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Updated: Oct 6 2020


  • Snapshot
    • A 54-year-old man presents to the emergency department 30 minutes after developing crushing sternal chest pain that radiates down the left arm and to the jaw. His symptoms are accompanied by anxiety. Medical history is significant for hypertension, hypercholesterolemia, and type II diabetes mellitus. On physical exam, the patient appears restless and is diaphoretic. An electrocardiogram is performed, which shows ST-segment elevated in leads V1-4. The cardiac catheterization lab is activated and the patient is awaiting stenting after appropriate acute management for acute coronary syndrome.
  • Introduction
    • Definition
      • a pathological process that causes damage to the
        • aorta
        • cerebrovasculature
        • coronary arteries
        • peripheral arteries
    • Epidemiology
      • risk factors
        • modifiable
          • hypertension
          • cigarette smoking
          • hyperlipidemia
            • especially hypercholesterolemia
        • nonmodifiable
          • age
          • male gender
          • family history
          • genetic abnormalities (e.g., LDL receptor gene mutations)
    • Pathophysiology
      • background
        • LDL transports cholesterol into peripheral tissues and HDL mobilizes cholesterol from the periphery and into the liver for excretion via bile
      • pathogenesis
        • injury (e.g., smoking, hypertension, and hypercholesterolemia) to the endothelium leads to endothelial dysfunction resulting in
          • increased vessel permeability
          • monocyte adhesion and emigration
        • macrophages become activated within the vessel intima and smooth muscles are recruited
          • smooth muscle cells migrate to the intima via FGF and PDGF
        • smooth muscle cells and macrophages engulf lipids (e.g., LDL), forming foam cells, along with recruitment of T lymphocytes forming a fatty streak
          • smooth muscle cells proliferate and there is deposition of the extracellular matrix, resulting in the fatty streak becoming a fibrofatty atheroma
            • slow forming plaques allow for the formation of collateral circulation
      • location
        • abdominal aorta > coronary artery > popliteal artery > carotid artery
  • Presentation
    • Symptoms
      • angina
        • if > 75% obstruction
        • myocardial demand ischemia
          • type of stable angina where individuals with known atherosclerotic coronary disease experience relative myocardial ischemia during episodes of high metabolic demand
          • subendocardial vessels are susceptible to ischemia during systole due to high resistance and systolic back flow from endocardial to epicardial vessels
            • left ventricular subendocardial muscle most likely due to left coronary vessel systolic compression
          • supply/demand mismatch can cause anginal pain and ischemic changes on EKG
      • claudication
      • can be asymptomatic
  • Complications
    • Aneurysms
    • Myocardial infarction
    • Ischemic stroke
    • Peripheral vascular disease
    • Atheromatous plaque disruption can result in thrombosis
      • thrombus fragments can break off and result in an embolism
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