Atherosclerosis Lecture

Jun 22, 2024

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Atherosclerosis Lecture

Introduction

  • Lecturer: Armando
  • Topic: Atherosclerosis (hardening and narrowing of arteries due to plaque formation)
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  • Pseudonym used by Armando

Definitions

  • Atherosclerosis: Narrowing of arteries due to plaque formation (waxy substance made predominantly of lipids)
  • Arteriosclerosis: Hardening of arteries

Heart and Coronary Arteries

  • Coronary arteries supply blood full of oxygen to cardiac muscle cells
  • Normal Scenario: Adequate blood flow maintains healthy heart function
  • Atherosclerosis Scenario: Plaque formation reduces or blocks blood flow, depriving cardiac muscle cells of oxygen

Symptoms and Consequences

  • Coronary Arteries: Vomiting, anxiety, angina, coughing, fainting
  • Severe Blockage: Heart attacks or heart failure due to myocardial ischemia (death of cardiac muscle cells)
  • Carotid Arteries: Weakness, headache, facial numbness, paralysis (can lead to stroke)
  • Peripheral Vascular Disease: Reduced blood circulation to other body parts (hair loss, erectile dysfunction, weakening of associated areas)
  • Renal Arteries: Appetite reduction, swelling of hands, increased blood pressure (due to renin release)

Plaque Formation Stages

  1. Initial Stage: Normal blood vessel with adequate blood flow
  2. Early Plaque: Plaque forms downwards in blood vessel layer
  3. Progressed Plaque: Plaque grows upwards, narrowing the vessel
  4. Severe Plaque: Plaque can rupture, forming a thrombus (clot), impeding blood flow

Mechanism of Plaque Formation

  1. Endothelial Dysfunction and LDL Deposit:
    • High circulating LDLs deposit in the Tunica Intima
    • LDLs become oxidized, activating endothelial cells
  2. White Blood Cell Adhesion:
    • Endothelial cells express receptors for white blood cells
    • Monocytes and T-helper cells move into the Tunica Intima
  3. Formation of Foam Cells:
    • Monocytes become macrophages, engulf oxidized LDLs, and become foam cells
    • Foam cells promote smooth muscle cell migration and proliferation
  4. Collagen Synthesis and Plaque Growth:
    • Increased smooth muscle cell proliferation leads to collagen synthesis
    • Foam cells die, releasing lipid content, contributing to plaque growth
  5. Rupture and Thrombosis:
    • Plaque build-up causes pressure and potential rupture
    • Thrombosis forms when plaque ruptures, leading to clotting and serious complications

Detailed Mechanism

  • Endothelial Dysfunction: Allows LDLs to move into Tunica Intima
  • Oxidation of LDLs: Traps LDLs in the Tunica Intima
  • Monocyte to Macrophage Conversion: Engulf oxidized LDLs and become foam cells
  • Foam Cells' Role: Release chemokines, IGF-1, attract more macrophages, and stimulate smooth muscle cells
  • Inflammation and Complications: Increase in foam cells, dead cells, collagen, and smooth muscle cells create the plaque
  • Increase in Blood Supply: To the Tunica Intima via vessels called Vasa Vasorum
  • T Cells' Role: Bind to adhesion receptors, release interferon gamma, promoting inflammation

Summary

  • Plaque formation is a complex process involving endothelial dysfunction, LDL oxidation, and multiple cell types
  • Plaque growth can lead to rupturing and severe cardiovascular complications

Conclusion

  • Understanding the detailed mechanisms helps in recognizing the seriousness of atherosclerosis
  • Importance of diagnosis and treatment to prevent severe outcomes like heart attacks and strokes

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