Flashcards in Cardiac Path Robbins Part 3 Deck (38)
valvular heart disease- may present with?
-valve doesn't open completely, occurs chronically
-impedes fwd flow
-chronic stenosis- may cause P overload hypertrophy- CHF
-valve doesn't close completely, may occur acutely or chronically
-allows reversed flow
-chronic insufficiency- may cause volume overload hypertrophy- CHF
most frequent causes of the major fxnal valvular lesions?
-aortic stenosis- calcification and sclerosis
-aortic insufficiency- dilation of asc aorta, often secondary to HTN/aging
-mitral stenosis- rheumatic heart disease
-mitral insufficiency- myxomatous degeneration (mitral valve prolapse)
calcific valvular degeneration- types
-calcific aortic stenosis
-calcific stenosis of congenitally bicuspid aortic valve
-mitral annular calcification
calcific aortic stenosis- occurs due to?
-most common valve abnormality!
-prevalence inc with age (70-80)
-"wear and tear" assoc with chronic HTN, hyperlipidemia, infl
calcific aortic stenosis- affects? effects?
-bicuspid valves- accelerated course (50-60's)
-affected valves contain osteoblast-like cells, which deposit an osteoid-like substance- ossifies
-calcifications in cusps- prevent complete opening of the valve
-pressure overload hypertrophy, CHF
calcific aortic stenosis- clinical featurs
-left ventricular hypertrophy- becomes ischemic
-onset of symptoms (angina, CHF, syncope)- poor prognosis!!!
-die within 5 yrs of angina development (if untreated); 3 yrs of syncope; 2 yrs of CHF
mitral annular calcification- what happens? occurs in who?
-calcific deposits in fibrous annulus
-normally doesn't affect valve fxn
-nodules may become sites for thrombus formation of infective endocarditis
-F > M, >60 males
-mitral valve prolapse
Calcific Stenosis of Congenitally Bicuspid Aortic Valve- caused by? clinical?
-Bicuspid aortic valve (BAV)- developmental abnormality
-chromosomes 18q, 5q, 13q!!
-2 fxnal cusps- the larger cusp as a midline raphe (where incomplete separation occurred)
-raphe- site of calcific deposits
-asymptomatic early in life
-late complications- aortic stenosis or regurgitation, infective endocarditis, aortic dilation
mitral annular calcification
-calcific deposits develop in fibrous annulus!!
-doesnt affect valvular fxn
-site for thrombus formation- inc risk of embolic stroke
-most common- women, >60, pts with mitral valve prolapse
mitral valve prolapse- what happens?
-valve leaflets prolapse back into LA during systole
-2-3% adults in US; 7:1 female; usually incidental
-leaflets become thickened and rubbery, due to proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption
-may occur as a complication of other causes of regurgitation (dilated hypertrophy)
mitral valve prolapse- symptoms
-most are asymptomatic!!
-incidentally found- mid-systolic clicks!!
-a minority experience- pain mimicking angina, dyspnea
mitral valve prolapse- complications
only cause of mitral stenosis??
RHD (rheumatic heart disease)
rheumatic fever-caused by?
-multisystem infl disorder following pharyngeal infection with group A streptococcus
-can cause chronic rheumatic heart disease
rheumatic heart disease- pathogenesis
-immune response to streptococcal M proteins- cross reacts with cardiac self-antigens
-acute RF- 10 days-6 wks after grp A strep infection (anti-streptolysin O; anti-DNase B)
rheumatic fever- can include?
cardiac features of acute RF
-pancarditis- Aschoff bodies! (lymphocytes, macrophages)
-infl and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)
-repeated streptococcal infections- cause these to recur
-LA enlargement- atrial fib/thrombosis; pulm congestion/RHF
chronic Rheumatic heart disease
chronic Rheumatic heart disease -mitral leaflet thickening
-fusion and shortening of commissures
-fusion and thickening of tendinous cords
-results in mitral stenosis!!!
-"fish mouth" stenoses- calcification and fibrous bridging across valvular commissures
-infection of valves and endocardium- characterized by vegetations consisting of microbes and debris, and tissue destruction
acute infective endocarditis
-rapidly progressive, destructive infection
-previously normal valve
-requires surgery and antibiotics
subacute infective endocarditis
-previously deformed valve (ex- chronic RHD)
-can be cured with antibiotics alone
nfective endocarditis- predisposing conditions
-valvular abnormalities- RHD
(used to be the major antecedent disorder! less common now), prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV
-bacteremia- another site of infection, dental work, contaminated needle
classic feature of IE
friable, bulky, destructive valvular vegetations!!
-left-sided valves more commonly affected (right-sided valves involved in IV drug abusers)
-friability- causes septic emboli
-vegetations- fibrin, infl cells, organisms
-subacute IE- granulation tissue
infective endocarditis- clinical presentation
-nonspecific symptoms- fever, weight loss, fatigue
-murmurs- present with left-sided lesions (90%)
infective endocarditis- complications
-microthromboemoli (splinter/subungual hemorrhages)
-erythematous/hemorrhagic nontender lesions on palms/soles (Janeway lesions)
-painful subcutaneous nodules in pulp of digits (Osler nodes)
-retinal hemorrhages (Roth spots)
infective endocarditis- organisms involved?
-S. viridans (valve abnormalities)- 50%
-S. aureus (normal/abnormal valves, IV drug abusers)- 20-30%
-S. epidermis (prosthetic valves)
-HACEK (Haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
nonbacterial thrombotic endocarditis- assoc with?
(used to be called marantic endocarditis- malnutrition)
-small, sterile thrombi on cardiac valve leaflets, along line of closure
-may be a source of emboli
-assoc with malignancies (mucinous adenocarcinomas), sepsis, catheter-induced endocardial trauma