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Common Congenital Heart Lesions - page 39 / 126





39 / 126

39 of 126

Macroscopic Features of Infarction

  • <4 hours - No abnormality

  • 4-12 hours - Occasional dark mottling

  • 12-24 hours - Dark mottling

  • 1-3 days - Mottling with yellow-tan necrotic center

  • 3-7 days - Central yellow-tan softening with hyperemic border

  • 7-10 days - Maximally yellow-tan and soft, depressed red-tan borders

  • 10-14 days - Red-gray, depressed borders

  • 2-8 weeks - Gray-white scar, progressive from border to core of infarct

  • >2 months - Mature scar

Late Changes

  • Characterized by 2 steps:

    • Removal of necrotic myocytes by macrophages (yellow softening)

    • Deposition of collagenÆfibrous scar

  • Yellow Softening: since irreversibly injured myocytes do NOT regenerate, they’re cleared by macrophages…this is a type of tissue reabsorption that for leaves the thin, dilated infarcted area susceptible for rupture for some time until fibrosis & scarring is complete

Functional Changes

  • Impaired ventricular contraction: AKA “ventricular systolic dysfunction”; CO is compromised b/c of loss of synchronous myocyte contraction

  • Impaired ventricular compliance: AKA “ventricular diastolic dysfunction”; results in elevated ventricular filling pressures

  • Stunned Myocardium: transient prolonged periods of ventricular systolic dysfunction that’s gradually recovered over time b/c of restored blood flow; seen in UA & regions adjacent to areas of acute MI

  • Ischemic Preconditioning: brief ischemic insults to a region of myocardium may allow it to be resistant to subsequent bouts of ischemia; possibly due to the expression of adenosine receptors

*Clinical significance: patients who survive an MI with anginal symptoms will have less morbidity & mortality that those without angina

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