Lecture 31: Cardiac Valve Pathology Flashcards Preview

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Flashcards in Lecture 31: Cardiac Valve Pathology Deck (67):

What are the three layers of the valve leaflet?

1. the fibrosa
-on the back surface of the valve (eg aortic side of aortic valve, ventricular side of mitral) in continuity with annulus fibrosa
2. the spongiosa
-in middle of fibrosa and ventricularis
-loose connective tissue
3. the ventricularis
-elastic fibers


What is the role of the fibrosa layer?

The back layer of the valves (facing the chamber blood rushes into)
Provides structural integrity to leaflet
-continuous with chordae tendinae in AV valves


What is the role of the spongiosa?

Layer in between fibrosa and ventricularis
Provides cushion


What is the role of the ventricularis?

Layer on the side where blood is coming from
Allows for elastic recoil


Are valves vascularized?

If they are, there might’ve
Been prior inflammation


What are the most important etiologic associations with AS?

1. dystrophic (from wear and tear and being senile) Calcification


What are the etiologic associations with MS?

1. chronic rheumatic heart disease


What are the etiologic associations with AR?

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


What are the etiologic associations with MR?

1. myxomatous degeneration
2. dilation of mitral valve ring with LV dilation due to LV failure


What does dystrophic calcification lead to?

Aortic stenosis
Dystrophic calcification = indicative of senility and wear/tear


What does chronic rheumatic heart disease cause?

Mitral stenosis


What does dilation of aortic root cause?

Aortic regurgitation


What does myxomatous degeneration cause?

Mitral regurgitation


What does dystrophic calcification most commonly affect?

Aortic valve leaflets most likely because subject to highest turbulence
Mitral valve ring (leading to MR)
Distinct from atherosclerosis


Why does wear and tear lead to AS?

Turbulent blood flow leads to wear and tear of the leaflets, especially where pressure gradients and turbulence are greatest
Leads to amorphous calcification (calcium deposit on the leaflets and valves)
Calcium deposit can occur on supporting structures (valve annulus) as well


What does dystrophic means?

Amorphous deposition of calcium phosphate


What are the gross features of aortic valve calcification?

1. nodular deposits in the middle of the leaflets protruding into the sinuses of Valsalva
2. No fusion of valve commissures (unlike rheumatic heart disease)
3. Most often results in stenosis but can lead to regurgitation as well
-Associated with concentric LV hypertrophy


What are the clinical symptoms of calcifications?

Angina, syncope, CHF
Symptoms of decompensated aortic stenosis


When does aortic stenosis start to be symptomatic?

When it is reduced to 1 cm^2
Can be reduced to smaller CSA because LV hypertrophies to compensate for narrowing to a point


What can happen to the nodular calcium deposits on the fibrosa side of aortic valve?

They can rupture which can lead to
i. embolization of calcific debris
ii. a nidus for infective endocarditis


What is a nidus?

A place in which something is formed/deposited
A site of origin


Can there be different leaflet numbers in aortic valve? Significance?

Yes can be unicuspid, bicuspid and tricuspid
Tricuspid = calcification in 80s
Bicuspid = calcification in 50s
Unicuspid = calcifications in 20s


What does a biscuspid aortic valve look like?

Has a raphe
Raphe represents area where two leaflets should’ve separated


What does a raphe in valves represent?

The point at which two leaflets should’ve separated but never did


What does a unicuspid Aortic valve look like?

Unicommissural vs. acommissural


What are the characteristics of calcification of Mitral Valve Annulus?

Can cause mitral regurg but usually asymptomatic
Rarely erodes into conduction system…but can do so
Occurs most often in the elderly and is associated with aortic valve calcification
Can also occur in patients with myxomatous degeneration and HTN
Can serve as a source of infection or embolus


What is acute rheumatic fever? Significance?

Throat infection from Group A streptococci
A systemic disease which can affect all layers of the heart
Can predispose one to chronic rheumatic heart disease


What are the key characteristics of chronic rheumatic heart disease?

Occurs years to decades after 1 or more episodes of acute rheumatic fever
Predominantly affects the mitral valve (but can affect any other valves)
Can lead to fusion of commissures, scarring of valve leaflets, and shortening/thickening/fusion of chordae tendinae
Leads to
i. stenosis
ii. regurgitation
iii. both stenosis and regurg


What is the hallmark of chronic rheumatic heart disease?

Commissural fusion of mitral valve
Fish mouth opening


What can CRHD predispose blood to?

May lead to atrial appendage thrombus


Can you get aortic stenosis/regurg from CRHD too?

Yes, difference is that you don’t see any calcifications but you do see fusion of commissures


What are the commissures?

The sites where free edges of adjacent leaflets attach to underlying chamber


What are the histological features of CRHD?

1. fibrosis in all 3 layers (or loss of the 3 layers)
2. Neovascularization


What does neovascularization in a valve indicate?

Chronic Rheumatic Heart Disease


What is the significance of having a scarred valves?

Predisposed to infection! Such as endocarditis


What are the consequences of MS?

LA dilation
Atrial fibrillation
Atrial thrombus
Arterial embolization


What are the consequences of having a LA appendage thrombus?

Because that shit can break loose and cause an embolus


What is a marker of prior inflammatory disease?

When you see neovascularization


What are the possible causes of aortic regurgitation?

1. Dilation of aortic root
2. Perforation or tear of valve leaflet
3. Retraction of valve leaflets
4. Fixation of valve leaflets by scarring or calcification
5. Results from eccentric hypertrophy of LV


What does myxomatous mean?

A pathological weakening of the connective tissue


What are the key characteristics of myxomatous degeneration of mitral valve?

1. Increased deposition of mucopolysaccharides in spongiosa (middle layer) with associated attenuation of fibrosa
2. Leaflets thicken, stretch, chordae elongate and leaflets can billow upward into LA
3. Can lead to Prolapse
Uncommonly symptomatic
Abnormal response to hemodynamic stress on the valve (perhaps due to genetics?)


What are the histological features of myxomatous degeneration?

Deposition of mucopolysacchatrides in the fibrosa


What are the gross features of myxomatous degeneration?

Thickened leaflets
Elongated chordae tendinae


What are the gross features of a prolapsed myxomatous mitral valve?

Can present with a rupture of the chordae


What are the clinically significant symptoms caused by myxomatous degeneration?

1. asymptomatic systolic click
2. MR due to annulus dilation or to chordal rupture (gradual and acute, respectively)
3. thrombus formation
4. dysrhythmia (MoA unclear)


What are symptoms associated with mitral stenosis?

1. elevation of LA pressure (can affect pulmonary vessels)
2. Pulmonary venous congestion due to increase in LA pressure
3. increased venous pressure transmitted to alveolar capillaries which may lead to interstitial and/or alveolar edema
4. increased pressure may be transmitted to pulmonary arterioles so pressure overload of RV
5. increased LAP can lead to pulmonary vein fibrosis
6. Increase in PA pressure can lead to structural changes in pulm arterioles (increase pulm resistance and fixed pulm HTN)


What is the connection between connective tissue disorders and myxomatous degeneration?

People with issues of connective tissue (Marfan’s syndrome) are more predisposed to cardiac valve degeneration
This suggests that there are underlying connective tissue and hereditary abnormalities that predispose these patients when subjected to hemodynamic stress


What are the histological changes of pulmonary artery in mitral stenosis?

Concentric intimal thickening (very similar to what happens in atherosclerosis or HTN)


What are the differences between acute and chronic changes from increased LAP?

Acute increased LAP = transient increased PVR
Chronic increased LAP can result in persistence pulmonary HTN


What is infectious endocarditis?

Infection of a heart valve
Manifested as bulky deposits of fibrin, platelets, inflammatory cells on valve
Most often bacterial but can be fungal, rickettsial, chlamydial or viral


What is the pathogenesis of bacterial endocarditis?

1. Requires pre-existing fibrin deposition on a heart (eg from a NBTE)
2. bacteremia, where bacteria enter the fibrin deposit
3. Once bacteria settles, leads to growth by fibrin and polys and intravascular immune complex formation


What is NBTE?

Non-bacterial thrombotic endocarditis


What is the clinical spectrum of bacterial endocarditis?

1. acute bacterial endocarditis
2. subacute bacterial endocarditis


What are the characteristics of acute bacterial endocarditis?

1. virulent bacteria, untreated is lethal within several weeks
2. caused by Staph aureus and gram negative enteric bacteria


What are the characteristics of subacute bacterial endocarditis?

1. less virulent bacteria
2. usually attaching previously damaged valve
3. Untreated lethal after 6 weeks
4. caused by streptococcus, esp. viridans


What are factors that predispose one to bacterial endocarditis?

1. congenitally abnormal valves
2. artificial valves
3. infection elsewhere
4. intravenous foreign bodies
5. immunosuppression
6. intravenous drug abuse (left or right sided valves)
7. Dystrophic calcification
9. Myxomatous degeneration


What are the gross features of endocarditis?

1. perforation of leaflet
2. vegetations


What are the clinical problems associated with bacterial endocarditis?

1. valvular regurgitation
2. embolism, specifically septic emboli
3. immune complex disease like glomerulonephritis and small vessel vasculitis


What can lead to glomerulonephritis?

Immune complexes that come off bacterial endocarditis


What is non-bacterial thrombotic endocarditis?

Known as NBTE
Occurs in patients with INJURY to endocardium
Due to turbulent blood flow
In setting of underlying hypercoagulability disorder, like low grade DIC, mucin producing adenocarcinomas and sepsis
Refers to sterile vegetations occurring on heart valves
Lack significant inflammation
Can resolve on its own


What are the key characteristics of non-bacterial thrombotic endocarditis?

Occurs in patients with injury to the endocardium in setting of hypercoagulability
Coagulation disorders = DIC, sepsis, burns or malignant neoplasms like mucin producing adenocarcinomas
Can predispose to superimposed infection


What are the histological features of NBTE?

Bland organizing fibrin


What are the causative organisms that lead to infective endocarditis?

1. normal valves = staph aureus
2. abnormal valves = strep, esp viridans
3. prostethetic valves = staph epidermidis, staph aureus, strep
4. IV drug abusers = staph aureus, fungi


What are the most common causative organisms of infective endocarditis on normal valves?

Staph aureus (gram –‘s)


What are the most common causative organisms of infective endocarditis on abnormal valves (subacute endocarditis)?

Strep viridans


What are the most common causative organisms for infective endocarditis on prosthetic valves?

1. Staph epidermidis (from skin)
2. Staph aureus
3. Strep


What are the most common causative organisms for infective endocarditis on valves of IV drug abusers?

1. Aspergillus
2. Candida
3. Staph aureus