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Flashcards in Valvular heart disease Deck (28)
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Clinical presentation of calcific aortic stenosis


-Hypertrophied myocardium causes ischemia and angina pectoris
-Both systolic and diastolic function may be impaired
-Surgical valve replacement is necessary

-Age associated wear and tear
-Statins don’t help with valvular calcific degeneration


Pathogenesis of calcific aortic stenosis

-If the valve is bicuspid, the issues precipitate faster
-Hydroxyapatite is the most common deposit
-Abnormal valves have cells that are like osteoblasts
-Chronic injury from hyperlipidemia, HTN, inflammation, atherosclerosis
-Left ventricular outflow obstruction leads to gradual narrowing of the valve orifice
-Increasing pressure gradient causes concentric LVH


Morphology of calcific aortic stenosis

-Mounded calcified masses within the aortic cusps
-Prevent the cusps from opening fully
-Layered architecture of the valves are preserved
-Commissural fusion is not usually seen


Clinical presentation of Calcific stenosis of congenitally bicuspid aortic valve

-Valves become incompetent due to aortic dilation, cusp prolapse, or infective endocarditis
-Usually asymptomatic early in life
-Aortic stenosis or regurgitation, infective endocarditis, and aortic dilation or dissection
-50% of cases become calcified


Pathogenesis of Calcific stenosis of congenitally bicuspid aortic valve

-Some show familial clustering with associated aorta or left ventricular outflow tract malformations
-NOTCH1 is strongly associated with these abnormalities


Morphology of Calcific stenosis of congenitally bicuspid aortic valve

-Two functional cusps of unequal size, larger cusp has a midline raphe
-Raphe is a common site for the calcific deposits


Clinical presentation of mitral annular calcification

-Women older than 60 or individuals with mitral valve prolapse

-Usually do not effect valvular function
-May cause: regurgitation, stenosis, or arrhythmias
-At a higher risk for embolic stroke
-Provides a location for infective endocarditis
-Visualized on echo or x ray by ring like opacities


Pathogenesis of mitral annular calcification

-Calcific deposits in the mitral valve typically occur in the fibrous annulus


Morphology of mitral annular calcification

-Irregular, stony hard, occasionally ulcerated nodules at the base of the leaflets


Clinical presentation of Mitral valve prolapse (myxomatous degeneration)


-Usually an incidental finding
-Mid-systolic clicks
-Minority display angina and dyspnea
-Serious complications: infective endocarditis, mitral insufficiency, stroke, arrhythmias
-Risk of serious complications is low but higher in men, older patients, and those with mitral regurgitation or arrhythmias

Most common cause of mitral valve surgery


Pathogenesis of mitral valve prolapse (myxomatous degeneration)

-Sometimes associated with Marfan syndrome (fibrillin-1) and dysregulates TGF-B signaling


Morphology of mitral valve prolapse (myxomatous degeneration)

-Leaflets are floppy and balloon back into the left atrium
-Interchordal ballooning (hooding) of the mitral leaflets that are enlarged, redundant, thick and rubbery
-Tendinous cords are elongated, thinned or even ruptured
-Myxomatous degeneration: thickening of the spongiosa layer from deposition of mucoid material
-Fibrous thickening of the leaflets, fibrous thickening of endocardium, thickening of the mural endocardium, thrombi on the leaflets, focal calcifications


Clinical presentation of rheumatic heart disease


Rate has declined due to increased diagnosis and treatment, and improved sanitation
-migratory polyarthritis, pancarditis, subq nodules, erythema marginatum, Sydenham chorea
-Acute: 10 days to 6 weeks after infection in children. Abs to streptolysin O and DNase B. Contain pericardial friction rubs, tachy, and arrhythmias
-After initial infection there is increased vulnerability to reactions with subsequent infections
-Damage to the valves is cumulative
-Surgical replacement of the valves

Rheumatic fever --> RHD

RHD only cause of mitral stenosis


Pathogenesis of rheumatic heart disease

-Acute, immunologically mediated, multisystem inflammatory disease occurring a few weeks after an episode of group A strep pharyngitis
-RHD: deforming fibrotic valvular disease involving the mitral valve
-CD4 cells against M proteins recognize cardiac self antigens causing cytokine production and macrophage activation


Morphology of rheumatic heart disease

Anitschkow cells: pathognomonic for RF. Caterpillar cells
-Aschoff bodies: distinctive lesions in the heart with T cells and anitschkov cells.
-Pancarditis: inflammation in any of the layers of the heart
-Fibrinoid necrosis in the cusps or tendinous cords
-Verrucae: vegetations along the lines of closure on the cusps
-MacCallum plaques develop in the left atrium due to regurgitant jets
-Mitral valve: leaflet thickening, commissural fusion, thickening and fusion of the tendinous cords
-Fish mouth or buttonhole stenoses
-Right ventricular hypertrophy and pulmonary vascular changes may occur


Clinical presentation of infective endocarditis

-Acute: infection of a previously normal heart valve by staph aureus that destroys. Difficult to destroy with drugs alone. May need surgery
-Subacute: strep viridans. That are insidious and overall less destructive. Cures can be achieved over weeks to months. Abx.
-Abx prophylaxis is necessary after previous RHF
-Acute: rapidly developing fever, chills, weakness and loassitude
-Mumurs on 90% of individuals
-DUKE criteria
-Glomerulonephritis, microthromboemboli, Janeway lesions, Osler nodes, and Roth spots


Pathogenesis of infective endocarditis

-Microbial infection of the heart valves or mural endocardium leading to the formation of vegetations of thrombotic debris and organisms
-Associated with the destruction of the underlying cardiac tissues
-Most common are bacterial
-Previously normal valves
-RHD may precede this but also mitral valve prolapse, degenerative calcific valvular stenosis, bicuspid aortic valve, artificial valves, and unrepaired and repaired congenital defects
-Microorganism seeding to bloodstream


Morphology of infective endocarditis

-Vegetations on heart valves that are friable and bulky
-Aortic and mitral valves are most common
-Vegetations are prone to embolization
-Granulation tissue
-Fibrosis, calcification and a chronic inflammatory infiltrate develop over time


Common organisms implicated in infective endocarditis

-S. viridans: after dental procedures
-S. aureus: acute and IV drug users
-S. Epidermidis: prosthetic valves


Clinical presentation of nonbacterial thrombotic endocarditis

-Can cause infarcts in the brain, heart, or elsewhere
-Often in debilitated patients (marantic endocarditis)
-Concomitantly with DVT and PE
-Striking association with mucinous adenocarcinoma that also causes Trousseau syndrome
-Endocardial trauma may also cause this


Pathogenesis of nonbacterial thrombotic endocarditis

-Deposition of small sterile thrombi on the leaflets of cardiac valves
-Develop on the line of closure of the leaflets or cusps


Morphology of nonbacterial thrombotic endocarditis

-Bland thrombi that are loosely attached to the underlying valve
-Non-invasive vegetations
-Often track along pulmonary artery catheters


Clinical presentation of endocarditis of SLE (Libman Sacks Disease)

-Steroids has decreased this risk
-Also can occur in the setting of antiphospholipid syndrome
-Mitral valve involvement is the most common


Pathogenesis of endocarditis of SLE (Libman Sacks Disease)

-Mitral and tricuspid valvulitis with small, sterile vegetations


Morphology of endocarditis of SLE (Libman Sacks Disease)

-Single or multiple, sterile, pink vegetations with a verrucous appearance
-Finely granular, fibrinous eosinophilic material
-Lesions also have fibrinous necrosis


Clinical presentation of Carcinoid Syndrome

-Systemic disorder with flushing, diarrhea, dermatitis, and bronchoconstriction


Pathogenesis of carcinoid syndrome

-Caused by release of serotonin from carcinoid tumors
-Cardiac lesions occur after there is a large hepatic metastatic burden
-Left side of the heart is protected from breakdown in the pulmonary vasculature
-Serotonin, kallikrein, bradykinin, histamine, prostaglandins, and tachykinins
-Levels of serotonin directly correlate to the severity of the cardiac lesions
-Similar lesions from taking fenfluramine or ergot alkaloids


Morphology of carcinoid syndrome

-Endocardium and the valves of the right heart are most affected
-Distinctive, glistening white intimal plaquelike thickenings of the endocardial surfaces
-Composed of smooth muscle cells and sparse collagen fibers in an MPS rich matrix
-Tricuspid insufficiency and pulmonary stenosis