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Cardiology > 18: Coronary Artery Pathophysiology & Syndromes > Flashcards

18: Coronary Artery Pathophysiology & Syndromes Flashcards

1
Q

What are the major determininants of oxygen **supply **and demand?

A

Supply:

  • O2 content
  • Coronary blood flow
    • Coronary perfusion pressure
    • Coronary vascular resistance
      • External compression
      • Intrinsic regulation
        • Local metabolites
        • Endothelial factors
        • Neural innervation

Demand:

  • Wall stress (P·r/2h) (Laplace)
  • Heart Rate
  • Contractility

**NB: **Imbalance between supply & demand –> ischemia

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2
Q

Describe the body’s intrinsic control of coronary tone.

A
  • Heart at rest consumes as much O2 as possible (2-3x more than other organs).
  • Heart cannot increase O2 extraction on demand.
  • Additional O2 requirements provided by increase in blood flow (autoregulation of coronary vascular tone).
    • **Q = ΔP/R **
    • NB: ΔP remains constant via baroreceptor regulation.
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3
Q

What is vascular tone?

A

Degree of constriction experienced by a blood vessel relative to its maximally dilated state.

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4
Q

How does external compression contribute to coronary vascular resistance?

A
  • Directly related to intramyocardial pressure
    • Greatest in systole
  • The subendocardium, which is adjacent to high intraventricular pressure, is most vulnerable to ischemic damage (increased resistance –> reduced flow).
  • NB: ↑HR –> ↑ Time in systole –> ↓Coronary blood flow –> Ischemia
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5
Q

What local metabolites regulate coronary vascular tone?

A
  1. Oxygen (vasoconstrictor)
  2. Adenosine (vasodilator)
  3. Lactate (vasodilator)
  4. Prostaglandins (vasodilator + platelet inh.)
  5. Hydrogen ions (vasodilator)
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6
Q

Describe how endothelial factors regulate coronary vascular tone.

A
  1. Endothelial-dependent vasodilators (ATP, ADP, bradykinin, histamine, Ach, thrombin, serotonin) stimulate endothelium derived relaxing factor (EDRF, a nitric oxide free radical).
  2. EDRF stimulates smooth muscle cell guanylate cyclase activity.
  3. Guanylate cyclase causes ↑cGMP, which inhibits calcium release (thus, ↑Ca2+ intracellularly), resulting in vasodilation.

NB: Organic nitrates (nitrate, nitroprusside) can act directly on SMCs (↑ G-cyclase activity).

NB: Shear stress can also promote EDRF.

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7
Q

List the endothelium-derived vasoactive substances and their regulators.

A
  1. Prostacyclin (EC) –> ↑cAMP (SMC) –> relaxation
  2. NO (EC) –> ↑cGMP (SMC) –> relaxation
  3. EDHF (EC) –> EDHF (SMC) –> relaxation
  4. Thrombin, angiotensin II, Epi –> Endothelin 1 (EC) –> SMC contraction
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8
Q

Describe the interaction between platelets and endothelial cells.

A

Normal:

  1. Prostacyclin & NO release from EC inhibit platelet aggregation and stimulate SMC relaxation.
  2. Aggregating platelets release ADP & 5-HT:** **upregulate prostacyclin & NO.
  3. Aggregating platelets release 5-HT & TXA2: promote SMC contraction.
  4. SMC relaxation dominates.

Dysfunctional:

  1. **CAD **risk factors (DM2, HTN, HLD, smoking, age) cause dysfunctional endothelium
  2. ↓NO & prostacyclin –> ↑platelet aggregation.
  3. SMC contraction dominates.
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9
Q

Describe how stenosis modifies coronary vascular resistance.

A
  • At maximal coronary flow, heart maintains normal output with a lesion diameter up to 70%.
  • At resting coronary flow, heart maintains normal output with a lesion diameter up to 90%.
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10
Q

Describe the transient ECG abnormalities seen during ischemia.

A
  • Subendocardial ischemia: ST depression (horizontal or downsloping), T wave inversion
    • “Non-ST-elevation MI/unstable angina (NSTEMI/UA)”
    • 1.4 million patients annually
    • Worse long-term mortality (multi-vessel disease, lower EF); more common
  • Transmural ischemia (total occlusion): ST elevation
    • ST-elevation MI (STEMI)
    • 0.6 million patients annually
    • Worse short-term mortality

NB: All ACS are caused by plaque rupture

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11
Q

What metabolite is used as a predictor for ACS prognosis?

A

Troponin; higher levels indicate greater risk of mortality.

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12
Q

What are the consequences of a large infarction?

A
  • Heart failure and ↓QOL
  • Atrial & ventricular arrhythmias
  • ICD (if EF < 35%) and biventricular pacemakers
  • Hospital readmissions
  • Resource consumption
  • Early and late mortality
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13
Q

Describe the Canadian Cardiovascular Society Angina Classification (CCSC).

A
  • Class I: Prolonged exertion evokes angina; no limit to normal activity
  • Class II: Walking >2 blocks evokes angina, slight limit to normal activity
  • Class III: Walking <2 blocks evokes angina, marked limit to normal activity
  • Class IV: Minimal or rest evokes angina, severe limit to normal activity

NB: Class I & II = stable angina; Class III & IV = unstable angina.

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14
Q

Describe **unstable angina **presentation.

A
  • Rest angina within 1 week
  • Now onset of CCSC Class III/IV within 2 months
  • Angina increasing in CCSC class to III or IV
  • Variant angina
  • Non-Q-wave MI
  • Post-MI angina (>24 hours)
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15
Q

Describe the endogenous protective mechanisms of plaque rupture.

A
  • Tissue factor pathway inhibitor (TFPI) inhibits conversion of VII to X.
  • Protein S & Protein C cause inactivated V & VIII.
  • Antithrombin III causes irreversible thrombin inhibition.
  • tPA promotes conversion of plasminogen to plasmin (breaks up fibrin clot); SFx: ↑platelet aggregation
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16
Q

How does a plaque rupture lead to coronary thrombosis?

A
  • Intraplaque hemmorrhage –> ↓vessel lumen diameter
  • Release of tissue factor –> activation of coagulation cascade
  • Exposure of subendothelial collagen & turbulent blood flow –> platelet activation and aggregation
17
Q

What are the consequences of coronary thrombosis?

A
18
Q

How does myocardial hypoxia cause cell death?

A
19
Q

Describe the dynamics of atherosclerotic plaque stability.

A

Factors increasing stress:

  • Thin fibrous cap
  • Large lipid pool
  • Less stenotic lesions (smaller plaque)
    • Law of Laplace: t = p·r –> bigger r
  • Ester/free cholesterol

Factors weakening cap:

  • ↓collagen synthesis
  • ↓smooth muscle cells
  • ↑macrophages & T cells
    • Secrete matrix metalloproteinases (digest cap), tissue factor, CRP and myeloperoxidase
    • **Statins **↓macrophage count
  • ↑collagen degradation

Cardiology (13 decks)

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