Histology of myocardial infarction Flashcards

1
Q

revision

What is cell injury and when does it occurs?

A
  • Cell injury occurs when cells are stressed beyond their ability to adapt
    • Hypertrophy
    • Hyperplasia
    • Atrophy
    • Metaplasia
  • Reversible cell injury
  • Irreversible cell injury and cell death
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2
Q

REVISION

Define and describe hypoxia and ischaemia

A

Hypoxia
- Extremely important cause of cell injury
- Deficiency of O2 → reduced aerobic respiration
- Causes:
- Reduced blood flow (ischemia)***
- Inadequate oxygenation of blood (cardiorespiratory failure)
- Decreased oxygen-carrying capacity of blood (severe blood loss, CO poisoning, anemia)

Ischemia
- Most common cause of cell injury in clinical medicine
- Reduced blood flow: mechanical arterial obstruction (most often); or reduced venous drainage
- Compromises:
- Supply of oxygen (aerobic metabolism ceases)
- Supply of metabolic substrate i.e. glucose
- Removal of metabolites
- Cell injury

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3
Q

Define infarction

A
  • Area of ischemic necrosis, occurs in any tissue in which ischemia leads to cell death/ tissue necrosis
  • Commonly myocardial, cerebral, pulmonary, bowel
  • Arterial:
    • Vast majority of infarctions
    • Occlusion by thrombosis or embolism
  • Venous:
    • Tissues usually congested → bypass channel permits vascular outflow
    • Infarct in organs with a single efferent vein (testis/ovary)
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4
Q

Revision

Define and describe necrosis

A
  • Morphologic changes that follow cell death in viable tissue
  • Can be visualized macroscopically and microscopically
  • Morphologic appearances due to:
    • Denaturation of cellular proteins
    • Enzymatic leakage and degradation of the cell
    • Inflammation

Types of Necrosis
- Coagulative necrosis:
- Denaturation of protein including enzymes → digestion of cells halted
- Preservation of the architecture of dead tissue for days/week
- Classic finding in ischemic necrosis caused by obstruction in a vessel (e.g. myocardial infarction and most forms of tissue infarction, except brain)
- Liquefactive necrosis:
- Digestion of dead cells → viscous liquid
- Classic finding in abscess (microbes stimulate enzyme release from leukocytes) → pus
- Classic finding in cerebral infarct (reasons unclear)
- Caseous necrosis:
- Distinctive form of necrosis → cheeselike (friable white appearance)
- Classic finding in TB
- Fat necrosis:
- Focal areas of fat destruction
- Classic finding in pancreatitis

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5
Q

Recall the arterial supply of the heart

A
  • Heart is supplied by the right and left coronary arteries
  • Both are branches of the ascending aorta
  • Should know about:
    • Right CA
      • Right marginal
      • Posterior interventricular
    • Left CA
      • Circumflex
      • Left anterior descending

see also anatomy of heart

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6
Q

Describe IHD

A

Ischemic Heart Disease
- Generic designation for closely related entities resulting from myocardial ischemia
- Leading cause of death in both males and females → single largest cause of mortality worldwide, accounting for over 12% of global deaths
- However, overall death rate has fallen ~50%
- Prevention (modifiable risk factors: smoking, cholesterol, etc.)
- Diagnostic and therapeutic advances (statins, angioplasty/stent, CABG)

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7
Q

Briefly describe pathogenesis of IHD

A
  • Risk of developing IHD depends on:
    • Number
    • Distribution (usually first few centimetres of LAD and LCX)
    • Structure (LAD, LCX, RCA) of atheromatous plaques
  • Degree of narrowing they cause
    • > 70% → critical stenosis
    • > 90% → inadequate flow, even at rest
  • How quickly the plaques evolve
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8
Q

List acute coronary syndromes and briefly describe how they precipitate

A
  • Unstable angina
  • Myocardial infarction (STEMI/ NSTEMI)
  • Sudden death
  • Precipitated by conversion of a stable atherosclerotic plaque to an unstable atherosclerotic plaque via:
    • Plaque erosion or ulceration with secondary occlusive luminal thrombus formation or
    • Intraplaque hemorrhage causing sudden luminal narrowing
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9
Q

Describe causes of acute plaque change

A
  • Events that trigger acute plaque change are poorly understood
  • Intrinsic:
    • Plaque structure and composition
  • Extrinsic:
    • Mechanical stress
      • Platelet reactivity
      • Rupture/fissuring
      • Erosion/ulceration
      • Haemorrhage
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10
Q

Describe the incidence of MI and risk factors

A

Incidence
- “Heart attack” - death of cardiac muscle due to prolonged ischemia
- Frequency increases with increasing age, however may occur at any age (10% <45 years; 45% <65 years)
- Leading cause of death in industrialized nations
- In the USA affects 1.5 million people p.a., 1/3 die, 1/6 die before reaching the hospital

Risk factors

  • Male
  • Risk factors for atherosclerosis
    • Hypertension
    • Cigarette smoking
    • Diabetes mellitus
    • Hypercholesterolemia
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11
Q

Describe the pathogenesis of MI

A

Pathogenesis
- STABLE PLAQUE
- ACUTE PLAQUE CHANGE
- Coronary arterial occlusion
- Increased myocardial demand
- Hemodynamic compromise
- Presence or absence of collateral vessels

Coronary Artery Occlusion
- Acute plaque change → disrupted plaque
- Platelets undergo adhesion, aggregation, activation
- Vasospasm (substance released from platelet)
- Activation of extrinsic pathway of coagulation → growing thrombus
- Within minutes, complete occlusion of the artery

NB

MI Not Associated With Atherosclerosis
- 10% of cases
- Vasospasm (e.g. cocaine)
- Emboli
- Vasculitis
- Hemoglobinopathies
- Amyloid
- Vascular dissection

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12
Q

Describe the myocardial response to MI

A

Myocardial Response
- Coronary arterial occlusion
- Loss of critical blood supply to the myocardium
- Profound functional, biochemical and morphological consequences

Myocardial Response
- Ischemia
- Cessation of aerobic glycolysis within seconds
- Loss of contractility <2 minutes
- Irreversible cell injury within 20-40 min will lead to necrosis of some myocytes
- Complete necrosis in 6 hours

  • Dependent on location, severity, and rate of development of the occlusion
  • Size of the vascular bed occluded
  • Duration of occlusion
  • Metabolic needs of the myocardium
  • Extent of collateral vessels
  • Alterations in BP, HR, and cardiac rhythm
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13
Q

Comapre and contrast transmural and subendocardial infarction

A

Transmural:
- Full thickness ischemic necrosis of the ventricular wall
- Permanent occlusion of an epicardial artery

Subendocardial:
- Non-transmural ischemic necrosis
- May involve the distribution of several coronary arteries (transient/partial obstruction)

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14
Q

Describe the progression of myocardial necrosis

A
  • One Hour: No macroscopic changes
  • Four Hours: +/- Wavy fibres
  • One Day: Subtle macroscopic changes, dark mottling; Coagulation necrosis, haemorrhage, scant neutrophils microscopically
  • Two Days: Mottled appearance with yellow/tan infarct center macroscopically; Coagulation necrosis + neutrophils microscopically
  • One Week: Hyperemic border + central tan softening macroscopically; Disintegration of necrotic myofibers, dying neutrophils, macrophages microscopically
  • Two Weeks: Maximally yellow/tan and soft, depressed infarct borders macroscopically; Phagocytosis, granulation tissue, early fibrosis microscopically
  • Two Months: White scarring macroscopically; Dense collagenous scar microscopically
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15
Q

Describe the consequences and complications of MI

A

Outside to Inside:
- Contractile Dysfunction
- Conducting system
- Pericardium
- Pericardial space
- Myocardium
- Endocardium
- Papillary muscles/valves

Contractile Dysfunction:
- Immediate post-MI and ongoing (10% of patients with transmural MI)
- Abnormalities of left ventricular function
- Left ventricular failure (hypotension, pulmonary edema)
- Cardiogenic shock

Arrhythmias:
- Many arrhythmias occur post-MI, especially in STEMI
- Sudden cardiac death often a lethal arrhythmia
- MI can directly affect the bundle of His in the septum
- Cardiac muscle irritability secondary to ischemia is a common cause

Pericarditis:
- Epicardial manifestation of underlying myocardial inflammation
- Fibrinohaemorrhagic
- Transmural infarct
- Resolves slowly over days
- Rarely, intense pericarditis can develop weeks after MI (Dressler syndrome)

Haemopericardium and Cardiac Tamponade:
- Escape of blood from the ventricles into the pericardial cavity (haemopericardium)
- Constriction of the heart with decreased diastolic filling (cardiac tamponade)
- Usually fatal

Myocardial Rupture:
- Mechanical weakening due to myocardial necrosis
- Occurs 3-7 days post-MI
- Rupture can involve the ventricular free wall, ventricular septum, or papillary muscle

Infarct Extension / Expansion:
- Extension: New necrosis adjacent to the existing infarct
- Expansion: Weak necrotic muscle stretches, enlarging the infarct without further necrosis

Ventricular Aneurysm:
- Late complication
- Expansion of the infarct and healing by fibrosis
- Aneurysm bulges during systole
- Complications include mural thrombus, arrhythmia, and left ventricular failure

Mural Thrombus:
- Adherent thrombus in the left ventricular cavity
- Local inflammation of the endocardium and abnormal contractility contribute to thrombus formation
- Potential for thromboembolism

Papillary Muscle Dysfunction:
- Dysfunction of the papillary muscles leading to mitral regurgitation
- Dysfunction can be caused by rupture, fibrosis and shortening, or ventricular dilation

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16
Q

List the timeline of MI complications

A

Time Line of Complications:

Arrhythmia:
- Immediate Arrhythmia Leading to Sudden Death
- Early Arrhythmias
- Ongoing Arrhythmias (e.g., Bundle Branch Block)

Contractile Dysfunction:
- Immediate Contractile Dysfunction within 60 Seconds
- Cardiogenic Shock
- Chronic Left Ventricular Failure

Pericarditis:
- Usual Onset: 2-3 Days After Myocardial Infarction
- Dressler’s Syndrome: Pericarditis Appearing Weeks After MI

Myocardial Rupture:
- Timing: 3-7 Days When Necrotic Myocardium Is Weakest

Mural Thrombosis with Risk of Embolism:
- Highest Risk: 10 Days After MI, Lasting for 3 Months

Aneurysm:
- Late Complication