand and supply
77
Q

What causes reperfusion injury?

A

After ischemia, reinroduction can cause death to vulnerable myocardial tissue

Possibly due to ion mismatch: Ca2+ rushes in, causing Z-lines to condense

Also may be due to rapid generation of ROS

78
Q

Thrombosis in the Right Coronary artery would cause infarction which sections of the myocardium?

A
  • Posterior LV wall
  • Posterior 1/3 of the interventricular septum
79
Q

List the 5 possible pathogenesis of ischemic heart disease

A
  1. Stenosing atherosclerosis of coronary arteries
  2. Platelet aggregation + formation of intramural thrombus
  3. Coronary vasospasm
  4. Nonatherogenic coronary disease
  5. Hemodynamic derangements
80
Q

How what tools and evidence help to diagnose ischemic heart disease?

A
  • ECG
    • “Exercise stress test”
    • ST depression or elevation
    • T wave changes
  • Scintigraphy (Radioactive tracer)
    • “Nuclear stress test”
    • Can see which areas are not perfused
  • Echocardiogram
    • Ischemic area will contract poorly -> wall motion abnormality
  • CT Angiography
  • Coronary angiography (Gold standard, but invasive)
81
Q

What are the 2 major clinical presentations of coronary atherosclerosis?

A
  1. Sudden reduction in blood flow due to plaque rupture -> Acute coronary syndrome
  2. Progressive narrowing due to negative remodeling -> Angina upon exertion
  • Vessel cannot increase blood flow to meet increased oxygen demand due to exercise
82
Q

Why are Troponin T and Troponin I assays the most popular for diagnosing MI?

A
  • They are specific to cardiac muscle
  • They are both sensitive and specific
  • Assay only takes 30 min to 1 hour
83
Q

What are the 3 major categories of treatment for ischemic heart disease?

A
  • Lifestyle modification
  • Pharmacologic intervention
  • Myocardial revascularization
84
Q

What are the clinical types of angina?

A
  1. Chronic, stable angina
  2. Atypical angina
  3. Anginal equivalents & silent ischemia
    (Shortness of breath)
  4. Other
    Decubitus, nocturnal, refractory, unstable, microvascular, neoplastic….
85
Q

Describe Class IV Angina

A
  • Inability to carry on any physical activity without discomfort

OR

  • Angina at rest
86
Q

Thrombosis in the Left Circumflex artery would cause infarction which sections of the myocardium?

A

Lateral LV wall

87
Q

What complications may arise after MI?

A

SACC PDF

  • Sudden cardiac death
  • Aneurysm with mural thrombus formation
  • Congestive heart failure
  • Cardiac arrhythmia
  • Papillary muscle dysfunction with valvular (esp. mitral) valve dysfunction
  • Dressler’s syndrome (fibrinous pericarditis)
  • Free wall rupture -> Tamponade
88
Q

What are the major risk factors for ischemic heart disease?

A

“HAS LIPIDS”

  • Heretity
  • Age
  • Sex (male)
  • Lipidemia
  • Increased weight
  • Pressure (is high)
  • Inactivity
  • Diabetes
  • Smoking
89
Q

List some examples of Ca2+ channel blockers

A

In general: -dipine, -il- (somewhere in the word_

Amlodipine

Felodipine

Nifedipine

Verapamil

Diltiazem

90
Q

What kind of drug is Nifedipine?

A

An anti-anginal Ca2+ channel blocker

(and other -dipine drugs)

CVB by Minnie (Madeleine) (43 decks)

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