Valvular Heart Disease Flashcards
Functional regurgitation
Valve incompetence due to pathology in support structures
Mitral stenosis
Rheumatic heart disease
Mitral insufficiency
Mitral valve prolapse
Aortic stenosis
Calcification
Aortic insufficiency
Dilation of ascending aorta
Calcification aortic stenosis
Most common valvular abnormality
Age related degenerative calcification
If aortic valve is congenitally bicuspid, comes to attention in 50 to 70
If previously normal, comes to attention in 60s to 80s
Calcification aortic stenosis morphology
Rheumatic stenosis has commissar always fusion (degenerative usually does not)
Mitral valve involvement in rheumatic heart disease
Calcification aortic stenosis clinical
Obstruction causes concentric LV hypertrophy
May cause systolic and diastolic (CHF) dysfunction
Senile aortic stenosis
Tricuspid aortic valve undergone calcification
Congenital bicuspid aortic valve
Cusps usually unequal
Mitral valve normal
Acquired bicuspid aortic valve
Post inflammatory commissural fusion in rheumatic heart disease
Mitral valve is also abnormal
Myxomatous degeneration of the mitral valve
Most often young women
Most common valvular disease in industrialized nations
One or both mitral leaflets are enlarged,hooded, redundant, or floppy
Rarely lead to serious complications
Myxomatous degenerative of mitral valve morphology
Hooding of mitral leaflets
Leaflets are thick and rubbery
Cords often elongated, thinned, and occasionally ruptured
Commissural fusion is absent unlike in rheumatic heart disease
Myxomatous degen of the mitral valve histology
Attenuation of collagenous fibrosa layer
Thickening of spongiosa layer
Deposition of mucous material in the leaflets
Myxomatous degen of the mitral valve PE
Midsystolic click
May have late systolic or holosystolic murmur
Rheumatic fever
Occurs a few weeks after an episode of group A streptococcal pharyngitis
Often involves heart acutely but may progress to chronic valvular disease
Acute rheumatic fever morphology
Aschoff bodies
Anitschkow cells
Pancarditis
Aschoff bodies
T lymphocytes
Occasional plasma cells
Plump macrophages
Found in all layers
Anitschkow cells
Plump macrophages
Abundant cytoplasm
Nuclear chromatin is central, slender, wavy ribbon
Larger ones form giant cells
Pericarditis
Fibrinous or serofibrinous exudate
Myocarditis
Aschoff bodies often perivascular
Endocarditis
See fibrinoid necrosis within the cusps or along the tendinous cords
Verrucae along line of closure of valves
MacCallum plaques
Rheumatic heart disease
Irregular subendocardial thickening usually in left atrium
Acute rheumatic fever pathogenesis
Damage to heart caused by:
Immune response to group A strep which cross reacts with host tissue
CD4+ cells specific for strep peptides also react with self proteins
Acute rheumatic fever clinical
Evidence of preceding group A strep pharyngitis (10 days to 6 weeks) and
Jones criteria:
2 major or 1 major and 2 minor
Most often in children ages 5 to 15
Lab antibodies to streptolysin O and DNAse B
Jones criteria
Major manifestations
Migratory polyarthritis
Carditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
Jones criteria
Minor manifestations
Fever
Arthralgias
Elevated acute phase reactant (C reactive protein)
Carditis
Pericardial friction rubs
Weak heart sounds
Tachycardia
Arrythmias
Consequence of rheumatic fever
Chronic rheumatic heart disease
Chronic rheumatic heart disease
Deforming fibrotic heart disease
Particularly mitral stenosis
Leaflet thickening
Commissural fusion
Shortening, thickening, and fusion of the tendinous cords
Chronic rheumatic heart disease morphology
LA dilation with possible mural thrombus
May cause RV hypertrophy 2* pulmonary congestion leading to vascular and parenchymal changes
Infective endocarditis
Serious infection of heart valves or mural endocardium
Invasion by a microbe-> formation of vegetation’s with destruction of underlying tissue
Usually do to bacteria
Can be in aorta, aneurysmal sacs, other blood vessels, prosthetic devices
Acute endocarditis
Highly virulent organisms
Frequently affect normal valves, as well as abnormal
Destructive, tumultuous infection
50% die even with antibiotics and surgery
Subacute endocarditis
Organisms with low virulence
Previously abnormal valve
Most recover after appropriate therapy
Agents causing Infective endocarditis
Strep viridans
- oral flora
- damaged abnormal valves
Staph aureus
- found on skin
- # 1 in drug abusers
Enterococci and HÁČEK
Staph epidermidis
-prosthetic valves
Infective endocarditis morphology
Friable vegetation’s composed of fibrin, inflammatory cells, bacteria
aortic and mitral valves are usual sites
Right-sided valves may be involved esp IV drug users
May produce abscess in myocardium-ring abscess
Infective endocarditis clinical
Fever
Fatigue, wt loss, flu like syndrome
Murmur (90%)
Less frequently Janeway lesions, Oiler nodes, Roth spots
Positive blood culture
Echocardiography- mass or abscess
Janeway lesions
Erythematous lesions on palms or soles in infective endocarditis
Older nodes
Subcutaneous nodules in pulp of digits in infective endocarditis
Roth spots
Retinal hemorrhages in infective endocarditis
Complications of artificial valves
Thromboembolic complications
- long term anticoagulation
- may cause hemorrhage complications
Structural deterioration of artificial valves
Major failure mode of bioprostheses
Other complications of artificial valves
Intravascular hemolysis from shear forces
Paravalvular leak from inadequate healing
Obstruction from overgrowth by fibrous tissue during healing
