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Y2S1-CVS-Pathology > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What are the three major blood supply of the heart?

A

1) Left anterior descending (LAD)

2) Left circumflex (LCX)

3) Right coronary artery

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2
Q

What is an ischemic heart disease?

A
  • AKA Coronary artery disease, Coronary heart disease
  • They are a group of related syndromes that result from myocardial infarction (an imbalance between the supply “perfusion” and demand of the heart for oxygen
  • In more than 90% of the cases it is due to the atherosclerosis of the coronary artery
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3
Q

What are the different classifications of IHD based on the clinical presentation?

A

1) Angina pectoris

2) Myocardial Infarction (MI)

3) Sudden cardiac death

4) Chronic HD with HF

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4
Q

What is a myocardial infarction?

A

Death to part of the cardiac muscle due to ischemia (there is necrosis due to infarction)

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5
Q

What is meant by sudden cardiac death?

A

Death within 1 hour of symptoms (arrhythmias) without a previous cardiac disease

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6
Q

Till which percentage of stenosis can the heart compensate?

A

75% after that symptoms will appear

  • 75%+ = symptoms while exercising
  • 90%+ = symptoms at rest
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7
Q

What is meant by acute coronary syndrome?

A
  • Sudden, reduced blood flow to the heart which is applied to (Unstable angina, Myocardial infarction, and Sudden cardiac death)
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8
Q

Describe the pathogenesis of ischemic heart diseases

A
  • Mainly due to diminished coronary perfusion relative to the myocardial demand due to:

1) Atherosclerotic narrowing of the coronary artery

2) Intraluminal thrombosis, overlying a disrupted plaque, platelet aggregation, or vasospasm

  • The prognosis of IHD depends on the extent of obstruction and severity (related to the location of the blockage) and on the dynamic changes in the coronary plaque morphology
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9
Q

What are the factors that contribute to the development of coronary atherosclerosis?

A

1) Decreased coronary perfusion

2) Erosion, Ulceration, Hemorrhage, rupture, thrombosis of the plaque

3) Inflammation

4) Coronary thrombus

5) Vasoconstriction

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10
Q

What are the factors that trigger changes in the plaque?

A

1) Intrinsic influences

  • For example Composition into the plaque

2) Extrinsic

  • Like Blood pressure
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11
Q

What are the types of plaque?

A

1) Stable plaque

  • Strong fibrous cap and smooth muscle proliferation, with a smaller lipid core (this is why ppl with atherosclerosis might not have problems for years)

2) Vulnerable plaque

  • Thin fibrous cap with a large necrotic core, which is easily ruptured
  • Fissures frequently occur at the junction of the fibrous cap and the adjacent normal arterial segment
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12
Q

What is angina pectoris?

A
  • Temporary, reversible ischemia due to hypoperfusion, which is not enough to produce ischemic necrosis or death
  • It is a “symptom complex” of IHD characterized by paroxysmal and recurrent attacks of substernal/precordial chest discomfort (constricting, squeezing, choking, or knifelike) due to a transient (15sec - 15min) Myocardial ischemia which does not induce infarction
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13
Q

What are the different patterns of angina pectoris?

A

1) Stable/typical angina

2) Prinzmetal/variant angina

3) Unstable/crescendo angina

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14
Q

What is stable/Typical angina?

A

The most common form, is due to reduced coronary perfusion to a critical level from a stenotic coronary atherosclerosis making the heart more vulnerable to emotions, physical activity, or any other activity that increases the cardiac workload

  • Usually relieved by rest or nitroglycerin (a strong vasodilator)
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15
Q

What is prinzmetal/variant angina?

A
  • Vasospasm reduced perfusion
  • Uncommon pattern of angina pectoris that occurs at rest, due to coronary artery spasm
  • Usually, the ST segment is elevated
  • The anginal attack is unrelated to the physical activity, heart rate, or blood pressure
  • It responds to vasodilators like nitroglycerin and CCB
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16
Q

How to differentiate between prinzmetal variant angina and myocardial infarction?

A

By using a biomarker test (Troponin T or I)

17
Q

What is unstable/crescendo angina?

A
  • Progression of a stable angina
  • Increasingly frequent pain (aggressive worsening of pain) at low cardiac demand or even at rest
  • Induced by a disruption of an atherosclerotic plaque with mural thrombosis, hemorrhage, or vasospasm that might embolize or induce vasospasm
18
Q

What is myocardial infarction?

A
  • AKA Heart attack
  • It is the irreversible death of the cardiac muscle due to ischemia, which heals by fibrosis
  • The leading cause of death in the US, more in males, and the major risk factors are DM, HTN, Smoking, and hypercholesterolemia
19
Q

Describe the pathogenesis of myocardial infarction

A
  • Coronary vessel occlusion: Atherosclerosis with thrombus (90% of cases), Others like vasospasm (10%)

1) Sudden disruption of an atheromatous plaques

2) Exposure to subendothelial collagen and necrotic plaque content

3) Platelets will undergo adhesion, aggregation, activation, and release of potent aggregators like TXa2, serotonin, and platelet factors 3 and 4

4) Vasospasm (due to mediators)

5) Coagulation (by other mediators)

6) The thrombus will immediately evolve occluding the lumen of the coronary vessel

  • After 30 minutes the changes are irreversible, and the cell dies from necrosis (coagulative)
20
Q

What are the clinical features of MI?

A

1) Rapid weak pulse

2) Profused sweating (diaphoretic)

3) Dyspnea

4) Chest pain

21
Q

How to diagnose MI?

A

1) Troponin (T & I) “They are the best markers, as they are sensitive and cardio-specific

2) Creatine kinase (CK-MB)

22
Q

What are the different patterns of infarction?

A

The location, size, and morphologic features depend on the size and distribution of the involved vessel, the rate of occlusion development and duration, the metabolic demands of the myocardium, and the extent of the collateral supply.

1) Transmural infarcts

  • When the coronary artery is blocked/obstructed, and thus the area supplying that region will suffer from necrosis
  • Involves the full thickness of the wall in the distribution of a given coronary artery, it is usually associated with coronary atherosclerosis, acute plaque change, and superimposed by thrombosis

2) Non-transmural infarcts (subendocardial)

  • When there is hypoperfusion, the area around the coronary “pericardium” will receive an acceptable amount of blood while the area further away will suffer from ischemia, shock can happen due to low perfusion
23
Q

Describe the microscopic morphology of MI

A

1) No change in the first 12 hours

2) Coagulative necrosis + neutrophils (12h - 3days)

3) Granulation tissue in 1-2 weeks (loose collagen and abundant capillaries)

4) Fine scarring if more than 3 weeks

5) Dense scarring if more than 2 months

  • The more the pink = more eosinophils = dying
24
Q

How can arrhythmia cause death after MI?

A

The scar made of fibrosis (dense collagen) gives strength to prevent the rupture of the heart and keeps it intact, but it won’t be good in contractility and electrical conduction and thus arrhythmias could lead to death

25
Q

Describe the evolution of the morphologic changes in MI

A
  • DAY 1-3, 3-7, 7-10 & Weeks 2-8 and > 2months are imp (dr said)

1) Day 1: Dying fibers, infiltration of PMNs

2) Day 1-3: Coagulation and infiltration

3) Day 3-7: Phagocytosis

4) Days 7-10: Well developed phagocytosis

  • Then granulation tissue, 2-8 weeks scar formation, then more than 2 months a fully developed scar
26
Q

What are the complications of myocardial infarction?

A
  • Poor prognosis (ant.wall is the worst, post.wall is worse, and the inferior wall is the best, due to electrical conduction)

1) Arrhythmias (requires DC shock)

2) Pump failure

3) Ventricular rupture

4) True aneurysm

5) Pericarditis (Dressler’s syndrome)

6) Recurrence

27
Q

What are the causes of sudden cardiac death?

A
  • Usually within 1 hour, it is a complication

1) CAD (atherosclerosis, 90% of cases)

  • Others:

2) Congenital structural or coronary arterial abnormalities

2) Aortic valve stenosis

3) Mitral valve prolapse

4) Myocarditis

5) Dilated/hypertrophic cardiomyopathy

6) PHTN

28
Q

What is the mechanism by which a sudden cardiac death occur?

A

A lethal arrhythmia (like ventricular fibrilation), usually occurs in young athletes with pul HTN and IHD

29
Q

What is meant by chronic IHD?

A
  • AKA Ischemic cardiomyopathy
  • It oftenly occurs in elderly who develops progressive heart failure as a consequence of ischemic myocardial damage
  • In most instance it is caused by failure of compensatory mechanisms (like hypertrophy) after MI
  • It is diagnosed by exclusion
  • There will be vacules and myocyte hypertrophy
30
Q

What are cardiomyopathies?

A

Cardiac diseases due to intrinsic myocardial dysfunction (heart muscle disease), it can be primary or secondary:

1) Primary: Confined to the myocardium

2) Secondary: Cardiac manifestations of systemic disorder

31
Q

What are the causes of cardiomyopathy?

A

1) Unknown

2) Inflammatory

3) Immunologic

4) Systemic metabolic disorder

5) Muscular dystrophy (duchenne)

6) Genetic disorder of MI fibers

32
Q

What are the different classifications of cardiomyopathies?

A

1) Dilated cardiomyopathy (DCM)

2) Hypertrophic cardiomyopathy (HCM)

3) Restrictive cadiomyopathy

33
Q

What is meant by dilated cardiomyopathy?

A
  • Progressive cardiac dilation and contractile dysfunction, usually with hypertrophy
  • Fradual development of cardiac failure with four chamber dilation of the heart
  • Autosomal dominant, autosomal recessive, and x-linked inheritance all have been proposed for particular families
  • It is a systolic disorder
  • Genetic, alcohol consumption and pregnancy are the major causes
34
Q

Describe the morphology of DCM

A

1) Macroscopic:

  • Four chamber dilation and hypertrophy are evident, and a small mural thrombus can be seen at the apex

2) Microscopically:

  • Myocyte hypertrophy and interstitial fibrosis (collagen is blue)
35
Q

What is meant by hypertrophic cardiomyopathy?

A
  • 100% genetic, in the sarcomeric proteins
  • Myocardial hypertrophy with a defective diastolic filling and in 1/3 of the cases the ventricular outflow is obstructed, characterized by a heavy muscular hypercontracting heart, representing a diastolic disorder
36
Q

Describe the morphology of hypertrophic cardiomyopathy

A

1) Massive myocardial hypertrophy, where the ventricular cavity loses its round shape and becomes banana-like due to the building of the

37
Q

What are the consequences of dilated cardiomyopathy and hypertrophic cardiomyopathy?

A

1) Heart failure

2) Sudden death

3) Atrial fibrilation

4) Stroke

38
Q

Summary of the three types of cardiomyopathies?

A
  • DCM 🡪 Cant contract efficiently 🡪 Systolic dysfunction 🡪 Heart compensates by slight hypertrophying-genetic and alcohol consumption main causes
  • HCM 🡪 Compensation by severe hypertrophy 🡪 Severe lumen narrowing 🡪 Diastolic dysfunction
  • Restrictive 🡪 Myocardium isn’t compliant 🡪 Can’t fill well 🡪 Diastolic dysfunction—emboli deposition

Y2S1-CVS-Pathology (12 decks)

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