Valvular Diseases Flashcards
describe the gross and histological morphology in systemic hypertensive heart disease
- gross:
- concentric hypertrophy of LV
- 400-600 g
- long-standing cases → right ventricular hypertrophy and dilation
- histo:
- enlarged myocytes with large hyperchromatic rectangular “box-car” shaped nuclei
describe clinical features of systemic hypertensive heart disease
- clinical features:
- early stages = asymptomatic
- angina pectoris
- signs and symptoms of LHF with progression
- cerebrovascular accidents (stroke) or renal failure as a consequence of HTN
- sudden cardiac death
describe acute cor pulmonale
- acute cor pulmonale
- pulmonary embolism causing sudden increase in burden on the right heart
- RV is dilated but no hypertrophy
describe causes of chronic cor pulmonale
- chronic cor pulmonale
- COPD = most common cause
- others: IPF, CF, marked obesity
- morphology:
- RV hypertrophy and often RA hypertrophy +/- dilatation
name the etiology of mitral stenosis
name the etiology of aortic stenosis
name the etiology of mitral regurgitation
name the etiology of aortic regurgitation
describe signs and symptoms of mitral stenosis vs. mitral regurgitation
- mitral stenosis
- dyspnea (pulm. edema), fatigue, hemoptysis
- signs: late low pitched diastolic murmur and crepitations in lungs
- mitral regurgitation (MR)
- dyspnea (pulm. edema), palpitation, fatigue
- signs: pansystolic murmur radiating to axilaa
describe signs and symptoms of aortic stenosis vs. aortic regurgitation
- aortic stenosis:
- angina, syncope, CHF
- signs: ejection systolic murmur loudest at base and radiates to the neck after S1
- aortic regurgitation
- volume overload LHF
- signs: bounding pulses, early diastolic murmur, displaced apex beat
describe the pathogenesis of rheumatic fever
describe how rheumatic fever affects the myocardium
- myocarditis:
- paravascular Aschoff bodies:
- central zone of eosinophilic matrix infiltrated by T-cells, plasma cells and activated macrophages within the CT of the heart
- Anitschkow cells: wavy ribbon-like chromatin (caterpillar cells)
- giant cells can be seen in all 3 layers of the heart
- paravascular Aschoff bodies:
describe how rheumatic fever can affect the endocardium and pericardium
- endocardium:
- edematous and thickened valves with foci of fibrinoid necrosis
- multiple tiny 1-2 mm wart-like vegetations along the lines of closure of mitral valve; no effect on cardiac fxn
- pericardium:
- fibrinous pericarditis
describe how rheumatic fever affects the mitral valve
- chronic mitral valvulitis: most frequent
- conspicuous irregular fibrous thickening (neovascularized) and calcification of the leaflets, often with fusion of the commissures and shortening of the chordae tendinae; fixed narrow opening (fish mouth, buttonhole)
- mitral stenosis and regurgitation
describe how rheumatic fever affects the aortic valve
- chronic aortic valvulitis:
- cusps are thickened, firm and adherent to each other
- valve orifice is reduced to rigid, triangular channel
describe clinical features of chronic rheumatic carditis
- valvulitis (M>A>T>P) murmurs
- cardiac hypertrophy and dilation
- CHF
- arrhythmias
- infective endocarditis
describe the diagnosis of RF
describe calcific aortic stenosis
- morphology:
- degenerative calcific stenosis (dystrophic calcification)
- leaflets are rigid and deformed by irregular calcified masses
- the calcium deposits lie behind the valve cusps and extend into the sinus of Vasalva → coronary ischemia
- marked LVH
describe clinical features of calcific aortic stenosis
- due to aortic stenosis:
- angina pectoris: increased requirement of hypertrophied myocardium
- syncope: poor perfusion of the brain
- death usually occurs due to CHF or arrhythmias
there is an intrinsic defect of ____ in mitral valve prolapse
there is an intrinsic defect of connective tissue synthesis and remodeling in mitral valve prolapse
describe the morphology of mitral valve prolapse
- morphology:
- soft pulled up rubbery mitral valve cusps
- ballooning of the valve leaflets into the LA during systole (mid-systolic click)
- the chordae tenindae, which are often elongated and fragile, may rupture in severe cases
- the mitral annulus may be dilated (regurgitation)
- soft pulled up rubbery mitral valve cusps
describe clinical features of mitral valve prolapse
- most patients are asymptomatic
- palpitations
- fatigue or atypical chest pain
- midsystolic click – abrupt tension on leaflets and chordae when valve tries to close
- severe complications in about 3% of cases:
- mitral regurgitation and CHF
- IE
- ventricular arrhythmias (may lead to SCD)
- thromboemboli stroke
- rarely syndrome characterized by scoliosis and high arched palate
describe acute endocarditis
-
acute endocarditis
- typically, infection of previously normal valve
- destructive and fulminant
- caused by highly virulent organisms
- mortality is high despite antibiotics and/or surgery
describe subacute endocarditis
- subacute endocarditis
- infxn of previously abnormal valve (deformed valves)
- less destruction
- caused by low virulent organisms
- most patients recover with appropriate therapy
name the causative organisms in native valve IE
name the causative organisms involved in prosthetic valve IE
describe the pathogenesis of IE
name predispoing factors for infective endocarditis
- preexisting cardiac abnormality:
- rheumatic valvular disease
- mitral valve prolapse
- congenital defects
- degenerative calcific aortic stenosis
- prosthetic heart valves
- IVDU = tricuspid valve
- transiet bacteremia:
- dental procedures, urinary catheterization, endoscopy
describe the complications and host consequences caused by persistent bacteremia (as a consequence of vegetation)
describe the complications and host consequences caused by tissue destruction (as a consequence of vegetation)
describe the complications and host consequences caused by fragmentation (as a consequence of vegetation)
describe the complications and host consequences caused by release of bacterial antigen (as a consequence of vegetation)
____ are the classic hallmark of IE and are prone to ___ that can lead to _____
explain this
vegetations are the classic hallmark of IE and are prone to embolization → septic infarcts, abscesses, mycotic aneurysms
- friable, bulky, potentially destructive lesions
- contain fibrin, inflammatory cells, bacteria
describe general features associated with IE
- fever
- clubbing of fingers
- splinter hemorrhages under nail beds
- Osler nodes: tender (painful) subcutaneous nodules
- Janeway lesions: nontender (not painful) maculae on palms and soles
- Roth spots: retinal hemorrhages with clear center
- systemic embolization → stroke, distal organ infarcts
name clinical features associated with acute bacterial endocarditis
-
acute bacterial endocarditis
- high grade fever with chills
- new cardiac murmur
- features of septicemia
-
subacute bacterial endocarditis
- low grade fever; malaise
- changing cardiac murmurs
- weight loss
- splenomegaly
describe the diagnosis and treatment of IE
- diagnosis
- Duke criteria
- repeated blood cultures for both aerobic and anaerobic organisms
- echocardiography
- treatment
- difficult infxn to eradicate because of the avascular nature of the valves
- antibacterial therapy (IV, long term)
describe nonbacterial thrombotic endocarditis (NBTE)
- characterized by the presence of sterile thrombi on the leaflets of previously normal valves
- encountered in debilitated patients e.g. cancer (hence the name marantic (from marasmus) endocarditis)
- usually asymptomatic
describe the pathogenesis and complications of NBTE
- pathogenesis:
- associated with endothelial abnormalities, hypercoagulable states, adenocarcinomas
- complications:
- embolization and IE
describe Libman-Sacks endocarditis
- characterized by presence of sterile vegetations on the cardiac valves in patients of SLE (LSE in SLE)
- deposition of immune complexes
describe complications of mechanical prosthetic valves
- complications:
- thrombo-embolism
- life anticoagulation → hemorrhage
- IE
- RBC destruction (hemolysis)
- inadequate healing → paravalvular leak
describe complications of tissue valves (bioprostheses)
- no anticoagulation needed
- complications
- less durable: matrix deterioation, rigidity, calcification → stenosis, can perforate
- IE
- inadequate healing → paravalvular leak
