this was the first lecture of the cardiac pathology series by dr. marcus miller, MD ND. we talked about the pathogenesis of coronary artery disease, atherosclerosis, and the ischemic heart diseases that can result from occlusion of the coronary artery. the first topic was atherosclerosis and the development and disruption of atherosclerotic plaques. in short, plaques are formed in the walls of blood vessels by high LDL levels which then penetrate into the intima of vessels and are oxidized, stimulating monocyte recruitment which leads to fatty streaks (clusters of macrophages that have ingested high levels of LDL). smooth muscle migration, extracellular matrix deposition, and formation of a fibrous cap around a core made largely of lipids and necrotic cellular debris eventually forms, protruding into the lumen of arteries.
if the fibrous cap of atherosclerotic plaques are disrupted by various factors such as sheer forces or simply a weakened area of the cap attracting inflammatory cells, the highly thrombogenic subendothelium and lipid core is exposed and thrombosis occurs, which generally leads to complete occlusion of the artery. if this occurs in the coronary artery, several conditions can result, such as angina pectoris refers to retrosternal chest pain that radiates to the left side that can be caused by ischemia or thrombosis.
the most severe condition results from ischemia that progresses to complete infarction of the myocardium, leading to an acute MI. infarction of the myocardium causes a switchover to anaerobic metabolism that decreases ATP levels in the myocardial cells-- this causes increased cellular permeability and decreased cellular function and eventual cell death. ATP levels can decrease as soon as 1-2 minutes and drop down to 50% of original levels in 10 minutes after the infarction. morphological changes of heart tissue include blue darkening and interstitial edema (4-12 hours), appearance of darker purple spots (12-24 hours), followed by tannish yellow areas of infarction (1-3 days), hyperemia, coagulation necrosis, decreased cell wall thickness (3-7 days). scar formation begins in 2-8 weeks and is completed in 2-3 months.
questions...
atherosclerosis...
1. where are atherosclerotic lesions usually located?
2. describe the role of smooth muscle in the development of atherosclerotic lesions.
3. what is the most commonly accepted theory of etiology for atherosclerosis?
4. what are some factors that contribute to endothelial damage?
coronary artery disease...
5. what is the most common cause of CAD?
6. describe a typical atherosclerotic plaque which might result in sudden thrombosis of the coronary artery.
7. describe the progression of the rupture of an atherosclerotic plaque in the coronary artery.
ischemic heart disease...
8. what are the four major results of ischemia of blood flow to the heart?
9. what is angina pectoris?
10. what is stable angina caused by? what are some unique symptoms?
11. An unstable angina is most likely the prodrome to what?
12. what is variant / Prinzmetal angina?
myocardial infarctions...
13. what is the most common pathogenesis of acute MI's?
14. what are some other possible etiologies of AMI's?
15. describe the reduction of ATP production with the amount of ischemia that leads to an MI.
16. describe the sequence of cellular injury that occurs with decreased ATP production in an MI.
17. when does irreversible cell death of myocardium occur?
18. what is the number 1 sequelae to an MI?
gross morphological changes in an MI during...
19. less than 4 hours...
20. 4-12 hours...
21. 12-24 hours...
22. 1-3 days...
23. 3 to 7 days...
24. 2 to 8 weeks...
25. 2 to 3 months...
answers
1. vessel bifurcations, large/mid sized arteries.
2. smooth muscle migrates from the media to the intima of atherosclerotic regions and builds up extracellular matrix around the plaque.
3. the "response to injury" theory in which endothelial damage causes inflammation which recruits monocytes, which then extravasate into the vessels and make fatty streaks, and then atherosclerotic plaques.
4. obesity, high LDL levels, diabetes mellitus, hyperglycemia, hypertension, turbulent blood flow, cigarette smoke.
5. fixed atherosclerotic narrowing or thrombus of disrupted atherosclerotic plaque of coronary artery.
6. the typical plaque that causes CAD is an unstable plaque that only causes mild or moderate stenosis and blocks less than 50% of the lumen prior to rupture and thrombosis.
7. a weakened fibrous cap attracts inflammatory cells which increases likelihood of rupture, which then exposes the thrombogenic subendothelium and lipid core, resulting in thrombosis.
8. myocardial infarction, angina pectoris, chronic heart failure, sudden cardiac death.
9. retrosternal chest pain that radiates to the left side and comes in paroxysmal and recurrent attacks, caused by ischemia that falls short of necrosis.
10. ischemia due to a fixed lesion; symptoms might include claudication and mesenteric angina.
11. generally a prodrome to an MI, transient ischemic attack or stroke.
12. angina caused by coronary artery vasospasm; pain at rest.
13. coronary artery plaque rupture and thrombosis.
14. coronary artery emboli from high cholesterol or infection, coronary artery vasospasm, hypoxia from underlying pulmonary disease or CO poisoning, arteritis.
15. ATP decreases starting 1-2 mins and can be reduced to 50% by 10 mins.
16. decreased ATP production inhibits action of Na/K ATPase pump which increases cell permeability. cell function further disrupted by degradative enzymes that are released from myocytes upon influx of calcium into cardiac muscle cells.
17. 15-20 minutes from onset of injury.
18. pericarditis.
19. often no change notable.
20. pale, blue, edematous.
21. darker spots of blue and purple.
22. tannish yellow areas of infarction.
23. hyperemia around infarcted areas, decreased wall thickness, coagulation necrosis.
24. greyish white scar formation.
25. scar formation complete.
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