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Arthrosclerosis and Ischemia > Pathology of myocardial ischemia and infarction > Flashcards

Pathology of myocardial ischemia and infarction Flashcards

1. Review the pathological manifestations of atherosclerotic coronary artery disease 2. Determinants of infarct size 3. Different pathological forms of MIs such as regional, diffuse, STEMI, NSTEMI 4. Gross and microscopic appearances of the different phases of an MI 5. Reperfusion myocardial injury 6. Clinical onsequences of MIs and thier pathological expressions

1
Q

Definition of myocardial ischemia

A

A state in which O2 supply to the myocardium is insufficient to meet its needs as a result of inadequate perfusion

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2
Q

Factors influencing myocadial O2 supply

A
  • diastolic perfusion pressure
  • coronary vascular resistance
  • O2 carrying capacity
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3
Q

Factors influencing myocardial O2 demand

A
  • wall tension
  • heart rate
  • contractility
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4
Q

Balance between supply and demand

A
  • when supply equals demand or increase in supply is met by the same increase in demand = no ischemia
  • demand > supply –> ischemia
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5
Q

What are causes of coronary artery disease (10)

A
  1. Atherosclerosis/ thrombosis (most important)
  2. Coronary emboli
  3. Coronary vasospas
  4. Ostial narrowing
  5. Congenital anomalities of coronary artery
  6. Arthritis
  7. Post -cardiac transplant vasculopathy
  8. Spontaneous arterial dissection
  9. Complications of coronary catherization
  10. Cocaine abuse
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6
Q

Most common reason why coronary artery atheroscerosis causes myocardial ischemia

A

-most infarcts (90%) are caused by plaque erosion and subsequent thrombosis

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7
Q

Consequences of calcification of coronary arteries

A

1) Luminal narrowing

2) Inability to dilate

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8
Q

Composition of atherosclerotic plaque

A
  • fibrous cap on the top - protective layer on surface (collagen and connective tissue and myofibroblasts -contractile and secretory part - make the matrix)
  • function of matrix - protect bloodstream from seeing the atheroma
  • atheroma = lipid core -if liberated in bloodstream causes instant thrombosis and sudden death
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9
Q

Compensation for narrowed lumen

A

-distal arterioles dilate

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10
Q

which plaques are the most dangerous (prone to rupture)

A
  • not plaques with alot of calcium (although this does make them narrowed and less pliable)
  • it is the soft plaques that are the most prone to rupture (and therefore to become a thrombus) - vulnerable plaque
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11
Q

Where plaque is most likely to rupture

A
  • at the shoulder region
  • where inflammatory cells accumulate and secrete cytokines and degredative enzymes (Matrix metaloproteinases and elastases)
  • eats away at soft thin region around shoulder and ruptures plack
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12
Q

Two mechanism formation of thrombus

A
  1. Plaque fissure

2. Plaque rupture

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13
Q

Plaque fissure

A
  • defect in the endothelium exposing underlying plaque tissue to flow of blood
  • thrombus forms on exposed surface
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14
Q

Plaque rupture

A
  • flap of fibrous cap has lifted
  • exposes underlying atheroma and it spills into the lumen
  • thrombus forms on exposed surface
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15
Q

Propagation of thrombus

A

1) Thrombus can remain relatively small
2) can enlarge and
i) remain stable
ii) become more fibrous and regress (brought into coronary artery wall)
iii) can block artery right in original position
3) can break off and float down into smaller vessel and occlude that (thrombo emboli)
- platelets that are part of the thrmbus contain platelets contain vasoactive factors - cause vasoconstriction in microvesicles (mechanical and chemical plug)
4) resolution –> rethrombosis and progressive stenosis

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16
Q

Infarction - definition

A

Cell/tissue death due to ischemia

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17
Q

Clinical definition of infarction

A

Evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia

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18
Q

Diagnosis of MI clinically

A

Rise and/or fall of cardiac biomarker (troponin) to >99th percentile + min 1 of:

1) symptoms of ischemia
2) ECG changes of new ischemia
- ST-T differences
3) Imaging evidence (new loss of viable myocardium, regional wall abnormality)

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19
Q

Timeline myocardial infarction

A

1) Myocardial dysfunction occur in 2 min from occlusion
2) Irreversible changes (necrosis) being approx 20 min following occlusion
3) Complete infarction may take 2-4 hours

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20
Q

Lethal cellular event in mi

A

-rapid drop in high energy phosphates
Real lethal event =
-cell membrane ion pumps don’t have a field to drive them (i.e. high energy phosphates) so fail
-membrane disruption because ions re-equilibrate across membrane and H2O follows
-cell death follows

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21
Q

How to detect myocardial necrosis

A
  • by elevation of specific enzymes
    i) CK-MB (rise 3-8 hr)
    ii) Troponin (rise 3-4 hr)
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22
Q

Troponin vs. CK-MB

A

-troponin rise faster and detectable fo longer period of time
-troponin more specific than CK-MB (which is found in some other organs in small amounts)
(troponins virtually undetectable in absence of cardiac disease

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23
Q

Other causes of increased troponins

A

x

24
Q

Area at risk

A
  • when occlude a coronary artery put an area of the myocardial bed at risk (area at risk)
  • more proximal occlude an artery = > area at risk
  • infarcts almost always start in
25
Q

Where do most infarcts start/ what parts can potentially be salvaged

A
  • in the immediate subendocardial zone
  • i.e. lateral borders of the heart seem to be predetemined
  • it is the part from the lateral border on (i.e. the depth of the wall) that may be able to be salvaged
26
Q

Wavefront phenomenon

A

Irreversible ischemic myocardial cell injury develops in an increasing number of cells as the duration of occlusion is prolonged
progresses Subendocardial –> subepicardium

27
Q

Subendocardial region

A

-inner half of the myocardium

28
Q

Why do most infarcts begin in the subendocardial region

A

1) Fewer collaterals than subepicardium
2) Vessels pass through more contracting myocardium
3) Increased wall tension relative to subepicardium
4) Higher metabolic demand of myocytes in the region

29
Q

Non -ST elevation MI

A
  • tends to be a subendocardial MI
  • often see S-T depression
  • management my be conservative or invasive including PCI/CABG
30
Q

ST elevation MI

A
  • transmural ischemia

- management involves either fibrinolyti therapy or primary PCI

31
Q

2 groups of infarcts by morphology

A

1) Segmental

2) Diffuse

32
Q

Segmental infarct

A

-single vessels coronary disease

33
Q

Causes of diffuse infarct

A

1) Multivessel CAD
2) Prolonged hypotension
3) Prolonged hypoxia
4) Shock
5) Over administration of inotropic drugs

34
Q

Percentage distribution of segmental MI’s

A

RCA -30%
Cx -20%
LAD -50%

35
Q

What determines infarct size

A
  1. Severity x duration of ischemia
  2. Size of area at risk
  3. Collateral coronary circulation
  4. Reperfusion of ischemic area
  5. Pre-ischemic state of myocardum
  6. Conccurent cardiac physiology
  7. Global (systemic) conditions -i.e. if anemic, systemic hypertension
36
Q

Histopathological sequence in myocardial infarction

A

1&2 Wavy fibres and interstitial edema

  1. Contraction bands
    - membrane pumps break down
    - SR liberates Ca2+= intraccellular Ca2+ overload
    - filaments exposed to Ca2+ contract- hypercontraction state (almost like tetani)
    - z lines bunched up together
  2. Neutrophilic infiltrate
    - neutrophils liberate degradative enzymes to dissolve dead tissue (so that can be removed by macrophage)
  3. Coagulation necrosis (proteins in cells coagulate = cell death)
    - heart is not dead all the way through often pathches of surviving myocytes (collaterals has something to do with this)
  4. Macrophage phagocytosis of necrotic myocytes (garbage trucks take away dead debris - a few days later)
  5. Granulation Tissue formation
  6. Formation of collagenous scar
37
Q

Features of Early infarct 1-3 days

A
  • infarct turn pale (as no blood flowing through)
  • myocardial pallor = mottling suggests non-reperfused early MI
  • then begins to turn yellow (destruction of cell wall = liberation of lipids = yellow)
38
Q

Features of resolving infarct 1-2 weeks

A
  • infarct contracts and forms a scar

- gray gelatinous/proteinaceous

39
Q

Infarct several weeks old

A
  • scar/granulating tissue contracting
  • progress until necrotic tissue ie replaced by a scar - can take a long time depending on how large the necrotic area is
40
Q

Appearance of healed MI -several months old

A

-white (collagen) fibrous scars

41
Q

Myocardial reperfusion injury

A

-reintroduction of oxygenated blood into a region of ischemia/necrosis

42
Q

Consequences of myocardial reperfusion

A

1) If achieved early (>2hrs) myocardial salvage
2) If delayed (> 6 hrs) potential for enhanced cell death
3) Reperfused infarcts tend to be very hemorrhagic (most common cause of hemorrhagia post mi = reperfusion)

43
Q

Agents of harmful side-effects in myocardial reperfusion/reperfusion injury

A
  • oxygen radicals

- intracellular Ca2+ overload

44
Q

Aim of reperfusion

A

-reduce the potential for the whole infarct

45
Q

Why reperfusion may cause further injury

A
  • reperfusion may introduce oxygen radicals

- thereby killing some of area meant to reperfuse

46
Q

Clinical consequences of mi

A

1) Arrhythmias
2) Ventricular dysfunction
3) Myocardial stunning
4) Myocardial hibernation
5) Cardiogenic shock
6) Infarct extension
7) Infarct expansion (remodeling)
8) Ventricular aneurysm

47
Q

Why MI can lead to arrhythmias

A

1) Decreased perfusion of conducting system tissues
2) Ischemia at the borders f the infarct - in the normal myocardium - this sensitizes the myocardial cells and promotes generation of ectopic arrhythemias
3) Accumulation of toxic metabolites (cellular acidosis)
4) Autonomic stimulation

48
Q

Why MI can cause ventricular dysfunction

A

1) Decreased performance from loss of functional myocardium

2) Increased volume because can’t ejected all of volume = increased LVEDV and increase LVEDP

49
Q

Myocardial stunning

A
  • product of severe ischemia that falls short of myocardial necrosis
  • persistent dysfunction even following restoration of normal myocardial blood flow
  • gradual return of contractility of myocardium (several days -weeks)
  • may be caused by reperfusion
50
Q

Myocardial hibernation

A
  • chronically impaired myocardial function due to persistently reduced blood supply
  • some chronic cellular damage
  • function may be restored by revascularization
51
Q

Cardiogenic shock

A
  • inadequate circulation as a consequence of primary pump failure
  • severe arrhythmias
  • proportional to infarct size
  • contributes to global ischemia and reinfarction
52
Q

Infarct extension (recurrent infarction)

A

-new infarction adjacent to or remote from original region

2-10 days from original event

53
Q

Infarct expansion (remodelling)

A
  • stretching/thinning of original infarct
  • proportional to original infarct size
  • usually antero-apical region (ventricular aneurysms) -occuring in LAD terrritory
54
Q

Basis for physiological effects of infarct expansion: increased wall stress

A

-infarct expands ventricular radius
-infarct decreases ventricular thickness
-increased LVEDV –> LVEDP
wall stress = Px r/2h

55
Q

Basis for physiological effect of infarct expansion

A
  1. increased wall stress
  2. Impairment of systolic contraction
  3. Increased probability of aneurysm formation

Arthrosclerosis and Ischemia (6 decks)

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