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Flashcards in Cardiac pathology 2 Deck (32)
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Valvular heart disease - stenosis

valve doesn’t open completely, occurs chronically
◦ Impedes forward flow
◦ Chronic stenosis may cause pressure overload hypertrophy → CHF


Valvular heart disease - insufficiency

valve doesn’t close completely, may occur acutely or
◦ Allows reversed flow
◦ Chronic insufficiency may cause volume overload hypertrophy → CHF


Calcific aortic stenosis

◦ Most common valve abnormality
◦ Prevalence increases with age (usually manifest at 60-80 years)
◦ “wear and tear” associated with chronic HTN, hyperlipidemia, inflammation
◦ Bicuspid valves show an accelerated course
◦ Affected valves contain osteoblast-like cells, which deposit an
osteoid-like substance → ossifies
◦ Mounded calcifications in cusps prevent complete opening of the valve
◦ Pressure overload hypertrophy, CHF


Mitral annular calcification

◦ Calcific deposits occur in the fibrous annulus
◦ Normally does not affect valve function
◦ Nodules may become sites for thrombus formation or infective endocarditis
◦F > M
◦ > 60 years
◦ Mitral valve prolapse


Mitral valve prolapse

Valve leaflets prolapse back into LA during systole

Affects 2-3% adults in US, with a 7:1 F:M, usually incidental (mid systolic click)

Leaflets become thickened and rubbery, due to proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption

May also occur as a complication of other causes of regurgitation (dilated hypertrophy)

Most are asymptomatic, a minority may experience:
◦ Pain mimicking angina
◦ dyspnea

Serious (but rare) complications may include:
◦ Infective endocarditis
◦ Mitral insufficiency
◦ Thromboembolism
◦ Arrhythmias


Rheumatic fever and rheumatic heart disease

multisystem inflammatory disorder following pharyngeal infection with group A streptococcus

Incidence decreased with more rapid diagnosis and treatment of strep infections

Acute rheumatic fever may include a carditis component, and over time may evolve to chronic rheumatic heart disease.


Rheumatic fever/heart disease pathogenesis

immune response to streptococcal M proteins cross reacts with cardiac (among other) self- antigens.
Acute RF occurs 10 days to 6 weeks after a grp A strep infection
◦ Anti-streptolysin O; anti-DNase B RF can include:
◦ Pancarditis, migratory polyarthritis, subcutaneous nodules, rash, Sydenham chorea


Cardiac features of acute RF

◦ Pancarditis, featuring Aschoff bodies
◦ Inflammation and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)
◦ Repeated streptococcal infections will cause these features to recur
◦ Chronic RHD: mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinous cords, resulting in mitral stenosis
◦ LA enlargement → atrial fib/thrombosis; pulmonary congestion/RHF


Acute infective endocarditis

rapidly progressing, destructive infection of a previously normal valve
◦ Requires surgery in addition to antibiotics


Subacute infective endocarditis

slower-progressing infection of
a previously deformed valve (such as in chronic RHD)
◦ Can often be cured with antibiotics alone


Infective endocarditis predisposing conditions

◦ Valvular abnormalities
◦ RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV

◦ Bacteremia
◦ Another site of infection
◦ Dental work/surgery
◦ Contaminated needle
◦ Compromised epithelium


Classic features of infective endocarditis

friable, bulky, destructive valvular vegetations

◦ Left-sided valves are more commonly affected (right-sided valves often involved in IV drug abusers)

◦ Friability leads to septic emboli

◦ Vegetations are mixtures of fibrin, inflammatory cells, and organisms
◦ Subacute vegetations may have a granulation tissue component


Infective endocarditis presentation

Patients may present with nonspecific symptoms
◦ Fever, weight loss, fatigue

Murmurs are usually present with left-sided lesions


Organisms involved in infective endocarditis

◦ S. viridans (valve abnormalities)
◦ S. aureus (normal valves, abnormal valves, IV drug abusers)
◦ S. epidermidis (prosthetic valves)
◦ HACEK (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)


Nonbacterial thrombotic endocarditis

◦ Small, sterile thrombi on cardiac valve leaflets, along the line of closure

◦ May be a source of emboli

◦ Associated with malignancies (especially mucinous adenocarcinomas), sepsis, or catheter-induced endocardial trauma


Dilated cardiomyopathy - pathogenesis

Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

◦ Thought to be familial in 30-50% of cases (TTN mutations may account for 20% of all cases); usually autosomal dominant.
◦ Alcohol is strongly linked to DCM
◦ Myocarditis
◦ Cardiotoxic drugs/substances: doxorubicin, cobalt, iron overload


Dilated cardiomyopathy morphology

dilation of all chambers
mural thrombi are common functional regurgitation of valves


Dilated cardiomyopathy - presentation

usually manifests between ages 20-50

progressive CHF → dyspnea, exertional fatigue, ↓ EF


Takotsubo cardiomyopathy

“Broken heart syndrome”

Excess catecholamines following extreme emotional or psychological stress
◦ >90% women, ages 58-75
◦ Symptoms and signs similar to acute myocardial infarction
◦ Apical ballooning of the left ventricle with abnormal wall motion and contractile dysfunction


Arrhythmogenic right ventricular cardiomyopathy

Right ventricular failure and arrhythmias
◦ Myocardium of the right ventricular wall replaced by adipose and fibrosis
◦ Causes ventricular tachycardia and fibrillation, sudden death Familial (usually autosomal dominant)


Hypertrophic cardiomyopathy

A genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to reduced stroke volume and often ventricular outflow obstruction

Numerous mutations known, involving sarcomeric proteins
◦ Most commonly β-myosin heavy chain

Morphology: massive myocardial hypertrophy, often with marked septal hypertrophy. Microscopically, myocyte disarray.


Consequences of extensive hypertrophy

◦ Foci of myocardial ischemia may occur
◦ Left atrial dilation and mural thrombus
◦ Diminished cardiac output and increased pulmonary congestion leads to exertional dyspnea
◦ Arrhythmias
◦ Sudden death


Restrictive cardiomyopathy

Decreased ventricular compliance (increased stiffness), leading to diastolic dysfunction.

May be secondary to deposition of material within the wall
(amyloid), or increased fibrosis (radiation).

Ventricles are usually of normal size, but both atria can be enlarged.



Extracellular deposition of proteins which form an insoluble β-pleated sheet.

May be systemic (myeloma) or restricted to the heart (usually transthyretin)
◦ Certain mutated versions of transthyretin are more amyloidogenic
◦ Amyloid can involve different parts of the heart, but when deposits are in the interstitium of the myocardium, a restrictive cardiomyopathy results.



Inflammation of the myocardium, most commonly due to a virus.
◦ Coxsackie A and B viruses are most common

Other infectious causes include
◦ Trypanosomes (Chagas disease)
◦ Various bacteria and fungi

Noninfectious causes include
◦ Immune mediated reactions, including RF, SLE, drug hypersensitivity


Congenital heart disease

“Sporadic genetic abnormalities are the major known causes of congenital heart disease.”
◦ The single most common genetic cause of congenital heart disease is trisomy 21
◦ About 40% patients with Down syndrome have at least one heart defect


Atrial septal defect

Usually asymptomatic until adulthood

The left-to-right shunting causes volume overload on the right side, which may lead to
◦ Pulmonary hypertension
◦ Right heart failure
◦ Paradoxical embolization
◦ May be closed surgically, with normal survival


Ventricular septal defect

Most common form of congenital heart disease

Effects depend on size, and presence of other heart defects

Many small VSDs close spontaneously

Large VSDs may cause significant shunting, leading to
◦ Right ventricular hypertrophy
◦ Pulmonary hypertension, which can ultimately reverse flow through the shunt, leading to cyanosis


Patent ductus arteriosis

May fail to close when infants are hypoxic, and/or have defects associated with increased pulmonary vascular pressure (VSD)

PDA produces a harsh, machinery-like murmur

Effect is determined by the shunt’s diameter
◦ Large shunts can increase pulmonary pressure and eventually shunt reversal and cyanosis


Tetralogy of Fallot

Four cardinal features:
◦ Obstruction of RV outflow tract ◦ Aorta overrides the VSD
◦ RV hypertrophy

Heart is enlarged and “boot shaped” because of the right ventricular hypertrophy

Clinical severity depends on the degree of subpulmonary stenosis
◦ Mild stenosis: L to R shunt. Classic TOF is R to L shunting with cyanosis