Pathology of Valve Disease

Question 1

3 layers of valve leaflets?

Answer 1

Fibrosa - on back (downstream) surface of valve, continuous with annulus fibrosa.
Spongiosa - central loose connective tissue.
Ventricularis - upstream side, rich in elastic fibers.

Question 2

Are normal valves vascularized?

Answer 2

Nope.

Question 3

What’s the “most important” etiology of aortic stenosis?

Answer 3

dystrophic calcification (wear and tear from old age)

Question 4

What’s the most important etiology of mitral stenosis?

Answer 4

chronic rheumatic heart disease

Question 5

What is the most important etiology of aortic regurgitation?

Answer 5

dilation of the aortic root (old age, HTN, atherosclerosis, Marfan syndrome)

Question 6

What are the 2 most important etiologies of mitral regurgitation?

Answer 6

Myxomatous degeneration.

Dilation of the mitral valve ring due to LV dilation from LV failure.

Question 7

What increases rates of dystrophic calcification?

Answer 7

Turbulent blood flow… shares some risk factors with atherosclerosis, such as HTN.

Question 8

Does dystrophic calcification cause valve leaflet fusion?

Answer 8

No, that’s more a thing with chronic rheumatic heart disease.

Question 9

Where do the nodules of dystrophic calcification of the aortic valve often protrude?

Answer 9

Into the sinus of Valsalva…. meaning… into the aorta.

Question 10

What age range does dystrophic calcification usually become symptomatic, if the valve was previously normal? If the valve is congenitally deformed?

Answer 10

eighth to ninth decade.

Congenital deformations -> more wear and tear -> early symptomatic dystrophic calcification.

Question 11

What’s the deal with calcification of the mitral valve annulus?

Answer 11

Ususually in older women, associated with myxomatous degeneration.
It causes regurgitation.

Question 12

When does chronic rheumatic heart disease have its onset, compared to the instance of acute rheumatic fever?

Answer 12

Occurs years to decades after acute rheumatic fever.

Question 13

What changes happen to the valves in chronic rheumatic heart disease?
To the chordae tendinae?

Answer 13

Valves thicken, commissures fuse, and they become vascularized.
Chordae tendinae shorten, thicken, and fuse.
(and scarred valves are predisposed to infection)

Question 14

Does chronic rheumatic heart disease produce stenosis or regurgitation?

Answer 14

It can cause either or both.

Question 15

What does mitral stenosis from chronic rheumatic heart disease look like?

Answer 15

A fish mouth.

Question 16

Complications of mitral regurgitation?

Answer 16

Increased pressure -> dilated LA.

Stasis in LA -> left atrial appendage thrombus.

Question 17

What does chronic rheumatic heart disease look like histologically?

Answer 17

Bland fibrosis in the valves - the distinction between the 3 layers of the valve is lost.
Neovascularization.

Question 18

What kind of remodeling of the LV does aortic regurgitation cause?

Answer 18

Eccentric (dilated) hypertrophy

Question 19

4 causes of aortic regurgitation?

Answer 19

Dilation of the aortic root.
Perforation or tear of leaflet - (infectious endocarditis)
Retracted leaflet (chronic rheum. heart dis.)
Fixed leaflets (dystrophic calcification, or chronic rheum heart dis.)

Question 20

Which valve does myxomatous degeneration usually affect?

Is it usually symptomatic?

Answer 20

The mitral valve, causing regurgitation.

It’s usually asymptomatic

Question 21

What does “myxomatous degeneration” mean?

Answer 21

Mucopolysaccharide deposition in spongiosa, attenuation of fibrosa.
Leaflets become floppy and “billow” i.e. prolapse into prior chamber (the LA).

Question 22

4 “clinical lesions” of myxomatous degeneration? What are the outcomes of 2 these “lesions”?
(this is the vaguest use of the word “lesion” I have yet seen)

Answer 22

Asymptomatic “systolic click.”
Mitral regurgitation - gradual from annulus dilation, or sudden from snapped chordae tendinae.
Thrombus formation -> embolus or endocarditis.
Dysrhythmia -> syncope or sudden death (unclear why).

Question 23

Underlying myxomatous degeneration….

Answer 23

may be a genetic defect in connective tissue similar to that in Marfan’s syndrome.

Question 24

What does mitral regurgitation do to the lungs?

Answer 24

increased pressure backs up… -> venous congestion, alveolar edema, SOB, orthopnea
(can also then mess up the right heart)

Question 25

What are 2 sequelae of chronic mitral regurgitation?

Answer 25

Fibrosis in pulmonary veins.
Changes in pulmonary arteries that increase resistance (concentric intimal thickening)…
leading to fixed pulmonary hypertension.

Question 26

How does bacterial endocarditis happen?

Answer 26

Fibrin on a valve leaflet gives bacteria (or whatever else) a place to anchor, where they grow.

Question 27

What’s a non-cardiovascular complication of bacterial endocarditis?

Answer 27

Immune complex deposition.

Question 28

Contrast acute from subacute bacterial endocarditis. (what causes it, who gets it, etc.)

Answer 28

Acute endocarditis: more aggressive bacteria (eg. S. aureus), can attack healthy heart valves, untreated is lethal within 6 weeks.

Subacute endocarditis: less aggressive bacteria (eg. Strep. viridians), usu. on previously damaged valves, untreated usu. isn’t lethal before 6 weeks.

Question 29

Valve-related conditions that predispose to bacterial endocarditis?

Answer 29

All the stuff we’ve talked about (dystrophic calcifcation, chronic rheumatic heart disease, myxomatous degeneration, congenital defects)… and artificial valves.

Question 30

4 non-valve-related factors that predispose to bacterial endocarditis?

Answer 30

Infection elsewhere
IV foreign bodies (e.g. catheters)
Immunosuppression
IV drug use (esp. right sided endocarditis)

Question 31

3 sequelae of bacterial endocarditis?

Answer 31

Regurgitation from valve damage.
Emboli -> infarct. Or septic emboli -> abscess elsewhere.
Immune complexes.

Question 32

How can endocarditis cause heart block?

Answer 32

If it damages / causes fibrosis of the conducting tracts that pierce the fibrous skeleton of the heart.

Question 33

Why are immune complexes from endocarditis bad?

Answer 33

They can cause acute necrotizing glomerulonephritis.

Question 34

Which bacteria really like prosthetic valves?

Answer 34

Staph. epidermidis.

Question 35

Which pathogens commonly cause endocarditis in IV drug users?

Answer 35

S. aureus, Candida, Aspergillus

Question 36

What causes non-bacterial thrombotic endocarditis (NBTE)? (hint: it’s not bacteria)

Answer 36

Valve damage in the setting of hypercoaguability (Virchow’s triad met, e.g.)
Not caused by a pathogen - there are no bugs when you look at the histology of this stuff.

Question 37

Examples of conditions that predispose to NBTE?

Answer 37

Mild disseminated intravascular coagulation (DIC), sepsis, burns, malignancies (esp. mucinous adenocarcinomas of the pancreas)

Question 38

Sequelae of NBTE?

Answer 38

Can cause emboli.
Doesn’t really damage the valve - is reversable.
Predisposes to actual infection.