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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

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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
Desribe the mechanism of action of Nitrates
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**
26
Which coronary is the most common site for thrombosis?
Left anterior descending artery (40%) Right coronary artery (27%) Left circumflex artery (11%)
27
What structures of the heart are supplied by the right coronary artery (RCA)?
* Anterior right ventricle * Posterior 1/3 fo the IV septum * Posterior right ventricle * Part of the posterior left ventricle
28
Which anti-ischemic agent prevents arrhythmia and does not alter blood pressure or heart rate?
Ranolazines (works by closing late inward Na+ gate -\> reduces Na+/Ca2+ exchange -\> prevents Ca2+ overload)
29
Describe the mechanism of action of Ca2+ channel blockers in treating ischemia
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
30
When would you expect myoglobin to rise, peak, and return to normal after MI?
* Rise 2h after infarction * Peak 6-8 h * Return to normal after 20-36
31
When would you expect lactate dehydrogenase to rise, peak, and return to normal after MI?
* Rise begins at 24h * Peak after 3 days * Return to normal after 8-9 days
32
How would **reduced aortic diastolic pressure** affect coronary blood flow?
Reduced aortic diastolic pressure would **reduce coronary blood flow**
33
What is ischemia?
O2 deprivation + inadequate removal of metabolites **due to reduced perfusion**
34
Describe the morphology of an **early** (1-6 hour) myocardial infarction
* No gross or light microscope findings * Electronic microscope reveals... * Wavy "lasagna noodle" muscle fibers * Leakage of myocardial enzymes (can be detected with dye)
35
After myocardial infarction, rupture of which walls would most likely lead to cardiac tamponade? When is this likely to occur?
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
36
When would you expect Troponin to rise, peak, and return to normal after MI?
* Rise in 4-6h * Peak 12-16 h * Return to normal after 10+ days
37
What are the goals of treatment for angina pectoris?
* Symptom control to increase quality of life * Prevention of life-threatening complications * MI, death * Prevention of disease progression
38
Which enzyme assay to diagnose MI rises most quickly after infarction?
Myoglobin
39
What pathology are myocardial scars prone to?
Aneurysm
40
How do lipid lowering agents (statins) work to treat ischemic heart disease?
* 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
After MI, how when would you begin to see coagulative necrosis?
6-12 hours
42
Describe the mechanism of action of beta-blockers
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
In a myoglobin assay to diagnose MI, what might cause a false positive?
Renal failure Skeletal muscle injury
44
What are the two major types of anti-ischemic Ca2+ channel blockers? How are they different?
* 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
Describe Class III Angina
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
What structures of the heart are supplied by the Left Anterior Descending Artery (LAD)?
* Anterior surface of the left ventricle * Partial anterior surface of the right ventricle * Anterior 2/3 of the IV septum * Apex
47
Describe the morphology of an MI 3-7 after the initial infarct
* 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
How would decreased right atrial pressure affect coronary blood flow?
Decreased right atrial pressure would **increase coronary blood flow**
49
Thrombosis in the Left Anterior Descending artery would cause infarction which sections of the myocardium?
* Anterior LV wall * Anterior interventricular septum
50
Which anti-ischemic agents work to decrease O2 demand (without changing O2 supply)?
Beta blockers
51
Why does hypertension increase one's risk of myocardial infarction?
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
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"
Class III Angina
53
Describe the characteristics of a transmural MI
* 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
What are anginal equivalents?
Symptoms of myocardial ischemia other than angina * Dyspnea * Nausea * Fatigue * Faintness More common in women, elderly people, diabetics
55
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"
Class II Angina
56
What enzymes can be used to diagnose MI? Which are most commonly used?
* 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
What is PTCA?
Percutaneous transluminal coronary angioplasty: surgical intervention for ischemic heart disease * Dilate coronary artery * Insert a metal stent * May be drug-eluting
58
What are the major side effects of Nitrates in treating ischemic heart disease?
Lightheadedness Headache Tolderance develops (don't take the medication at night, allows for re-set)
59
Which angina class is described as: "Inability to carry on any physical activity without discomfort, or angina at rest"
Class IV Angina
60
What are the major classes of pharmacologic intervention for ischemic heart disease? List major drug types in each class
* Anti-Ischemic agents * Nitrates * Beta-blockers * Ca2+ Channel blockers * Ranolazine * Antiplatelet agents * Anti-hypertension medication * Renin/angiotensin inhibitors * Lipid lowering agents
61
How do antiplatelet agents work to treat ischemic heart disease?
Decreaseing platelet aggregation prevents thrombotic events that could cause complete occlusion of a narrow artery
62
What causes the majority of all myocardial infarctions?
Thrombosis of a coronary artery Forms at the site of an ulcerated or ruptured atheromatous plaque
63
Thrombosis in ____________ would cause infarction in the anterior LV wall and/or the anterior interventricular septum
Left Anterior Descending artery
64
In a lactate dehydrogenase assay to diagnose MI, what might cause a false positive?
Lactate dehydrogenase is found in many different muscle types * Heart muscle * Skeletal muscle * Liver * RBC * Kidney * Neoplasms
65
Which isoenzymes of lactate dehydrogenase are relevant to MI?
LD1: Heart, RBC, renal LD2: Reticuloendothelial **Reversal lf LD1 : LD2 implies MI**
66
Describe Class I Angina
"Ordinary activity does not cause angina - Angina with strenuous, rapid, or prolonged exertion only"
67
What is angina pectoris?
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
What are the 2 types of myocardial infarction?
Transmural Subendothelial
69
Which patients should **not** recieve non-dihydropyridine Ca2+ channel blockers as treatment for ischemic heart disease?
Patients with LV dysfunction Patients taking another medication that lowers heart rate (non-dihydropyridine Ca2+ channel blockers lower HR)
70
Which structures of the heart are supplied by the left circumflex artery?
* Lateral left ventricle
71
When is CABG used over PTCA?
In more severe cases, or if multiple occlusions exist
72
How would increased myocardial contraction affect coronary blood flow?
Increased myocardial contraction would **decrease coronary blood flow**
73
What would happen to perfusion if there was no difference between the aortic diastolic pressure and the right atrial pressure?
Perfusion would cease
74
Thrombosis in ____________ would cause infarction in the posterior LV wall and/or the posterior 1/3 of the interventricular septum
​Right Coronary Artery
75
Describe the morphology of a 12-24 hour myocardial infarction
* Infiltration by neutrophils (peak in 3 days) * Sign of inflammation * Muscle cells lose nuclei and cross-striations
76
How can reperfusion injury after surgery be prevented?
* 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
What causes reperfusion injury?
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
Thrombosis in the Right Coronary artery would cause infarction which sections of the myocardium?
* Posterior LV wall * Posterior 1/3 of the interventricular septum
79
List the 5 possible pathogenesis of ischemic heart disease
1. Stenosing atherosclerosis of coronary arteries 2. Platelet aggregation + formation of intramural thrombus 3. Coronary vasospasm 4. Nonatherogenic coronary disease 5. Hemodynamic derangements
80
How what tools and evidence help to diagnose ischemic heart disease?
* 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
What are the 2 major clinical presentations of coronary atherosclerosis?
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
Why are Troponin T and Troponin I assays the most popular for diagnosing MI?
* They are specific to cardiac muscle * They are both sensitive and specific * Assay only takes 30 min to 1 hour
83
What are the 3 major categories of treatment for ischemic heart disease?
* Lifestyle modification * Pharmacologic intervention * Myocardial revascularization
84
What are the clinical types of angina?
1. Chronic, stable angina 2. Atypical angina 3. Anginal equivalents & silent ischemia (Shortness of breath) 4. Other Decubitus, nocturnal, refractory, unstable, microvascular, neoplastic....
85
Describe Class IV Angina
* Inability to carry on any physical activity without discomfort OR * Angina at rest
86
Thrombosis in the Left Circumflex artery would cause infarction which sections of the myocardium?
Lateral LV wall
87
What complications may arise after MI?
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
What are the major risk factors for ischemic heart disease?
"HAS LIPIDS" * Heretity * Age * Sex (male) * Lipidemia * Increased weight * Pressure (is high) * Inactivity * Diabetes * Smoking
89
List some examples of Ca2+ channel blockers
In general: **-dipine, -il-** (somewhere in the word\_ Amlo**dipine** Felo**dipine** Nife**dipine** Verapam**il** D**il**tiazem
90
What kind of drug is Nifedipine?
An anti-anginal Ca2+ channel blocker | (and other -dipine drugs)

CVB by Minnie (Madeleine) (43 decks)

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