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Cardiovascular > Atherosclerosis & Ischemia > Flashcards

Atherosclerosis & Ischemia Flashcards

1
Q

The normal heart pumps in: Series/Parallel

A

Series

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2
Q

What does coronary blood flow depend on? (2)

A

1) Perfusion gradient

2) Coronary resistance

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3
Q

What raises oxygen demand? (3)

A

Increased pump work (HR, LV pressure & volume, “vigour” of contraction)

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4
Q

Ischemia occurs when:

A

Increase of coronary blood flow is insufficient to meet the increase of oxygen demand

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5
Q

What happens when ischemia persists and is severe?

A

Myocardial necrosis

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6
Q

What is the functional contractile unit in myocytes?

A

Sarcomeres

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7
Q

What is at the ends of each sarcomere?

A

Z lines

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8
Q

What are the contractile proteins? (2)

A

Myosin - thick filaments, actin - thin filaments

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9
Q

What are the regulatory proteins associated with actin/myosin? (4)

A

Troponin C, T, and I, and tropomyosin

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10
Q

What has the most rapid spontaneous phase 4 depolarization?

A

SA node

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11
Q

What stimulates the release of Ca2+ from the sarcoplasmic reticulum?

A

The rise in Ca2+, from opening of Ca2+ channels caused by sarcolemma depolarization.

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12
Q

What is troponin C’s function?

A

It blocks the formation of strong attachments between myosin heads and actin in the resting state.

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13
Q

Myosin heads undergo flexion in the (presence/absence) of ATP.

A

Presence

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14
Q

Actin filaments are attached to:

A

Z lines

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15
Q

What allows myosin heads and actin to bind?

A

Increase of Ca2+, which binds troponin C and exposes the actin binding sites on the myosin so strong cross bridges can form.

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16
Q

What is the preferred cardiac fuel in the fasting state? What percentage of cardiac needs do they supply?

A

Free fatty acids. 60-70%

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17
Q

What is the origin of the left main coronary artery (LMCA)?

A

Left sinus of Valsalva (referred to as left coronary sinus by cardiologists)

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18
Q

What is the origin of the right coronary artery (RCA)?

A

Right sinus of Valsalva (referred to as the right coronary sinus)

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19
Q

Clinically there are considered to be three coronary arteries. What are they?

A

Left anterior descending coronary artery (LCA)
Circumflex coronary artery (Cx)
Right coronary artery (RCA)

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20
Q

What part of the heart does the LCA supply?

A

Anterior wall of left ventricle and most of the inter ventricular septum

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21
Q

What part of the heart does the circumflex coronary artery supply?

A

Lateral wall of left ventricle

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22
Q

What part of the heart does the RCA supply?

A

Posterior part of the inter ventricular system, SA and AV nodes

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23
Q

Where do coronary veins converge? Where is this?

A

Coronary sinus; which runs along the posterior surface of the heart in the AV groove and empties into the right atrium.

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24
Q

How can coronary arteries be grouped?

A

Conductance vessels vs. resistance vessels

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25
Q

What are conductance vessels? Give 2 examples

A

Vessels that run over the surface of the heart and penetrate through the muscle mass to bring blood. Epicardial and myocardial penetrating vessels.

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26
Q

What are resistance vessels? Give 2 examples

A

Applies resistance against the aortic root pressure. Arterioles and capillaries

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27
Q

Coronary flow to the left ventricle occurs in:

A

Diastole

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28
Q

What is the equation for coronary perfusion gradient?

A

Aortic root pressure - LV pressure = CPP

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29
Q

Describe the coronary perfusion gradient during systole.

A

Aortic root pressure and LV pressure are equal (approx 120mmHg). There is no gradient, so therefore no coronary flow.

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30
Q

Describe the coronary perfusion gradient during diastole.

A

Aortic root pressure is about 90mmHg, and LV pressure is about 10mmHg. The gradient is 80mmHg - blood flows into coronary arteries.

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31
Q

What is the ratio of diastole to systole at resting HR? What is its significance

A

2:1. This duration is the amount of time the blood has to fill coronary arteries. When ratio decreases (less time in diastole), HR rises and less blood enters.

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32
Q

What are determinants of coronary resistance? (2)

A

1) Myocardial compression

2) Tone of resistance vessels

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33
Q

How does myocardial compression affect coronary resistance?

A

During systole, contraction of myocardium squeezes intramyocardial vessels and prevents any significant systolic blood flow. During diastole, myocardium is relaxed and its diastolic LV chamber pressure determines myocardial compression.

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34
Q

Where does most of the resistance arising from cross-sectional area of coronary bed come from?

A

Arterioles & precapillary sphincters

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35
Q

Describe how metabolic mechanisms are responsible for changes in vascular tone.

A

Coronary resistance responds to varying myocardial oxygen demand. When there is ischemia, adenosine levels rise, along with H+, K+ and CO2, and O2 drops. This causes vasodilatation of arterioles and relaxation of pre capillary sphincters.

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36
Q

Describe how endothelial mechanisms are responsible for changes in vascular tone?

A

Endothelium releases EDRF (NO) continuously to maintain vasodilatory tone; this increases with ischemia. PGI2 is a vasodilator, and endothelia is a vasoconstrictor; both are produced by endothelium.

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37
Q

Describe how neurogenic mechanisms are responsible for changes in vascular tone?

A

Sympathetic innervation of coronary bed. Alpha receptors responsible for vasoconstrictor effects, while beta receptors responsible for vasodilatory effects. Parasympathetic stimulation produces vasodilation.

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38
Q

Describe how myogenic mechanisms are responsible for changes in vascular tone?

A

Pressure/flow sensitive smooth muscle in arteriolar walls relaxes or constricts in relation to perfusion pressure. Autoregulation to maintain myocardial perfusion at constant levels occurs in the face of widely varying mean aortic pressures from 130-40mmhg.

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39
Q

What causes vasodilatory effect in the coronary arteries? (4 main ones)

A
  • Rise in adenosine, H+, K+, CO2; drop in O2
  • EDRF and PGI2 released from endothelium
  • Beta receptors (SNS) & PNS stimulation
  • Autoregulation
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40
Q

What situations can lower the oxygen content in coronary arteries? (2)

A
  • High altitudes
  • Malfunctioning lung
    (Generally not central to clinical issues)
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41
Q

What is the Law of Laplace

A

Wall stress = rp/2h (r = radius, p = pressure, h = thickness)

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42
Q

What is the LV radius also referred to as?

A

Preload

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43
Q

A greater intraventricular pressure during systole (increases/decreases) the oxygen requirement

A

Increases

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44
Q

What determines the intraventricular systolic pressure? (3)

A

1) Resistance of aortic valve (normally 0)
2) Peripheral vascular resistance (BP)
3) Compliance of aorta & major vessels
- This is referred to as the total resistance to LV ejection, referred to as impedance

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45
Q

LV hypertrophy is a compensatory response in order to:

A

Decrease oxygen demand

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46
Q

What is contractility? What is its impact on muscle length?

A

It is the “vigour” or “speed” of cardiac contraction. A greater contractility results in a more rapid shortening of muscle.

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47
Q

What happens to the contractility curve during exercise (vs. at rest)?

A

Curve shifts left - greater contractility per end diastolic volume

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48
Q

How does heart rate affect oxygen demand?

A

Higher heart rate = higher oxygen demand

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49
Q

Why does increased myocardial supply require increases in coronary blood flow? (3)

A

1) Myocardium depends almost totally on aerobic metabolism
2) Coronary venous O2 saturation is low (25-30%) and so O2 extraction cannot be increased
3) The myocardium cannot incur a significant O2 debt (contractile performance fails in seconds)

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50
Q

What is resting coronary flow?

A

~300mL/min

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51
Q

In maximal oxygen demand, how much can coronary blood flow be increased by?

A

5-fold

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52
Q

What is the difference between resting coronary blood flow and maximum coronary blood flow called?

A

Coronary reserve

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53
Q

What is “an increase in demand, and supply fails to keep pace?”

A

Demand ischemia

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54
Q

What do we call schema that results from a fall in supply, and demand persists or does not decrease sufficiently?

A

Supply ischemia

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55
Q

How does ischemia cause symptoms? (Mechanism)

A

Ischemia results in a reduction of myocardial performance, and production of adenosine, which causes noxious stimulation of afferent sympathetic receptors and the perception of chest discomfort

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56
Q

Describe the supply/demand balance of oxygen during exercise.

A

This is a physiologic mechanism. Onset of exertion: Increase in HR, BP, LV-end diastolic radius & contractility. This demand is met by increasing coronary flow (primarily by dilatation of arterioles & pre capillary sphincters in response to local metabolic stimuli). Coronary reserve is able to meet this balance.

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57
Q

Describe the supply/demand balance of oxygen in pathology (eg. atherosclerotic stenosis)

A

Flow is impeded by:

1) Geometry of stenosis (reduction of cross-sectional area & length)
2) Degree of residual capacity for dilatation (stenoses usually centric, may cause dilation)
3) Presence of superimposed platelet aggregation and thrombus

At rest, coronary flow is normal, and there is no reduction to maximum coronary flow until stenosis reduces lumen by about 70%. Then there is a progressively increased reduction in maximal flow attainable (rises exponentially) until at about 90% reduction of lumen, when there is no virtually no capacity to increase flow in relation to demand.

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58
Q

Symptoms of angina on exertion indicates a reduction of ____% area reduction of a major coronary artery

A

at least 75%

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59
Q

What is the total occlusion of a major coronary artery usually the result of?

A

Rupture of the cap of an atherosclerotic plaque, leading to exposure of thrombogenic plaque contents, and the formation of an occlusive thrombus at the site of rupture.

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60
Q

ATP generation fails after ______ with total occlusion?

A

3-4 beats

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61
Q

The affected segment begins to infarct when occlusion of coronary artery persists for __________.

A

> 15 minutes

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62
Q

What is “fibroatheroma”?

A

Arteriosclerosis with prominent fatty and fibrous buildup

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63
Q

What is “Atherothrombosis”?

A

Arteries that have both atherosclerosis and prominent thrombosis either within the atherosclerotic plaque or within the adjacent lumen.

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64
Q

Which layer of the vascular wall is mainly affected by atherosclerosis?

A

Intima

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65
Q

What does atherogenesis include? (3)

A

1) Interaction of the inner surface of the wall with circulating bolo factors within the lumen
2) Factors carried to the outer wall by neural endings
3) Vasculature’s own blood supply (vasa vasorum)

66
Q

What is the term for the “risk of morbidity and mortality in spite of the best available therapies”?

A

Residual risk

67
Q

Atherogenesis is a ________ & ________ inflammatory process.

A

Chronic & indolent

68
Q

The atherogenesis process can be visible as early as the _________ (age) and manifestations occur __________.

A

Late teens/early 20s. “Decades later” (elderly)

69
Q

What are the focal points/predilections where atherosclerosis commonly occurs? (2)

A

Branch points, areas of turbulent flow

70
Q

Atherosclerosis is generally seen first in ___________, then the ________, ________, ________, ________ and then finally the _________.

A

1) Dorsal aspect of abdominal aorta
2) Proximal coronaries/popliteal arteries, descending thoracic aorta, internal carotids
3) Renal arteries

71
Q

Name the 3 structural layers of an artery and their components (3 each)

A

1) Intima - endothelial cells & internal elastic lamina
2) Media - smooth muscle cells, extracellular matrix, external elastic lamina
3) Adventitia - vasa vasorum, nerve endings, adventitial tissue

72
Q

Normal endothelium serves a ____________ function.

A

Homeostatic

73
Q

A normally functioning endothelial cell is designed to maintain: (3)

A

1) An antithrombotic surface
2) A non-adherent surface
3) A relatively relaxed smooth muscle cell with a low propensity to synthesize extracellular matrix and a low propensity to replicate or migrate

74
Q

What is an antioxidant produced by the endothelial cell?

A

Superoxide dismutase

75
Q

Name 4 antithrombotic products produced by the endothelium.

A

1) Heparin sulfate
2) Thrombomodulin
3) Plasminogen activators
4) Nitric oxide

76
Q

Under normal conditions, what functions do the endothelial cells have?

A

1) Suppression of endothelial cell capacity to elaborate receptors that bind WBCs to its surface
2) Suppression of capacity to elaborate mediators of smooth muscle cell constriction

77
Q

What is responsible for modulating the size and blood carrying capacity of the larger sized arteries?

A

Smooth muscle cell

78
Q

Smooth muscle cells have a capacity to dramatically alter their own form and function in response to noxious stimuli (e.g. _____________) and withdrawal of suppressive signals from the endothelium (eg. _____________)

A

Inflammatory cells. Nitric oxide.

79
Q

Where is the extracellular matrix normally found? What is it produced by?

A

Found mainly in medial layer. Produced by a basal level of synthetic function of the smooth muscle cells.

80
Q

What does the extracellular matrix contain?

A
  • Fibrillar collagen (gives strength)

- Proteoglycans, elastin (gives flexibility)

81
Q

In addition to providing strength, what other functions (2) does collagen have?

A

1) Inhibit SMC growth

2) Preserve SMC longevity (by making them less likely to undergo apoptosis)

82
Q

What is the most widely used concept to explain atherogenesis?

A

“Response to injury hypothesis”

83
Q

What are some possible mediators/causes of vascular injury in the vascular bed? (4)

A

1) Diverse chemical irritants (tobacco smoke, lipids, glucose)
2) Physical forces
3) Hemodynamic stress (at branch points - disrupts smooth/laminar flow)
4) Systemic hypertension

84
Q

What 2 processes occur in the earliest stages of atherogenesis?

A

1) Failure of endothelial barrier function

2) White cell adherence to endothelial cell

85
Q

T/F: Both innate and adaptive immunity are involved in atherosclerosis.

A

True (accruing evidence for adaptive).

86
Q

How do endothelial cells respond to flow? (3)

A

1) Change shape
2) Align themselves in direction of flow
3) Induce nitric oxide system

87
Q

What is a good representation of endothelium health before any other abnormalities are evident?

A

Nitric oxide pathway

88
Q

How is nitric oxide produced? What enzyme is involved and what regulates it?

A

Conversion of L-arginine by the nitric oxide synthase; enzyme is upregulated in presence of shear stress or acetylcholine.

89
Q

What (6) things do normal endothelium regulate?

A

1) Transport of substances into and out of subendothelial space
2) Thrombosis
3) White cell adhesion
4) Vasomotion of vascular smooth muscles
5) Growth and apoptosis of the vascular smooth muscle cells in the media
6) Oxidative state

90
Q

What characterizes endothelial dysfunction? (7)

A

1) Altered permeability
2) Prothrombotic state on vessel surface
3) White cell adhesion receptors on surface
4) Inadequate vasodilation
5) Increased secretion of growth factors
6) Increased oxidative state
7) Endothelial dysfunction can be shown to be present before any physical changes in the artery are present and to persist throughout progression of atherosclerosis

91
Q

Name 4 leukocyte adhesion molecules released when the endothelium is injured.

A

VCAM-1, ICAM-1, E-selectin, P-selectin

92
Q

Name 3 chemoattractants released when the endothelium is injured.

A

MCP-1, IL-8, Interferon inducible protein 8

93
Q

What is “diapedesis”?

A

Transmigration of white cells between EC’s allowing white cells to get to subendothelial space.

94
Q

How do foam cells form?

A

Monocytes turn into phagocytic macrophages and express a scavenger receptor, with no feedback inhibition mechanism. The macrophage engorges itself with modified LDL containing cholesterol & cholesteryl ester, forming cholesterol crystals that form necrotic core of foam cells.

95
Q

How do dendritic cells contribute to atherogenesis?

A

They activate T cells, which produce TH1 cytokines that further activate macrophages & vascular cells, some regulatory and produce anti-inflammatory cytokines (IL-10, TGF-b), and B-cell activation

96
Q

What traps lipids in the subendothelial space? What happens in the subendothelial space?

A

Proteoglycans traps lipids. Lipids are rendered prone to modification - mLDL (oxidized LDL through oxidation, glycated LDL through glycation)

97
Q

What is the effect of mLDL to endothelium and smooth muscle cells?

A

Toxic effect. Contributes to transformation that these 2 cells undergo during atherogenesis. They also induce further leukocyte recruitment/inflammation thereby enhancing numbers of monocytes & macrophages. They also induce autoantibody formation, which further aggravates local inflammation.

98
Q

Describe the normal state of smooth muscle cells.

A

Relaxed, non-migratory, non-replicating, low/basal level of synthetic function for elaboration of ECM

99
Q

What are smooth muscle cells responsive to? Which one is for dilation, which one is for contraction?

A

Prostacyclin, nitrous oxide, endothelin, angiotensin, and inflammatory mediators (IL-6, TNF-a, etc). Dilation = NO; contraction = angiotensin II

100
Q

Describe the transformed state of smooth muscle cells responsible for atherogenesis.

A

Spastic, replicating, migratory, highly synthetic

101
Q

What system generates oxygen free radicals?

A

NADPH oxidase systems

102
Q

What is the arterial remodeling process called?

A

Glagov remodeling

103
Q

Describe compensatory remodeling. What is the eventual effect on lumen size?

A

Outward or centrifugal remodeling that maintains lumen size as atheroma bulk increases. Eventually the lumen becomes smaller.

104
Q

Enhanced synthetic function of smooth muscle cells leads to…?

A

Excessive production of extracellular matrix, further enhancing the trapping of monocytes and inflammatory cells within vascular wall

105
Q

What is released/elaborated (by activated EC’s, SMC’s, and foam cells) when the plaque becomes more mature?

A

Tissue factor, PAI-1

106
Q

Plaque disruption and exposure to the circulating blood stimulates which 2 processes on the surface of disrupted plaque? What does this result in?

A

1) Platelet adhesion
2) Thrombin formation
- These may create a small/large thrombus that may be transient or permanent.

107
Q

What are the early signs of development of atherosclerosis? (2)

A

1) Endothelial dysfunction

2) Intimal thickening

108
Q

By what age is the fatty streak visible by? What is its significance?

A

Age 20. It doesn’t protrude/obstruct flow, and may progress or regress.

109
Q

What causes the fatty streak formation?

A

Response to injury of endothelial cells leading to entry of lipids into subendothelial space, causing a pro-inflammatory state, leading to leukocyte recruitment –> foam cells

110
Q

What is the hallmark of transition from fatty streak to a fibroflatty lesion/fibrous atheroma in plaque progression? What is it mediated by?

A

Smooth Muscle Cell Migration, mediated by products produced by foam cells/activated platelets/activated endothelial cells

111
Q

What is “neovascularization”?

A

Growth of vasa vasorum into the wall

112
Q

What is plaque disruption? When does it occur?

A

It initiates thrombosis (which can be minimal to totally occlusive, and from transient to permanent); it can occur during any phase of atherosclerosis that has some bulk. It can heal but generally not without also contributing to more bulk - “tug of war” of repair & disruption

113
Q

What leads to a vulnerable plaque structure? (2)

A

1) Death of smooth muscle cell

2) Excess foam cells

114
Q

What is in the necrotic core of a vulnerable plaque? Where is it most vulnerable?

A

Spillage of lipids & debris cause increased volume of necrotic core; hemodynamic vulnerability is max at the shoulder where foam cells and other inflammatory cells reside

115
Q

A thick fibrous cap is characteristic of a (stable/vulnerable) plaque.

A

Stable

116
Q

Describe the stabilizing & non-stabilizing effects of calcification.

A

1) Stabilizing - if it occurs within the necrotic core - less prone to rupture
2) Non-stabilizing - if it occurs on the surface of plaque

117
Q

What are some characteristics of vulnerable plaques? (4)

A
  • Thin fibrous cap
  • Devoid of smooth muscle cells
  • Large lipid core
  • Abundance of foam cells
118
Q

What are some characteristics of stable plaques? (4)

A
  • Thick fibrous cap
  • Many smooth muscle cells & collagen
  • Little/no lipid core
  • Few foam cells & inflammatory cells
119
Q

How is plaque integrity disrupted? (3)

A

1) Rupture/erosion of cap
2) Collapse due to calcific nodules in the cap
3) Intra-plaque hemorrhage through disruption of vasa vasorum

120
Q

How can endothelial dysfunction be detected clinically? (2)

A
  • Adequacy of vasodilatory response to shear stress

- Endothelium-dependent vasodilators (eg. acetylcholine)

121
Q

What are some ways of visualizing atherosclerosis? (7)

A
  • Autopsy (post-mortum)
  • Optical coherence tomography
  • Intravascular ultrasound
  • Trans-cutaneous ultrasound
  • Calcium scan
  • CT angiography
  • Invasive angiography
122
Q

What do ischemic syndromes imply about underlying atherosclerosis?

A

1) Demand ischemia (classic angina/claudication) - fixed stenosis
2) Non-demand ischemia (stenosis is “dynamic” - can be Prinzmetal’s angina, local thrombosis, combination of both; embolization, hemorrhage of vasa vasorum)
3) Rigidity and aneurysm formation with ensuing fragility and pressure effects leading to dissection/rupture
4) Collateralization

123
Q

How does ASA work to improve morbidity/mortality of atherosclerosis?

A

Reduction of platelet activity –> reduce processes of thrombosis initiated by platelet activation

124
Q

How do statins work to improve morbidity/mortality of atherosclerosis? (4)

A
  • Reduce # of LDL particles
  • Diminution in foam cell formation
  • Plaque anti-inflammatory effects
  • Overall improvement of endothelial dysfunction
125
Q

How does smoking increase morbidity/mortality of atherosclerosis?

A
  • Associated with oxidized LDL, low HDL, endothelial dysfunction, increased platelet reactivity, increased SNS activity
126
Q

How do anti-hypertensives work to improve morbidity/mortality of atherosclerosis? (3)

A
  • Barotrauma to endothelial cells
  • Increased angiotensin II –> oxidation = increased permeability
  • Overall improvement of endothelial dysfunction
127
Q

How does diabetes increase morbidity/mortality of atherosclerosis?

A
  • Glycated LDL leads to endothelial dysfunction –> promotes thrombosis; clustering of other risk factors
128
Q

How does weight & non-active lifestyle increase morbidity/mortality of atherosclerosis?

A
  • Abdominal obesity = high lipids, BP & sugar

- Lack of exercise = low flow (low shear stress) = endothelial dysfunction

129
Q

Define “treatment gap”

A

Patients do not get (sufficient) therapy in spite of currently available treatments

130
Q

Define “residual risk”

A

On-going risk of morbidity & mortality in patients provided the best of current evidence-based therapy

131
Q

Define “optimal medical therapy” in atherosclerotic disease.

A

Use of non-procedural interventions proven to reduce the morbidity and mortality of atherosclerotic disease

132
Q

List 7 interventions considered “optimal medical therapy” in atherosclerotic disease.

A

1) Maintain ideal weight
2) Aerobic activity
3) Abstinence from smoking
4) Use of statins to lower LDL
5) Use of ASA to diminish platelet reactivity
6) Reduction of elevated BP (ACEIs, ARBs, diuretics, B-Blockers, CCBs)
7) Reduction of HbA1c using diabetic medications

133
Q

What is the 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”

134
Q

What are 3 determinants of myocardial O2 supply?

A

1) Diastolic perfusion pressure
2) Coronary vascular resistance
3) O2 carrying capacity

135
Q

What are 3 determinants of myocardial O2 demand?

A

1) Wall tension
2) Heart rate
3) Contractility

136
Q

(Atherosclerosis/thrombosis) is responsible for the more severe mortality and morbidity outcomes.

A

Thrombosis - rupture of plaques

137
Q

What are some causes (9) of coronary artery disease?

A

1) Coronary emboli
2) Coronary vasospasm
3) Ostial narrowing
4) Congenital anomalies of coronary artery
5) Arteritis
6) Post-(cardiac) transplant vasculopathy
7) Spontaneous arterial dissection
8) Complications of coronary catheterization
9) Cocaine abuse

138
Q

What are some pathologic characteristics of ruptured atherosclerotic plaque?

A

Artery is calcified/rigid - cannot be spread out; decreased ability to dilate; fixed

139
Q

What is contained in the fibrous cap, and what is its function?

A

It has collagen, connective tissue, myofibroblasts, allowing it to be secretory and contractile. It secretes matrix to prevent blood exposure to the atheroma below. Exposure would cause thrombus formation and eventual/sudden death.

140
Q

What is characteristic of coronary artery disease (vs. coronary heart disease)? (3)

A
  • Asymptomatic atherosclerosis

- <3 quadrants obliterated

141
Q

What is characteristic of coronary heart disease (vs. coronary artery disease)? (3)

A
  • Symptomatic atherosclerosis
  • > 70% reduction in luminal area
  • > 3 quadrants obliterated
142
Q

Why is blood flow not limited despite reduction in luminal area in early plaque growth?

A

Arterial media expands to accommodate

143
Q

Describe the process from atherosclerosis to thrombus/complications.

A

1) Plaque fissure/erosion - defect in endothelium exposes plaque tissue to bloodstream
2) Plaque rupture - separation of thin fibrous cap exposes underlying atheromatous debris; flap of fibrous cap is lifted, so atheroma material spreads into lumen
3) Thrombosis - thrombus forms on exposed surface
4) Propagation - thrombus may enlarge, remain stable or resolve via fibrinolytic mechanisms
5) Embolization - fragments of thrombus detach & travel downstream to occlude smaller caliber vessels = thromb oemboli
* Thrombus may resolve, rethrombose, or progress to stenosis

144
Q

What is the definition of ischemia?

A

“Cell/tissue death due to ischemia”

145
Q

What is the clinical definition (diagnosis) of ischemia?

A

1) Rise and/or fall of cardiac biomarker (Eg. troponin) to >99th percentile normal reference limit, plus at least 1 of:
a) Symptoms of ischemia
b) ECG changes of new ischemia (ST-T changes, LBBB)
c) Imaging evidence - new loss of viable myocardium, regional wall abnormality
2) Pathological evidence of MI

146
Q

Describe the timeline of MI.

A
  • 2 minutes after occlusion: Myocardial dysfunction may occur
  • 20 minutes: Irreversible changes (necrosis) begins
  • 2-4h: Complete infarction
147
Q

What is the “lethal cellular event” of an MI?

A

Cell membrane ion pumps fail

148
Q

What are some biomarkers of an MI? How do they compare?

A

Troponins (vs. CK-MB)

  • Rise faster (3-4h) vs 3-8h in CK-MB
  • Specific; virtually undetectable in absence of cardiac disease
  • Detectable for a longer period than CK-MB
149
Q

Describe the “Wavefront Phenomenon” of an MI.

A

When occlude a coronary artery –> put an area of heart at risk; other areas not compromised. More proximal occlusion = more area at risk. Infarct starts at immediate subendocardial zone. Lateral borders are pre-determined, but can salvage the depth that becomes infarcted

150
Q

What is the subendocardial region? What is its significance?

A
  • Inner half of myocardium
  • Most infarcts begin here (goes outwards)
  • Most vulnerable to ischemia
151
Q

Why is the subendocardial region most vulnerable to ischemia? (4)

A

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

152
Q

Differentiate STEMI from NSTEMI.

A 
STEMI = ST elevation MI, transmural ischemia, managed with fibrinolytics or primary PCI
NSTEMI = Non-ST elevation (spares epicardium), subendocardial ischemia, often STP depression, managed with conservative/invasive measures, including PCI/CABG
153
Q

Differentiate regional infract vs. diffuse infarct.

A 
Regional = segmental infarct; single vessel CAD
Diffuse = multivessel CAD, with prolonged hypotension, hypoxia, and shock
154
Q

What are the percentage distributions of MIs across the 3 coronary arteries?

A

LAD - 50%
RCA - 30%
CX - 20%

155
Q

What determines infarct size? (7)

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 myocardium
6) Concurrent cardiac physiology
7) Global (systemic) conditions (eg. anemia, hypertension)

156
Q

Describe histopathology of an MI with a rough timeline

A

1) First few minutes - Wavy fibres, interstitial edema intracellularly; Ca2+ dependent contraction bands occur to liberate calcium as intracellular Ca2+ is overloaded
2) 6-12h later - PMNs enter, go through necrotic bed to release degradative enzymes; proteins coagulate, membranes break down, and pH shifts
3) Few days - Macrophages carry away debris, fibroblasts enter for scarring and capillary sprouts grow into myocardium; scarring occurs

157
Q

Describe the gross pathology of an MI with a rough timeline

A

1) 1 hour - Heart thickness unchanged
2) 1-3 days - Infarct turns pale (no RBCs/perfusion through it), lipids liberated later –> turns yellow
3) 1-2 weeks - Infarct contracts and starts to scar; gelatinous/proteinaceous/edematous appearance
4) Several weeks - Continued scarring, depending on size of infarct
5) Months to years - White scars, formed by collagen - denotes old MI

158
Q

Describe reperfusion injury.

A

Reperfusion = Reintroduction of oxygenated blood into a region of ischemia/necrosis
- Reperfusion can salvage myocardium if done early (6h) can lead to enhanced cell death, as oxygen can be a substrate for free radicals and increase intracellular calcium (overload)

159
Q

What types of myocardial dysfunction are related to reperfusion? (4)

A

1) Myocardial stunning
2) No-reflow phenomenon
3) Reperfusion arrhythmias
4) Lethal reperfusion injury

160
Q

How do reperfusion injury-related infarcts usually present? (3)

A
  • Often large (size increased by 50%)
  • Hemorrhagic
  • Earlier appearance of inflammatory cells and healing

Cardiovascular (2 decks)

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