Atherosclerosis and AMI

1234567891011121314
Across
  1. 2. With prolonged occlusion of coronary artery, a wave of irreversible myocardial injury spreads from the ___________ layer of cardiac tissue into the subepicardial layer.
  2. 4. The _____ transforms into macrophage to phagocytose oxidised LDL-C
  3. 5. This is considered to the first cellular event in the formation of atherosclerotic plaque.
  4. 11. Foam cells release ___________________ which signals to recruit smooth muscle cells (SMCs) from the tunica media onto the plaque.
  5. 12. In initial steps of plaque formation, plaques usually grow in an _____ direction of the vessel.
  6. 14. Overtime, the inner layer of coronary arteries accumulates with fatty deposits, leading to the formation of plaques, and narrowing of the arteries. This phenomenon is referred to as _______ (easy one, isn't it, take the next one!)
Down
  1. 1. This is considered to be an important trigger for Atherosclerosis.
  2. 3. This layer of arteries is the outer layer and consists of connective tissue to anchor arteries to the surrounding tissues.
  3. 6. Cigarette toxins can also act as irritants and cause dysfunction of the endothelium, making arteries more susceptible to the entry of LDL cholesterol into the ______ layer of the arteries.
  4. 7. During advanced atherosclerotic lesion, macrophages can also release _____________ enzyme that degrades collagen.
  5. 8. Phagocytosis of LDL cholesterol results in macrophage filled with LDL-C that undergo apoptosis and develop _____.
  6. 9. When numerous active and dead macrophages and other inflammatory cells accumulate, this develops. (Hint: An atheroma that has a fibrous structure)
  7. 10. LDL-C infiltrates into the intimal layer as it contains a hydrophilic structural protein known as ______, allowing it to adhere to extracellular matrix proteoglycan and LDL receptors on the endothelial surface.
  8. 13. Smooth muscle cells produce extracellular matrix such as _____ to form a stable fibrous cap.