Ischemic Heart Dz

Question 1

IHD pathogenesis in 90%?

Answer 1

reduced coronary blood flow d/t atherosclerotic narrowing

Question 2

causes of decreased blood flow (4)?

Answer 2

1. fixed atherosclerotic narrowing
2. acute plaque change
3. thrombosis overlying ruptured plaque
4. vasospasm

Question 3

how much narrowing causes stx w/ exercise? at rest?

Answer 3

70%. 90% at rest.

Question 4

what is the most common artery affected? 2 others also affected?

Answer 4

first several cm of LAD. also left circumflex, entire R coronary artery.

Question 5

what are things that could happen to plaques resulting in myocardial ischemia?

Answer 5

1. rupture/fissures/ulcerations (exposes underlying thrombogenic substances)
2. hemorrhage into atheroma (expands plaque and further narrows lumen)

Question 6

what is the result of acute plaque change?

Answer 6

acute coronary syndromes: acute MI, unstable angina, sudden cardiac death

Question 7

what are influences that contribute to acute plaque changes? intrinsic and extrinsic factors

Answer 7

intrinsic: structure and composition of plaque (foam cells/lipids, thin fibrous cap, MODERATELY STENOTIC LIPID RICH ATHEROMAS W SOFT CORE, abundant inflammation, few SMCs, and mechanical stress at jxn of fibrous cap and adjacent normal wall
extrinsic: adrenergic stimulation (upon awakening, emotional)

Question 8

how does coronary thrombosis decrease blood flow?

Answer 8

can be partial or total. total = acute transmural MI or sudden death. incomplete (mural thrombus) causes unstable angina, acute subendocardial infarction, sudden death, or emboli

Question 9

how does vasoconstriction lead to decreased blood flow?

Answer 9

compromises lumen size, increases mechanical forces that contribute to plaque rupture, leads to severe but TRANSIENT reduction in coronary blood flow

Question 10

what are some stimulators of vasoconstriction?

Answer 10

adrenergic agonists, locally released platelet contents, endothelial dysfunction leading to impaired secretion of endothelial relaxing factors, mediators released from mast cells

Question 11

4 basic syndromes of IHD?

Answer 11

angina pectoris, MI, chronic IHD, sudden cardiac death

Question 12

clinical angina pectoris? grossly?

Answer 12

15 seconds to 15 minutes of chest pain caused by transient myocardial ischemia. no cell necrosis.

Question 13

3 patterns of angina pectoris?

Answer 13

stable: attributed to chronic stenosing coronary AS
prinzmetal: due to coronary artery spasm, at rest
unstable: becomes more frequent, often at rest, induced by disruption of plaque with superimposed partial thrombosis (often prodrome of acute MI)

Question 14

MI risk factors

Answer 14

increasing age and predisposition to atherosclerosis: HTN, cigarettes, DM, increased cholesterol and or lipids

Question 15

pathogenesis of MI?

Answer 15

90%: acute plaque change resulting in thrombus and occlusion of coronary artery
10%: vasospasm, emboli or unexplained

Question 16

types of MI?

Answer 16

transmural, subendocardial

Question 17

transmural MI qualities?

Answer 17

1. full thickness of ventricular wall
2. confined to distribution of 1 vessel
3. fixed coronary obstruction w superimposed acute plaque change and complete obstructive thrombosis

Question 18

subendocardial MI qualities?

Answer 18

1. necrosis limited to inner 1/3 (watershed area)
2. may extend laterally beyond perfusion of 1 vessel
3. fixed coronary obstruction w acute plaque change but w non-occlusive thrombus or lysis of thrombus or hypotension

Question 19

how long till irreversible damage is done?

Answer 19

20-40 minutes (coagulative necrosis)

Question 20

effect of early thrombotic therapy?

Answer 20

3-4 hrs. trying to reperfuse and limit size of infarct.

Question 21

gross morphology of MI at under 12 hours?

Answer 21

not apparent. with tetrazolium stain, see pale areas 2-3 hrs post occurrence.

Question 22

gross morphology of MI at 12 - 24 hrs

Answer 22

dark red-blue mottling (d/t stagnant blood)

Question 23

gross morphology of MI at 1-14 days

Answer 23

early: sharply defined yellow-tan area
late: still central yellow-tan area but hyperemic peripheral zone (d/t repair)

Question 24

gross morphology of MI at over 2 weeks?

Answer 24

gray-white scar begins to form

Question 25

histology of MI at 4-12 hours?

Answer 25

wavy fibers

Question 26

histology of MI at 12hr-7 days

Answer 26

coagulative necrosis well-established and ongoing. initially pyknotic nuclei, very pink myocytes. followed by PMNs (1-3 days max), loss of nuclei and striations. by 7 days macrophages at border

Question 27

histology of MI at 7-14 days

Answer 27

10-14 days granulation tissue well-est, collagen deposition begins
(7-10 days = phagocytosis)

Question 28

histology of MI at over 14 days?

Answer 28

progressively more collagen deposition, eventually dense fibrous scar

Question 29

when does an acute MI reperfusion injury usualy occur?

Answer 29

after thrombolysis, balloon angioplasty or bypass grafts. prevents necrosis if w/in 20 mins. grossly see hemorrhage into infarcted tissue

Question 30

histo of reperfusion injury?

Answer 30

necrosis with contraction bands d/t influx of Ca.

Question 31

what processes facilitate reperfusion injury?

Answer 31

could be: oxygen free radicals from leukocytes, microvascular injury causing hemorrhage and endothelial swelling that occludes caps (no flow), or platelet and complement activation

Question 32

MI clinical features

Answer 32

chest pain: sever, radiating into L arm, neck, jaw, epigastrium, several mins to hrs, no relief by nitroglycerin
rapid weak pulse, sweating, dyspnea d/t pulm edema
10-15% w/o stx
ECG patterns
Labs: cardiac enzymes, CRP

Question 33

complications of MI

Answer 33

contractile dysfunction
cardiogenic shock
arrhythmia
myocardial rupture (3-7 days later): free wall, ventricular septum, papillary muscle
pericarditis (2-3 days)

Question 34

more complications of MI

Answer 34

mural thrombus & thromboembolism
ventricular aneurysm (late)
papillary muscle dysfunction (secondary to scarring/fibrosis)
progressive heart failure (late)

Question 35

acute MI prognosis

Answer 35

depends on size of infarct, also site and transmural extent. long term depends on quality of L ventricular fxn and extent of vascular obstruction ( < 40% is bad)

Question 36

chronic ischemic heart dz seen in?

Answer 36

elderly ppl w progressive heart failure d/t ischemic myocardial damage: post-infarction cardiac decompensation (exhaustion of hypretrophied fibers), or severe coronary artery dz w/o infarction but w/ myocardial dysfunction

Question 37

Chronic IHD morphology?

Answer 37

enlarged heart w/ LVH and dilation, coronary AS, scars, subendocardial myocyte vacuolization

Question 38

what is SCD?

Answer 38

unexpected death d/t cardiac causes, w/ or w/o stx. due to lethal arrhythmia: asystole or v-fib.

Question 39

morphology of SCD?

Answer 39

coronary atherosclerosis, acute plaque change, MI, scars from old MIs or pathology associated wtih non-atherosclerotic causes