Cardiac Path Robbins Part 3 Flashcards
valvular heart disease- may present with?
- stenosis
- insufficiency
valvular stenosis
- valve doesn’t open completely, occurs chronically
- impedes fwd flow
- chronic stenosis- may cause P overload hypertrophy- CHF
valvular insufficiency
- 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!!
- NOTCH1 loss-of-fxn
- 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
(rare)
- infective endocarditis
- mitral insufficiency
- thromboembolism
- arrhythmias
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?
- pancarditis
- migratory polyarthritis
- subcutaneous nodules
- rash
- Sydenham chorea
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
infective endocarditis
-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
- Staph aureus!!
- requires surgery and antibiotics
subacute infective endocarditis
- slower-progressing infection
- previously deformed valve (ex- chronic RHD)
- viridans streptococci!!
- 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
- GN
- 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
Endocarditis of Systemic Lupus Erythematosus
(Libman-Sacks Disease)
- mitral and tricuspid valvulitis with small, sterile vegetations
- use of steroids- dec the incidence of this complication!
- lesions- small, single/multiple, sterile, pink vegetations with a warty (verrucous) appearance
- vegetations- finely granular, fibrinous eosinophilic material
- valvulitis- fibrinoid necrosis
Carcinoid syndrome
-systemic disorder marked by flushing, diarrhea, dermatitis, bronchoconstriction that is caused by bioactive compounds such as serotonin released by carcinoid tumors!
carcinoid heart disease- refers to?
- cardiac manifestations caused by bioactive compounds
- occurs in 1/2 of pts with the systemic carcinoid syndrome
carcinoid heart disease- lesions
- dont occur until there’s a massive hepatic metastatic burden (liver normally catabolizes circulating mediators)
- endocardium and valves of right heart- primarily infected!!!- first cardiac tissues bathed by the mediators released by GI carcinoid tumors
- left side of herat protected- pulm vascular bed degrades the mediators!
carcinoid heart disease- pathogenesis
- mediators released by carcinoid tumors- serotonin, kallikrein, bradykinin, histamine, prostaglandins, tachykinins
- serotonin and urinary excretion of serotonin metabolite (5-hydroxyindoleacetic acid)- correlate with severity of cardiac lesions
- unknown how serotonin induces cardiac changes!
carcinoid heart disease- morphology
- distinctive, glistening white intimal plaquelike thickening of endocardial surfaces of the cardiac chambers and valve leaflets
- lesions- smooth m cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix material
- right-sided involvement- tricuspid insuff and pulm stenossis
2 types of valvular prosthesis
- mechanical valves
- tissue valves (bioprostheses)
60% of substitute valve recipients- develop what?
-prosthetic-related problem within 10 yrs of surgery
complications of prosthetic valves
- thromboembolism- major consideration for mechanical valves!!!
- structural deterioration- all bioprostheses become incompetent due to calcification and tearing!!
- infective endocarditis
- inadequate healing (paravalvular leak), exuberant healing (obstruction), hemolysis (due to high shear forces)
