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Heart Valves
- function
- what happens when valves are deformed?
- • Valves are important in maintenance of
- unidirectional blood flow
- • Deformed valves produce significant
- hemodynamic disturbance on cardiac chambers
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Valvular stenosis
- what is it?
- effects
- aka valve obstruction
–Increased resistance to blood flow results in increased pressure in emptying chamber
–Cardiac chambers adapt by concentric hypertrophy
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Valvular regurgitation
- what is it?
- effects?
– incompetence: valves don't close all the way
- Blood flows back into emptying chamber resulting in volume overload
–Cardiac chambers adapt by eccentric hypertrophy
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Major Causes of acquired valve disease
- 1. aortic stenosis
- 2. aortic regurgitation
- 3. mitral stenosis
- 4. mitral regurgitation
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SENILE CALCIFIC AORTIC STENOSIS
•Degenerative & calcific valvular disease due to progressive & advanced age-related “wear & tear” of normal aortic valves
•Patients over 65, often in 80s & 90s
•Increasing incidence of aortic stenosis due to rising age of population
•Functional valve area diminished resulting in obstruction to outflow (pressure overload)
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SENILE CALCIFIC AORTIC STENOSIS: Gross Findings
- –Heaped-up calcified masses at bases of aortic cusps protruding through outflow surfaces into sinus of Valsalva & preventing opening of cusps
–No commissural fusion
–Usually normal mitral valve
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CALCIFIC STENOSIS OF CONGENITAL BICUSPID AORTIC VALVE
- •Congenital bicuspid aortic valve occurs with
- estimated frequency of ~1.0 – 2.0% of live births
Instead of having 3 leaflets, valves have 2
•Predisposed to progressive degenerative calcification
•Calcific aortic stenosis in congenitally bicuspid valves usually occurs before age 65
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CALCIFIC STENOSIS OF CONGENITAL BICUSPID AORTIC VALVE:
Gross Findings
- - Only 2 functional cusps, usually of unequal
- size
–Midline raphe of larger cusp due to incomplete separation during development
– Raphe = major site of calcific deposits
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ACUTE RHEUMATIC FEVER
what is it?
sequela?
incidence and mortality?
•Immune-mediated, multisystem inflammatory disorder occurring 2-4 wks after group A streptococcal pharyngitis in about 3% of pts
•Most important sequela of RF = chronic valvular deformities, esp. mitral stenosis
- •Incidence & mortality of RF declined
- significantly in many parts of the world
– Improved socioeconomic conditions
– Rapid diagnosis & treatment of streptococcal pharyngitis
–Unexplained decrease in virulence of group A streptococcus
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DIAGNOSIS OF ACUTE RHEUMATIC FEVER
Diagnosis established via Jones criteria
–Evidence of preceding infection with group A streptococcus
–+ 2 major criteria (or)
– +1 major and 2 minor criteria
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ACUTE RHEUMATIC FEVER: gross findings
- –Fibrinous pericarditis
–Small, irregular warty vegetations along lines of closure
– McCallum plaques = irregular endocardial thickenings usually in left atrium
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ACUTE RHEUMATIC FEVER:
Aschoff body
–Most distinctive lesion of acute rheumatic fever
–Can be found in all layers of heart = pancarditis
–Foci of necrotic collagen surrounded by lymphocytes, plasma cells, & Anitschkow cells
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Acute Rheumatic Fever:
- Anitschkow cells
–Pathognomonic for RF
–Plump macrophages with abundant cytoplasm, central round-to-ovoid nuclei with central, slender, wavy chromatin
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Chronic RHEUMATIC HEART DISEASE
• <10% acute RF cases progress to chronic RHD w/ latent period of 20-30 yrs bf symptoms appear
•Chronic RHD most frequent cause of mitral stenosis (99% cases)
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CHRONIC RHEUMATIC HEART DISEASE: Gross Findings
- Valvular deformities
- –Fibrous thickening of leaflets
– Commissural fusion & shortening (“fish mouth” deformity)
–Thickening & fusion of chordae tendinae
–Neovascularization
Mitral valve almost always abnormal
– 65-70% MV involved alone
–25% both MV & AV involved
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Mitral Valve Prolapse
- prevalence
- sequela
•Most common valve defect involving >3% of adults in US, most often young women
•Most common indication for mitral valve replacement
•Usually incidental finding on physical exam; however, ~3% pts have serious sequelae
–Infective endocarditis
–Mitral regurgitation
–Systemic embolization
–Arrhythmias
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Mitral Valve Prolapse: Gross Findings
–Intercordal ballooning of mitral leaflets – often enlarged, redundant, thick, rubbery
–Elongated, thinned, & occasionally ruptured chordae tendinae
–Annular dilatation
–Commissural fusion is absent
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Mitral Valve Prolapse: histopathology
–Attenuation of fibrosa layer
–Marked accumulation of myxomatous material in spongiosa layer
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INFECTIVE ENDOCARDITIS
what are the 2 types?
- 1. acute infective endocarditis
- 2. subacute infective endocarditis
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Acute Infective Endocarditis
–Destructive, fulminant infection with highly virulent organism (e.g. S. aureus)
–Frequently on previously normal heart valve
–Death occurs within days - wks of >50% pts despite antibiotics & surgery
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subacute infective endocarditis
– Less destructive, insidious infection by low virulence organism with protracted clinical course (e.g. S. viridans)
–Usually affects deformed heart valves
–Most pts recover after appropriate antibiotic therapy
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Infective endocarditis
- •Pts with underlying congenital or acquired
- defects are at increased risk (regurgitant > stenotic valves)
• AV & MV most common sites of involvement
• TV involvement seen in IV drug users
Complications:
–Septic embolization
–Sudden death
–Ring abscess
–Pyogenic myocarditis
–Valvular insufficiency
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Infective endocarditis:
Pathological Findings
–Friable, bulky, & potentially destructive vegetations containing fibrin, inflammatory cells, & organisms on valves
–SBE vegetations have granulation tissue at bases suggesting chronicity
–Chronic inflammation, fibrosis, & calcification may be present with time
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NONBACTERIAL THROMBOTIC (MARANTIC) ENDOCARDITIS
•Commonly present in patients with hypercoagulable state with systemic activation of coagulation such as DIC
•May be related to:
–Underlying malignancy: Affects people who are dying of other causes
–Other debilitating diseases (severe burns, sepsis)
•Embolization may occur
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Nonbacterial thrombotic endocarditis
- gross pathology
- histopathology
Gross pathology:
–Small, sterile, nondestructive, loosely adherent single or multiple vegetations along line of closure
- Histopathology
- –Composed of bland thrombus without inflammation or induced valve damage
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PERICARDITIS
- •Inflammation of visceral & parietal
- linings of heart
•Usually secondary to various cardiac diseases, thoracic or systemic disorders, metastases from neoplasms, or surgical procedures on heart
•Primary pericarditis unusual & almost always of viral origin
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Pericaditis: causes
- -infectious agents that usually come in
- through the lungs
- Immunologically mediated
- Ideopathic (viruses)
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3 Types of Pericarditis
- 1. serous pericarditis
- 2. hemorrhagic pericardits
- 3. caseous pericarditis
- 4. finbrinous pericarditis
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Serous pericarditis
–Usually due to noninfectious inflammatory conditions (RF, SLE, scleroderma, tumors,uremia)
–Scant inflammatory infiltrate comprised of PMNs, lymphocytes, & macrophages on pericardial surface
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Hemorrhagic pericarditis
- –Blood mixed with fibrinous or suppurative
- effusion
–Most commonly caused by malignancy, bacterial infection, underlying bleeding diathesis, TB, and after cardiac surgery
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Caseous pericarditis
–Most commonly TB
–Rare, but most frequent antecedent of fibrocalcific constrictive pericarditis
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FIBRINOUS PERICARDITIS
•Most frequent type of pericarditis
•Composted of serous fluid admixed with fibrinous exudate
•Common causes:
–Myocardial infarction (heart attack)
–Post-pericariotomy syndrome (Dressler syndrome)
–Uremia
–Radiation
–Collagen vascular diseases
–Rheumatic fever
–Trauma
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