Cardiology I

Question 1

Answer 1

Remote thrombosis with recanalization

2 small, narrow channels

Question 2

Answer 2

Atherosclerosis of coronary artery

Severe narrowing

Blue area = calcification

Question 3

Answer 3

Pink to red recent thrombosis in narrowed coronary artery

Lumen occluded

Cholesterol clefts (narrow white spaces)

Question 4

Answer 4

High magnification of atheroma shows many foam cells & occasional cholesterol cleft

Some dark blue inflammatory cells

Question 5

Answer 5

Aortic atherosclerosis (mild-bottom to severe-top)

Top has extensive ulcerations

Question 6

Answer 6

Abdominal aortic aneurysm

Bulge just above aortic bifurcation

Prone to rupture

Pulsatile mass on PE

Question 7

Answer 7

Microscopic cross section of aorta

Large atheroma on left (contains cholesterol clefts)

Far left - hemorrhage

Question 8

Answer 8

Foam cells + cholesterol clefts

Question 9

Answer 9

Severe aortic atherosclerosis

Atheromatous plaques have ulcerations + formation of mural thrombus

Question 10

Answer 10

Cholesterol clefts

Cholesterol emboli rare

Question 11

Answer 11

Left coronary artery from aortic root on left

Extending across middle of picture to right is anterior descending branch

Severe atherosclerosis w/ extensive calcification + significant narrowing (far right)

Question 12

Answer 12

Coronary atherosclerosis complicated by hemorrhage into atheromatous plaque

May acutely narrow arterial lumen

Question 13

Answer 13

Shows large LV and small RV

Pale region surrounded by hyperemia = MI from anterior to septum

Neovascularization around MI area

Transmural because extends thru full thickness of ventricular wall

Question 14

Answer 14

Earliest change seen in MI (day 1) - CONTRACTION BAND NECROSIS

Myocardial fibers lose cross striation, lose nuclei, irregular dark pink wavy contraction bands extend across fibers

Question 15

Answer 15

Infarction (1-2 days)

Dark red contraction bands on myocardial fibers

Almost all myocardial cell nuclei disappeared

Beginning of acute inflammation

Question 16

Answer 16

Extensive hemorrhage + myocardial fiber necrosis w/ contraction bands & loss of nuclei

Question 17

Answer 17

NOT FROM LECTURE

3-4 days old

Extensive acute inflam. cell infiltrate; myocardial fibers so necrotic, that outlines barely visible

Question 18

Answer 18

Intermediate MI 1-2 weeks old

Normal remaining myocardial fibers at top

Below are many macrophages with many capillaries & little collagenization

Question 19

Answer 19

LV free wall in R, septum in center

MI in anterior LV free wall & septum

White appearance of endocardial surface -> extensive scarring

Question 20

Answer 20

Complication of MI = rupture myocardium

Most likely to occur in 3-5 days following initial event (myocardium softest)

White arrow = point of rupture (anterior-inferior MI of LV free wall & spetum)

Dark red blood clot in hemopericardium, risk for tamponade

Question 21

Answer 21

Arrow = point of rupture

MI 3 weeks before & another MI occurred, rupturing through already thin ventricular wall 3 days later

Question 22

Answer 22

Previous extensive transmural MI involving free wall of LV

Normal thickness of wall at top, but inferiorly, only THIN FIBROUS WALL. Infarction was so bad that after healing, ventricular wall was replaced by thin band of collagen -> ANEURYSM -> noncontractile -> decreased SV -> strain remaining myocardium.

Stasis of blood also predisposes aneurysm to mural thrombosis.

Question 23

Answer 23

Ventricular aneurysm with thin wall

Increased risk for mural thrombus (present in pic)

Question 24

Answer 24

Aortic dissection may lead to hemipericardium when blood dissects thru media proximally –> can lead to cardiac tamponade

Question 25

Answer 25

Longitudinally opened aorta revealing limited dissection Red-brown thrombus extends around aorta Creates double lumen to aorta

Question 26

Answer 26

Aorta dissection went into muscular wall Blood can dissect up (close off carotids) or down (shut off coronaries) aorta

Question 27

Answer 27

Right carotid artery compressed by blood dissecting upward from tear with aortic dissection. Symptoms of aortic dissection: severe chest pain (distal dissection) or stroke (carotid dissection) or MI (coronary dissection)

Question 28

Answer 28

Microscopic cross section of aorta Red blood clot compressing aortic lumen due to aortic dissection

Question 29

Answer 29

Infective endocarditis Aortic valve has large, irregular tan vegetation Staphyloccocus produces "acute" bacterial endocarditis Streptococcus viridans produce "subacute" bacterial endocarditis

Question 30

Answer 30

Normal aortic valve shows 3 thin delicate cusps Can see coronary artery orifices just above Smooth endocardium, red-brown mycardium Aorta has smooth intima with no atherosclerosis

Question 31

Answer 31

Normal tricuspid valve Thin chordae tendinae that attach leaflets to papillary muscles of ventricular wall

Question 32

Answer 32

Normal myocardial fibers in longitudinal section Central nuclei & syncytial arrangement of fibers, some have pale pink intercalated disks

Question 33

Answer 33

Normal coronary artery Large lumen with no narrowing by atheromatous plaques Musuclar arterial wall normal proportion

Question 34

Answer 34

Normal (muscular?) artery lumen

Question 35

What is the most commonly affected coronary artery in MI?

Answer 35

LAD - Left anterior descending coronary artery (50%)

Question 36

Blockage in LAD would cause an MI where?

Answer 36

Anterior wall of LV, anterior septum, & apex

Question 37

What is the 2nd most commonly affected coronary artery in MI?

Answer 37

RCA - Right coronary artery (30-40%)

Question 38

What does the RCA supply?

Answer 38

In 90% of people, it supplies the posterior-inferior LV wall and posterior 2/3 of interventricular septum, posterior-inf. RV

Question 39

What is another less commonly affected coronary artery in MI?

Answer 39

Circumflex coronary artery (10-20%) Comes from the Left coronary artery

Question 40

What does the circumflex artery supply?

Answer 40

Lateral LV (except apex)

Question 41

When is the earliest you can identify an MI via pallor?

Answer 41

8-12 hours after infarct (accorinding to Dr. Kaya) 1-3 days (according to Robbins)

Question 42

Answer 42

LV wall shows large recent MI

Question 43

Answer 43

Remote MI Likely circumflex artery affected (lateral wall) and RCA (posterior wall)

Question 44

Histology of MI

Answer 44

Question 45

Answer 45

Hemorrhage (seen especially after reperfusion of of damaged myocardium)

Question 46

Answer 46

Neutrophils "Mickey Mouse" Inflammatory response infiltrating myocardium

Question 47

Answer 47

5-7 Days after MI - process of repair Neutrophils undergo apoptosis, now monocytes & macrophages Can see capillaries (neovascularization)

Question 48

Answer 48

Necrotic myocardium removed & replaced by scar tissue (no muscle)

Question 49

Answer 49

Complication of MI - free wall rupture

Question 50

Answer 50

Complication of MI - Ventricular septum rupture Creates L to R shunt --\> Harsh systolic murmur and hypoxia (SOB)

Question 51

Answer 51

Complication of MI - Papillary muscle rupture Valvular incompetence

Question 52

Answer 52

Ventricular aneurysm - ballooning out due to weakening of wall

Question 53

Answer 53

Ventricular aneurysm

Question 54

Answer 54

Aortic dissection

Question 55

Answer 55

Aortic dissection into media and ruptured

Question 56

Answer 56

Aortic dissection

Question 57

Answer 57

Aortic dissection

Question 58

What is an atherosclerotic plaque composed of?

Answer 58

Cells (SMC, fibroblast, macrophages, leukocyte) Connective tissue: collagen, elastin, fibrin, proteoglycans Lipid: intracellular/extracellular

Question 59

What are complications of coronary atherosclerosis?

Answer 59

1. Critical stenosis of lumen 2. Acute thrombosis 3. Hemorrhage into plaque 4. Aneurysm & rupture of wall

Question 60

What are the 2 major types of acute MI?

Answer 60

1. Subendocardial (10%): Necrosis limited to inner 1/3 - 1/2 of myocardium (mau be due to global reduction in perfusion or single vessel occlusion) * Multifocal, patchy, circumferential, coronary thrombosis rare, often due to hypotension/shock, No epicarditis, Don't form aneurysms or lead to ventricular rupture 1. Transmural (90%): Necrosis involves basically entire myocardial wall thickness (usually single vessel occlusion) * Unifocal, solid, in distribution of specific coronary artery, coronary thrombosis common, often cause shock, Epicarditis common, May result in aneurysm/ventricular rupture

Question 61

Describe a remote (healed) MI macroscopically

Answer 61

Characterized by scar tissue where normal myocardium replaced by fibrous CT Normally, scar tissue is firm, white, and ventricular wall thinned

Question 62

Describe the evolution of morphologic changes in MI over time

Answer 62

Question 63

What is ventricular rupture? When is it most common? 3 types & consequences?

Answer 63

Due to weakening of myocardium (due to necrosis & progressive removal of necrotic tissue) following transmural infarction Most common 3-5 days after MI Types: free wall rupture (hemopericardium, tamponade); septal rupture (L to R shunt); Papillary muscle rupture of mitral valve (acute valvular insufficiency)

Question 64

What is a ventricular aneurysm?

Answer 64

Due to remote MI composed of fibrous tissue (non-contractile). Weakened ventricle lead to out pouching of thinned ventricle. May cause blood stasis --\> mural thrombus within aneurysm

Question 65

Which part of the aorta is most affected by atherosclerosis?

Answer 65

Infra-renal abdominal aorta

Question 66

What is an aortic dissection? What is it associated with? How do you differentiate the types?

Answer 66

Dissection of blood within wall of aorta - causing blood-filled channel. Blood from dissection may cause 2nd distal tear in intima -\> double lumen aorta Assoc. with HTN, disorders of CT (Marfan's syndrome) Type A (occurs before aortic arch), type B (occurs after arch)