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Flashcards in Valvular Disease Patho Deck (47)
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3 microscopic layers of each valve leaflet

1. fibrosa: back surface of valve (aortic side of aortic valve, ventricular side of mitral) in continuitry with annulus fibrosa 2. spongiosa : central layer comprised of loose CT 3. ventricularis/atrialis: closest to the inflow surface and rich in elastic fibers


Normal valves are __________.

-not vascularized


Most important etiologic associations with valve defects: AS, MS, AR, MR

AS: dystrophic (wear and tear, aka senile) calcification -MS: chronic rheumatic heart disease -AR: dilation of aortic root (old age, HTN, atherosclerosis, Marfan) -MR: myxomatous degeneration, dilation of mitral valve ring with LV dilation due to LV failure


Dystrophic calcification most often affects ________ and _________. Discuss the cause.

-aortic valve leaflets, and mitral valve ring -turbulent blood flow leads to wear and teardamage to leaflets, esp. where pressuregradients and turbulence are greatest,leading to amorphous (dystrophic)calcification (notatherosclerosis of valves, but shares some risk factors)


Aortic valve calcification results in ______ in the _____ of leaflets, protruding into the __________. There is no ____________. Functionally this most often results in ________, but regurgitation as well. There is associated LV ____________.

-nodular deposits -middle, protruding into sinuses of Valsalva -no fusion of valve commissures (vs. Rheumatic heart disease) -most often results in stenosis -assoc with concentric LVH


Clinical sxs of dystrophic calcification. When does it tend to reach clinical significance.

-angina, syncope, CHF -8-9th decades (senile calcific AS) when aortic valve orifice is reduced to <1 cm2


dystrophic calc of tricuspid aortic valve


nodular fibrosis and calcification in dystrophic calcification


Timing of clinical sxs due to aortic valve calcification

-previously nl heart valve: 8-9th decade

-congenitally deformed aortic valves= earlier sxs onset

-bicuspid valves at 5-6th decade (unequal with raphe on large or equal without raphe)

-unicuspid valves: 2-4th decades : unicommmissural or acommmisural

-trend: greater deformity= greater turbulence= sooner calcification


bicuspid aortic valve with raphe (not calcified here) but can also be born without raphe


left is unicommissural

-right is acommissural


Calcification of MV annulus

-elderly, more often in women, more often in patients with myxomatous degernation or chronically increased LV pressures

-commonly detected on CXR or US; usually asymptomatic but can cause mitral regurg

-rarely erods into conduction system 


calcification of MV annulus


calc of mitral valve annulus! not leaflets!!


Acute rheumatic fever vs chronic rheumatic heart disease

-ARF: systemic disease! whichc an affect all layers of the heart as well as extracardiac sites (joints, skin, CNS); inflammatory disease triggered by an abnormal immune reaction to pharyngitis caused by Group A B hemolytic strep

-CRHD: affects cardiac valves, years after 1 or more attacks of ARF; mitral valve affected with or without aortic valve (less common)


Chronic RHD occurs _______________. Affect which valves? What does chronic injury cause?

-years to decades after 1 or more episodes of ARF

-affects mostly cardiac valves on LH esp mitral or mitral + aortic

-chronic injury causes scarring of valve leaflets with thickening, retraction, and neovasc. of leaflets as well as fusion of commissures. Shortening, thickening, and fusion of chordae tendonae


Gross path of chronic rheumatic heart dz

chronic injury causes scarring of valveleafletswith thickening, retraction, andneovascularization of leaflets, as wellasfusion of commissures. Also causesshortening, thickening and fusion of chordae tendineae (may also cause regurg)


The valvular changes in CRHD can produce function _____, ______ or both.




Pure MS from CRHD results in ___________________ . Added MR produces ____________, as does AS or AR.

-left atrial dilation, atrial fibrilation, atrial thrombbus which possible embolization

-added MR produces LVH, as does AS or AR


Scarred valves from CRHD are predisposed to ________.



MS secondary to CRHD

-view from above: fish mouth,; thickened leaflets and fused commissures

-side view: shortened, thickened fused chordae


Aortic regurgitation due to CRHD looks like what?

-shortened, rolled up leaflets


Chronic rheumatic heart disease on microscopy

-bland fibrosis of leaflets with loss of 3 layers

-potential neovascularization


arrow pointing out neovasc in CRHD


Causes of AR, which is the most common? and what is end result?

-dilation of aortic root is by far the most common cause (old age, medial degeneration, marfan's)

-perforation or tear of leaflet (infectious endocarditis)

-retraction of valve leaflets: scarring due to CRHD

-fixation of valve leaflets: scarring or calcification

-results in eccentric LVH


AR due to dilation of aortic root

-can also be due to shortened rolled upleaflets from CRHD!


Myxomatous degeneration of MV

-increased deposition of mucopolysaccharides in spongiosa with associated attenuation of fibrosa

-leaflets thicken, stretch, chordae elongate, and leaflets can billow upward into LA (prolapse) functionally producing regurg

-uncommonly sxs

-Pathogenesis is unknown, but may involve a subtle,
sometimes inherited disorder of structural proteins, so that normal physical stresses on the valve result in
increased deposition of extracelllular matrix, as well as stretching of the chordae..


What does MV prolapse sound like?

-mid systolic click


myxomatous degeneration: spongiosa layer is blue with polysaccharides


myxomatous degeneration of valve: looks like clouds on long stems!