CVM Valve Pathology stoopidest

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stoopidest  on April 12, 2011

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cvm pathology

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CVM Valve Pathology stoopidest

major causes of valvular pathology
congenital defect

bacterial infectious endocarditis

nonbacterial thrombotic endocarditis

metabolically mediated endocarditis

aging and attendant degeneration
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Definitions

major causes of valvular pathology congenital defect

bacterial infectious endocarditis

nonbacterial thrombotic endocarditis

metabolically mediated endocarditis

aging and attendant degeneration
isolated valvular disease disease affecting a single valve
combined valvular disease disease affecting multiple valves
valvular stenosis inability of valve to open fully

leads to reduced forward flow through valve
valvular insufficiency inability of valve to close fully

allows for backward flow through valve
functional regurgitation incompetence in a valve caused by structural problems in the heart rather than any inherent defect in the valve

e.g. may involve dilation of the ventricle which alter the chordae tendenae preventing them from effectively pulling the valve closed
most common acquired valvular disease aortic stenosis
dystrophic calcification deposition of calcium phosphate crystals found in normal concentrations on to an abnormal structure
metastatic calcification deposition of calcium phosphate crystals found in abnormally high concentrations on to normal structures
calcific aortic stenosis [CAS] deposition of calcium on an abnormal aortic valve; this process occurs at normal physiologic calcium concentrations, ie is usually dystrophic
potential effects of calcific aortic stenosis [CAS]LVH -> ischemia -> MI or LV failure, congestion

calcium deposits on valve leaflets prevent the valve from opening fully

as a result, the LV may experience pressure overload, it may hypertrophy resulting in increased O2 demand with the attendant risk of ischemia and MI

CAS may also contribute to LV failure, congestion, and then RV failure
CAS murmur high-pitched systolic murmur with crescendo-decrescendo pattern

heard at right sternal border at 2-3 ICS; may radiate to the apex

becomes longer with handgrip [b/c left-sided]
the most common congenital heart malformation bicuspid aortic valve

this valve is usually asymptomatic, but may predispose to CAS, endocarditis and may be a/w other aortic anomalies
mitral annular calcification [MAC] deposition of calcium on the annular ring, a support structure, of the mitral valve

often asx, but may contribute to regurgitation, stenosis, arrhythima or even sudden death

nodules may embolize with r/o stroke; nodules are also potential sites of infection
conditions a/w mitral annular calcification the following may contribute to or be caused by MAC:
hypertension
aortic stenosis
hypertrophic cardiomyopathy
mitral valve prolapse [MVP] insufficiency of mitral valve due to weak valve leaflets which may prolapse back into the left atrium

valve leaflets may be floppy, loose, thick, rubbery

most common in younger women; often asx

a/w congenital connective tissue defects; often seen in Marfan's Syndrome [fibrillin-1 defect]
secondary valve changes a/w MVP thickening or fibrosing of valve leaflets

thickening of LV endocardium

thickening of LA in response to prolapsing leaflets

LA thrombi

calcification
complications relating to MVP infectious endocarditis

insufficiency with r/o cordae tendenae rupture

embolization

arrhyhmias
MVP murmur mid-to-late systolic murmur, often preceded by a click

murmur is not precipitated by exertion

valsalva moves the murmur closer to S1

inspiration moves the murmur closer to S2
course of rheumatic fever 1. strep A pharyngitis
2. rheumatic fever [6-10 wks later]
3. pancarditis, arthritis
4. chronic rheumatic heart disease with mitral valve stenosis
Aschoff bodies foci of lymphocytes and Anitschkow cells found in any layer of cardiac tissue in pancarditis of acute rheumatic fever
Anitschkow cells large, round or ovoid marcophages with owl-eye multinucleation, caterpillar-like chromatin, and abundant cytoplasm

these cells are found in Aschoff bodies in acute rheumatic pancarditis
common clinical findings a/w rheumatic fever 1. polyarthritis
2. pancarditis, including mitral valve inflammation and vegetations
3. subcutaneous nodules
4. erythema marginata
5. Sydenham chorea
clinical findings a/w acute rheumatic pancarditis 1. murmurs
2. weak heart sounds
3. pericardial friction rub
4. tachycardia
5. arrhythmias
cardiac structures commonly affected by rheumatic heart disease mitral valve [in all cases]:
- leaflet thickening
- commisural fusion
- thickening of tendinous cords

LA:
- dilation
- thrombi with r/o embolization

aortic valve [25% of cases]
- stenosis

also: pulmonary congestion may develop leading to RVH and failure
typical effect of valvular stenosis on the heart pressure overload -> concentric hypertrophy

turbulent jets of blood flow may also cause thrombi on the endocardium
typical effect of valvular insufficiency on the heart volume overload -> series hypertrophy, i.e. dilation
most frequent causes of aortic valve stenosis calcification of normal valve or of congenitally bicuspid valve
most frequent cause of aortic valve insufficiency dilation of ascending aorta, esp in hypertension and aging
most frequent cause of mitral stenosis rheumatic heart disease
most frequent cause of mitral insufficiency mitral valve prolapse
conditions contributing to acquired aortic stenosis chronic conditions including:
- HPT
- hyperlipidemia
- inflammation

these factors also play a role in atherosclerosis
clinical features of aortic stenosisNB: once symptoms appear, prognosis is not good; asymptomatic CAS is commonly fine

narrowing of valve orifice -> ventricular pressure build-up and high pressure gradient b/w the chambers

- LVH from pressure overload
- ischemia of hypertrophic tissue
- angina

progression can lead to systolic dysfunction and CHF
infectious endocarditis [IE] a serious infection characterized by colonization or invasion of the heart valves or the mural endocardium by a microbe, usually bacterial
acute infectious endocarditis infection of normal valve by highly virulent microbe producing necrotizing, ulcerating, destructive lesions

difficult to cure and often fatal
most common causes of IE mitral valve prolapse
degenerative calcific valvular stenosis
bicuspid aortic valve
artificial (prosthetic) valves
unrepaired and repaired congenital defects
history of IE
most common bacterial pathogen causing IE strep viridans

NB: s. viridans is normal oral flora
HACEK organism haemophilus
actinobacilus
cardiobacterium
eikenella
kingella

NB: the organisms are oral commensals and can cause IE
percentage of IE cases attributed to s. aureus 10-20%

s. aureus is a common epidermal flora and is the most common cause of IE in IVDA
clinical features of IE fever, chills, weakness, lassitude

new murmurs, esp in left-sided IE, from IE-derived valvular anomalies/defects

Janeway lesions, Osler nodes, retinal hemorrhages
most common sites of IE infection mitral and aortic valves

tricuspid IE may be seen in IVDA
morphological hallmark of IE vegetations: accumulations on the valves;
these consist of:
- bacteria
- thrombotic elements
- fibrin
- inflammatory cells

vegetations may be single or multiple and may appear on one or more valves

vegetations present the r/o of embolization -. abscesses and septic infarcts
characteristics of normal pericardial fluid 30-50 mL in volume of thin, clear, straw-colored fluid
key factor in determining effect of pericardial effusion on heart functionrate of fluid accumulation:
- slow effusion allows the pericardium to dilate so it can accommodate large amounts of fluid, up to 500 mL

- rapid effusion into non-dilated pericardium can constrict the atria, venae cava or ventricles interfering with normal heart function and may lead to tamponade; 200-300 mL can have this effect
cause of pericarditis primary pericarditis is rare and usually viral in origin

secondary pericarditis is the more common form, is usually acute, and is caused by:
- various cardiac disease
- metastasis
- thoracic or systemic infections
- surgery
types of pericarditis - serous
- fibrinous/serofibrous
- purulent
- hemorrhagic
- caseous
causes of serous pericarditis noninfectious inflammatory processes, e.g.:
- RF
- SLE
- sclerodoma
- uricemia
- tumors

infectons in adjacent structures may also cause serous pericarditis w/o actually infecting the pericardium

NB: unlikely to organize
causes of fibrinous/serofibrinous pericarditis NB: this is the most common form of pericarditis
fluid is a serous exudate w/fibrinous components

causes may include:
- acute MI
- Dressler syndrome [post-MI]
- RF
- SLE
- chest radiation
- uremia
- trauma
- surgery
most common clinical sign of fibrinous pericarditis pericardial friction rub
pain
signs of CHF
causes of purulent pericarditismicrobe infection deriving from:

- direct extension from neighboring infections [e.g empyema of the pleural cavity, lobar pneumonia, mediastinal infections, or extension of a ring abscess through the myocardium or aortic root]
- seeding from the blood
- lymphatic extension
- direct introduction during cardiotomy
microscopic features of purulent pericarditis red, granular serosal surface covered w/exudate
signs of inflammation are present

full resolution is rare and usually leads to scarring, organization, and ultimately constrictive pericarditis
morphology of fibrinous pericarditis dry serosal surface with fine granular roughening

may become organized
morphology of serofibrinous pericarditis yellow-brown, cloudy, turbid fluid w/immune cells and RBCs resulting from a more intesne inflammatory response

serofibrinous pericarditis may become organized
clinical features of purulent pericarditis spiking fever, chills
pericardial friction rub
pain
signs of CHF
causes of hemorrhagic pericarditis - usually metastasis of malignant tumors [neoplastic cells are often found in the exudate]
- baxterial infection
- bleeding diathesis
- TB
subtypes of chronic/healed pericarditis soldier's plaque
adhesive pericarditis
adhesive mediastinopericarditis
constrictive pericarditis
constrictive pericarditis fibrous scarring of the pericardium which encases the heart and prevents dilation or hypertrophy

- inability to dilate becomes problematic in exertion when increased CO is required

NB: mimics restrictive cardiomyopathy
adhesive pericarditis fibrotic fusion of the layers of the pericardium following pericarditis

usually has no effect on heart function
adhesive mediastinopericarditis obliteration of the pericardial sac following pericarditis and resulting in the fusion of the parietal layer to mediastinal structures

may severely inhibit cardiac fxn as the heart has pull on the now attached structures when it contracts

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