CH8 - Cardiac Pathology Flashcards
What is ischemic heart disease (IHD)?
Group of syndromes related to myocardial ischemia
What is the leading cause of death in the US?
ischemic heart disease (IHD)
What is ischemic heart disease (IHD) usually due to?
atherosclerosis of coronary arteries, which decreases blood flow to the myocardium
What are the risk factors for IHD?
They are similar to those of atherosclerosis; incidence increases with age.
What is stable angina?
chest pain that arises with exertion or emotional stress.
What is stable angina due to?
atherosclerosis of coronary arteries with > 70% stenosis;
Why does stable angina arise with exertion?
decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion
What does stable angina represent?
reversible injury to myocytes (no necrosis)
How does stable angina present?
As chest pain lasting < 20 minutes that radiates to the left arm or jaw, diaphoresis, and shortness of breath
What does the EKG show in stable angina?
ST-segment depression due to subendocardial ischemia
What is stable angina relieved by?
rest or nitroglycerin
What is unstable angina?
chest pain that occurs at rest.
What is unstable angina usually due to?
rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
What does unstable angina represent?
reversible injury to myocytes (no necrosis)
What does the EKG show in unstable angina?
ST-segment depression due to subendocardial ischemia
What is unstable angina relieved by?
Nitroglycerin
In unstable angina there is a high risk of what?
progression to myocardial infarction
What is prinzmetal angina?
episodic chest pain unrelated to exertion.
What is prinzmetal angina due to?
coronary artery vasospasm
What does prinzmetal angina represent?
reversible injury to myocytes (no necrosis)
What does the EKG for prinzmetal angina show?
ST-segment elevation due to transmural ischemia.
What is prinzmetal angina relieved by?
nitroglycerin or calcium channel blockers
What is myocardial infarction?
Necrosis of cardiac myocytes
What is myocardial infarction usually due to?
rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
In addition to atherosclerotic plaque what are some other causes of myocardial infarction?
coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (e.g., Kawasaki disease).
What are the clinical features for myocardial infarction?
include severe, crushing chest pain (lasting > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea; symptoms are not relieved by nitroglycerin.
In myocardial infarction what does the infarction usually involve?
the left ventricle (LV); right ventricle (RV) and both atria are generally spared.
What artery is most commonly involved artery in MI?
LAD; left anterior descending artery ? 45% of cases
What does occlusion of the left anterior descending artery (LAD) lead to?
infarction of the anterior wall and anterior septum of the LV
What does occlusion of right coronary artery (RCA) lead to?
infarction of the posterior wall, posterior septum, and papillary muscles of the LV;
What is the 2nd most commonly involved artery in MI?
RCA, right coronary artery
What does occlusion of the left circumflex artery lead to?
infarction of lateral wall of the LV.
What does the initial phase of infarction lead to?
subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction);
What does the EKG show for the initial phase of infarction?
(subendothelial infarction) ST-segment depression.
After the initial phase of infarction, what does continued or severe ischemia lead to?
transmural necrosis involving most of the myocardial wall (transmural infarction)
What does the EKG show in transmural infarction?
ST-segment elevation
What do the laboratory tests detect for myocardial infarction?
elevated cardiac enzymes.
What is the most sensitive and specific marker (gold standard) for Ml?
troponin I
What are the troponin I levels after 2-4 hours?
Levels rise 2-4 hours after infarction
When do troponin I levels peak?
at 24 hours
When do troponin I levels return to normal?
By 7-10 days.
What is CK-MB is useful for?
detecting reinfarction that occurs days after an initial MI
When do creatine kinase MB (CK-MB) levels rise?
4 - 6 hours after infarction
When does creatinine kinase MB levels peak?
They peak at 24 hours
When does creatinine kinase MB levels return to normal?
by 72 hours.
What does treatment for myocardial infarction include?
1) Asprin 2) Supplemental O2 3) Nitrates 4) beta-blockers 5) ACE inhibitor 6)Fibrinolysis or angioplasty
How does aspirin and/or heparin help treat MI?
limits thrombosis
How does supplemental 02 help treat MI?
minimizes ischemia
How do nitrates help treat MI?
vasodilate coronary arteries
How does beta-blockers help treat MI?
slows heart rate, decreasing O2 demand and risk tor arrhythmia
How does ACE inhibitors help treat MI?
decreases LV dilation
How does fibrinolysis or angioplasty help treat MI?
opens blocked vessel
What happens in fibrinolysis or angioplasty post-MI?
it opens bloced vessel; 1) contraction band necrosis 2) reperfusion injury
What is contraction band necrosis?
After fibrinolysis or angioplasty post-MI there is reperfusion of irreversibly damaged cells resulting in calcium influx, leading to hypercontraction of myofibrils
What is reperfusion injury?
After fibrinolysis or angioplasty post-MI, the return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes
< 4 hours from time of infarction what are the gross and microscopic changes?
No gross changes, and no microscopic changes
What are the complications < 4 hours from time of infarction?
Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
4-24 hours from time of infarction what are the gross and microscopic changes?
[Gross] Dark discoloration and [microscopic] Coagulative necrosis
What are the complications from 4-34 hours from the time of infarction?
arrhythmia
1-3 days from time of infarction what are the gross and microscopic changes?
[gross] Yellow pallor, [microscopic] Neutrophils
What are the complications for 1-3 days from time of infarction?
Fibrinous pericarditis presents as chest pain with friction rub
What does fibrinous pericarditis present as?
chest pain with friction rub
4-7 days from time of infarction, what are the gross and microscopic changes?
[gross] Yellow pallor, [Microscopic] Macrophages
What are the complications 4-7 days from time of infarction?
Rupture of ventricular free wall, interventricular septum, or papillary muscle
What does rupture of ventricular free wall lead to?
cardiac tamponade
What does rupture of interventricular septum lead to?
shunt,
What does rupture of papillary muscle lead to?
mitral insufficiency
1-3 weeks from time of infarction, what are the gross and microscopic changes?
[gross] Red border emerges as granulation tissue enters from edge of infarct, [microscopic] Granulation tissue with plump fibroblasts, collagen, and blood vessels
Months from time of infarction, what are the gross and microscopic changes?
[gross] White scar, [microscopic] Fibrosis
What are the complications for 1 Month from the time of infarction?
Aneurysm, mural thrombus, or Dressier syndrome
What is sudden cardiac death?
Unexpected death due to cardiac disease, occurs without symptoms or <1 hour after symptoms arise
What is sudden cardiac death usually due to?
fatal ventricular arrhythmia
What is the most common etiology for sudden cardiac death?
acute ischemia; 90% of patients have preexisting severe atherosclerosis.
What are the less common causes for sudden cardiac death?
mitral valve prolapse, cardiomyopathy, and cocaine abuse
What is chronic ischemic heart disease?
Poor myocardial function due to chronic ischemic damage (with or without infarction);
What does chronic ischemic heart disease progress to?
congestive heart failure (CHF)
What is congestive heart failure?
Pump failure; divided into right- and left-sided failure
What are the causes of left-sided heart failure?
ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy
What are the clinical features for left-sided heart failure due to?
decreased forward perfusion and pulmonary congestion.
What are the clinical features for left-sided heart failure?
1) decreased perfusion and pulmonary congestion 2) activation of rennin angiotensin system
In left-sided heart failure what does pulmonary congestion lead to?
pulmonary edema.
In left-sided heart failure why is there paroxysomal nocturnal dyspnea?
Its due to increased venous return when lying flat
In left-sided heart failure, pulmonary edema results in what?
dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles
How can left-sided heart failure lead to intra-alveolar hemorrhage?
Small, congested capillaries may burst, leading to intraalveolar hemorrhage
In left-sided heart failure what is intra-alveolar hemorrhage marked by?
hemosiderin-laden macrophages (heart-failure cells)
In left sided heart failure how are the kidneys involved?
Decreased flow to kidneys leads to activation of renin-angiotensin system
In left sided heart failure does the kidney affect the rennin angiotensin system?
Fluid retention exacerbates CHF
What is the main treatment for left sided heart failure?
treatment is ACE inhibitor.
What is right-sided heart failure most commonly due to?
left-sided heart failure;
Aside from left sided heart failure what are some other important causes for right sided heart failure?
Left to-right shunt and chronic lung disease (cor pulmonale)
What are the clinical features for right sided heart failure due to?
congestion
What are the clinical features for right sided heart failure?
- Jugular venous distension 2. Painful hepatosplenomegaly with characteristic nutmeg liver; may lead to cardiac cirrhosis 3. Dependent pitting edema
In right sided heart failure what is the dependent pitting edema due to?
increased hydrostatic pressure
What are the congenital heart defects?
Arise during embryogenesis
When do congenital heart defects usually arise?
usually weeks 3 through 8
In what percentage of live births do you see congenital heart defects?
seen in 1% of live births
Most congenital heart defects are?
sporadic.
Congenital heart defects often result in?
shunting between left (systemic) and right (pulmonary) circulations.
Defects with left-to-right shunting
may be relatively asymptomatic at birth, but the shunt can eventually reverse
What does increased flow through the pulmonary circulation result in?
hypertrophy of pulmonary vessels and pulmonary hypertension.
What does increased pulmonary resistance eventually result in?
reversal of shunt
What does the reversal of shunt in congenital defects with left to right shunt lead to?
late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing.
What do defects with right-to-left shunting usually present as?
cyanosis shortly after birth.
What is ventricular septal defect (VSD)?
Defect in the septum that divides the right and left ventricles
What is the most common congenital heart defect?
ventricular septal defect (VSD)
What is ventricular septal defect (VSD) associated with?
fetal alcohol syndrome
What does ventricular septal defect (VSD) result in?
left-to-right shunt,
What determines extent of shunting in ventricular septal defect (VSD)?
size of defect and age at presentation
What happens with small defects in ventricular septal defect (VSD)?
they are often asymptomatic
What happens with large defects in ventricular septal defect (VSD)?
can lead to Eisenmenger syndrome
What is the treatment for ventricular septal defect (VSD)?
involves surgical closure; small defects may close spontaneously
What is atrial septal defect?
Defect in the septum that divides right and left atria;
What is the most common type of atrial septal defect?
It is ostium secundum (90% of cases)
What type of atrial septal defect is type is associated with Down syndrome?
Ostium primum
What does atrial septal defect result in?
left-to-right shunt and split S2 on auscultation
Why is there split S2 on auscultation in atrial septal defect?
increased blood in right heart delays closure of pulmonary valve
What is an important complication of atrial septal defect?
Paradoxical emboli
What is patent ductus arteriosus?
Failure of ductus arteriosus to close
What is patent ductus arteriosus associated with?
congenital rubella
What does patent ductus arteriosus result in?
left-to-right shunt between the aorta and the pulmonary artery
During development what does the ductus arteriosus normally do?
shunts blood from the pulmonary artery to the aorta, bypassing the lungs
What are the symptoms for patent ductus arteriosus?
Asymptomatic at birth with holosystolic machine-like murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis
What does the treatment for patent ductus arteriosus involve?
indomethacin, which decreases PGE2 resulting in PDA closure
What is the effect of PGE on patent ductus arteriosus?
PGE maintains patency of the ductus arteriosus
What is tetralogy of fallot?
It is characterized by (1) stenosis of the right ventricular outflow tract, (2) right ventricular hypertrophy, (3) VSD, and (4) an aorta that overrides the VSD
In tetralogy of fallot what does the right-to-left shunt lead to?
early cyanosis;
In tetralogy of fallot what determines the extent of shunting and cyanosis?
the degree of stenosis
In tetralogy of fallot what patient behavior is observed?
they learn to squat in response to a cyanotic spell
In tetralogy of fallot why does squatting help with the cyanotic spell?
increased arterial resistance decreases shunting and allows more blood to reach the lungs.
What is seen on x-ray in tetralogy of fallot?
Boot-shaped heart on x-ray
What is transposition of the great vessels characterized by?
pulmonary artery arising from the left ventricle and aorta arising from the right ventricle
What is the transposition of the great vessels associated with?
maternal diabetes
What does transposition of the great vessels presents with?
early cyanosis; pulmonary and systemic circuits do not mix.
In transposition of the great vessels what is required for survival?
creation of shunt (allowing blood to mix) after birth is required for survival.
What is the effect of PGE in transposition of the great vessels?
can be administered to maintain a PDA until definitive surgical repair is performed.
What does transposition of the great vessels result in?
hypertrophy of the right ventricle and atrophy of the left ventricle
What is truncus arteriosus?
Characterized by a single large vessel arising from both ventricles 1. Truncus fails to divide.
What does truncus arteriosus present with?
early cyanosis
Why is there early cyanosis in truncus arteriosus?
deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate
What is tricuspid atresia?
Tricuspid valve orifice fails to develop; right ventricle is hypoplastic.
What is tricuspid atresia often associated with?
ASD, resulting in a right-to-left shunt; presents with early cyanosis,
What is coarctation of the aorta?
Narrowing of the aorta,
What is coarctation of the aorta classically divided into?
infantile and adult forms
What is the infantile form of coarctation of the aorta associated with?
a PDA
In the infantile form of coarctation of the aorta where is the coarctation located?
after (distal to) the aortic arch, but before (proximal to) the PDA
What does the infantile form of the coarctation of the aorta present as?
lower extremity cyanosis in infants, often at birth
What is the infantile form of coarctation of the aorta associated with?
Turner syndrome
What is the adult form of coarctation of the aorta associated with?
Its not associated with a PDA
Where is the coarctation for the adult form of coarctation of the aorta?
coarctation lies after (distal to) the aortic arch
How does the adult form of coarctation of the aorta present?
as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood
In the adult form of coarctation of the aorta what is seen on x-ray?
Notching of ribs
Why is there notching of the ribs seen on x-ray for the adult form of coarctation of the aorta?
Collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray
What is the adult form of coarctation of the aorta associated with?
bicuspid aortic valve
What is the purpose of heart valves?
To prevent back flow
What are the has four valves of the heart?
tricuspid, pulmonary, mitral, and aortic
What does valvular lesions generally result in?
stenosis (decreased caliber of the valve orifice) or regurgitation (backflow)
What is acute rheumatic fever?
Systemic complication of pharyngitis due to group A beta-hemolytic streptococci
Who does acute rheumatic fever affect?
children 2-3 weeks after an episode of streptococcal pharyngitis strep throat
What is acute rheumatic fever caused by?
molecular mimicry, bacterial M protein resembles proteins in human tissue
What is diagnosis of acute rheumatic fever based on?
Jones criteria.
What evidence is needed for the Jones Criteria?
Evidence of prior group A beta-hemolytic streptococcal infection with the presence of major and minor criteria
What would indicate prior group A beta-hemolytic streptococcal infection?
Elevated ASO or anti-DNase B titers
What is the minor Jones criteria?
Minor criteria are nonspecific and include fever and elevated ESR.
What is the major Jones criteria?
1) migratory polyarthritis 2) pancarditis 3) subcutaneous nodules 4) erythema marginatum 5) Sydenham chorea
What is Migratory polyarthritis?
In Jones criteria, swelling and pain in a large joint (e.g., wrist, knees, ankles) that resolves within days and migrates to involve another large joint
What is Pancarditis?
a) endocarditis b) myocarditis c) pericarditis
In endocarditis which valve is involved more commonly?
Mitral valve is involved more commonly than the aortic valve.
How is endocarditis characterized?
by small vegetations along lines of closure that lead to regurgitation
What is myocarditis in pancarditis?
its with Aschotf bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material
What is the most common cause of death during the acute phase?
myocarditis
What is pericarditis in pancarditis lead to?
friction rub and chest pain
What is involved with erythema marginatum in the major criteria of Jones criteria
annular, nonpruritic rash with erythematous borders, commonly involving trunk and limbs
What is Sydenham chorea in the major criteria of Jones criteria?
It is rapid, involuntary muscle movements
What usually happens to an acute attack of rheumatic fever?
usually resolves, but may progress to chronic rheumatic heart disease;
What does repeat exposure to group A beta-hemolytic streptococci result in?
relapse of the acute phase of rheumatic fever and increases risk for chronic disease.
What is chronic rheumatic heart disease?
Valve scarring that arises as a consequence of rheumatic fever
What does chronic rheumatic heart disease result in?
stenosis with a classic fish mouth appearance
What does chronic rheumatic heart disease almost always involve?
the mitral valve
What does the involvement of the mitral valve in chronic rheumatic heart disease lead to?
thickening of chordae tendineae and cusps
What does chronic rheumatic heart disease occasionally involve?
the aortic valve
What does the involvement of the aortic valve in chronic rheumatic heart disease lead to?
fusion of the commissures
What do complications in chronic rheumatic heart disease include?
infectious endocarditis
What is aortic stenosis?
Narrowing of the aortic valve orifice
What is aortic stenosis usually due to?
fibrosis and calcification from wear and tear
When does aortic stenosis present?
in late adulthood (> 60 years)
What does a bicuspid aortic valve increase the risk for?
aortic stenosis and hastens disease onset.
How many cusps does a normal aortic valve have?
three cusps,
What is the effect of fewer cusps on the aortic valve?
it results in increased wear and tear on each cusp
What is the relationship between aortic stenosis and chronic rheumatic fever?
aortic stenosis may arise as a consequence of chronic rheumatic valve disease;
What distinguishes rheumatic disease from wear and tear in aortic stenosis?
coexisting mitral stenosis and fusion of the aortic valve commissures
In aortic stenosis what happens during cardiac compensation?
it leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard
What does the complications of aortic stenosis include?
1) Concentric left ventricular hypertrophy 2) angina and syncope with exercise 3) microangiopathic hemolytic anemia
In aortic stenosis what does concentric left ventricular hypertrophy lead to?
It may progress to cardiac failure
In aortic stenosis what does angina and syncope with exercise lead to?
Limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain
In aortic stenosis what does microangiopathic hemolytic anemia lead to?
RBCs are damaged (producing schistocytes) while crossing the calcified valve
In aortic stenosis what does treatment involve?
valve replacement after onset of complications.
What is aortic regurgitation?
Backflow of blood from the aorta into the left ventricle during diastole
Aortic regurgitation arises due to what?
aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)
What is the most common cause of aortic regurgitation?
isolated root dilation
What are the clinical features for aortic regurgitation?
- Early, blowing diastolic murmur 2. Hyperdynamic circulation due to increased pulse pressure
What is pulse pressure?
it is the difference between systolic and diastolic pressures
What is the relationship between pressure and aortic regurgitation?
Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume
How does aortic regurgitation present?
with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), and head bobbing
What does aortic regurgitation result in?
LV dilation and eccentric hypertrophy (due to volume overload)
What is the treatment for aortic regurgitation?
valve replacement once LV dysfunction develops
What happens in mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole
What is the incidence of mitral valve prolapse in US adults
Seen in 2-3% of US adults
What is mitral valve prolapse due to?
myeloid degeneration (accumulation of ground substance) of the valve, making it (loopy)
What is the etiology for mitral valve prolapse?
Unknown
What might mitral valve prolapse be seen in?
Marfan syndrome or Ehlers-Danlos syndrome
What does mitral valve prolapse present with?
an incidental mid-systolic click followed by a regurgitation murmur that is usually asymptomatic
With mitral valve prolapse, when does the mid-systolic click get louder?
Click and murmur become louder with squatting
Why does squatting make the mid-systolic click get louder in mitral valve prolapse?
increased systemic resistance decreases left ventricular emptying
What are the complications for mitral valve prolapse?
they are rare, but include infectious endocarditis, arrhythmia, and severe mitral regurgitation.
What is the treatment for mitral valve prolapse?
valve replacement.
What is mitral regurgitation?
Reflux of blood from the left ventricle into the left atrium during systole
Mitral regurgitation usually arises as a complication of what?
mitral valve prolapse
Aside from mitral valve prolapse, what are some other causes of mitral regurgitation?
Left ventricular dilatation (left-sided cardiac failure), infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a myocardial infarction.
What are the clinical features for Mitral regurgitation?
- Holosystolic [blowing] murmur;
In mitral regurgitation why is the holosystolic murmur louder with squatting?
increased systemic resistance decreases left ventricular emptying and expiration, increased return to left atrium
What does mitral regurgitation result in?
Volume overload and left-sided heart failure
What is mitral stenosis?
Narrowing of the mitral valve orifice
What is mitral stenosis usually due to?
chronic rheumatic valve disease
What are the clinical features for mitral stenosis?
- Opening snap followed by diastolic rumble 2. Volume overload leads to dilatation of the left atrium
In mitral stenosis what does the dilation of the left atrium leading to volume overload result in?
i. Pulmonary congestion with edema and alveolar hemorrhage ii. Pulmonary hypertension and eventual right-sided heart failure iii. Atrial fibrillation with associated risk for mural thrombi
What is endocarditis?
Inflammation of endocardium that lines the surface of cardiac valves
What is endocarditis usually due to?
bacterial infection
What is the most common overall cause of endocarditis?
Streptococcus viridans
What is streptococcus viridans?
it is a low virulence organism that infects previously damaged valves (chronic rheumatic heart disease and mitral valve prolapse).
What does streptococcus viridans result in?
small vegetations that do not destroy the valve (subacute endocarditis)
How does streptococcus viridans affect the endocardial surface?
develops thrombotic vegetations (platelets and fibrin) on damaged endocardial surface, transient bacteremia leads to trapping of bacteria in the vegetations, prophylactic antibiotics decrease risk of endocarditis.
What is the most common cause of endocarditis in IV drug users?
Staphylococcus aureus
What is Staphylococcus aureus?
High-virulence organism that infects normal valves, most commonly the tricuspid.
What does Staphylococcus aureus result in?
large vegetations that destroy the valve (acute endocarditis)
What is Staphylococcus epidermidis associated with?
endocarditis of prosthetic valves
What is Streptococcus bovis associated with?
endocarditis in patients with underlying colorectal carcinoma
What are HACEK organisms associated with?
are associated with endocarditis with negative blood cultures.
HACEK
Haemophilus, Actinobacius, Cardiobacterium, Eikenella, Kingella
What are the clinical features of bacterial endocarditis?
1) Fever 2) Lesions 3) Janeway lesions 4) anemia of chronic disease
What is the fever in bacterial endocarditis due to?
bacteremia
What is the murmur in bacterial endocarditis due to?
vegetations on heart valve
What are the Janeway lesions, splinter hemorrhages in nail bed and osier nodes in bacterial endocarditis due to?
embolization of septic vegetations
What are Janeway lesions?
erythematous nontender lesions on palms and soles.
What are Osier nodes?
tender lesions on fingers or toes
What is anemia of chronic disease due to?
chronic inflammation
What are the laboratory findings for endocarditis?
- Positive blood cultures 2. Anemia of chronic disease 3. Transesophageal echocardiogram is useful for detecting lesions on valves
What are the general lab findings of anemia of chronic diseae?
low Hb, low MCV; high ferritin, low TIBC, decreased serum iron, and decreased l% saturation
What is the transesophageal echocardiogram useful for?
detecting lesions on valves
What is non-bacterial thrombotic endocarditis due to?
sterile vegetations that arise in association with a hypercoagulable state or underlying adenocarcinoma.
What does non-bacterial thrombotic endocarditis result in?
Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation.
What is Libman-Sacks endocarditis due to?
sterile vegetations that arise in association with SLE.
What does Libman-Sacks endocarditis result in?
Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation
What is cardiomyopathy?
Group of myocardial diseases that result in cardiac dysfunction
What are the types of cardiomyopathy?
Dilated cardiomypathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy
What is dilated cardiomyopathy?
Dilation of all four chambers of the heart
What is the most common form of cardiomyopathy?
Dilated cardiomyopathy
What does dilated cardiomyopathy result in?
Results in systolic dysfunction (ventricles cannot pump),
What does the systolic dysfunction resulting from dilated cardiomyopathy lead to?
biventricular CHF
What are the complications of dilated cardiomyopathy?
mitral and tricuspid valve regurgitation and arrhythmia.
What is the most common cause of dilated cardiomyopathy?
Its idiopathic
What are some other causes of dilated cardiomyopathy?
- Genetic mutation (usually autosomal dominant) 2. Myocarditis (usually due to coxsackie A or B) 3. Alcohol abuse 4. Drugs (doxorubicin) 5. Pregnancy
In pregnancy, when is dilated cardiomyopathy?
Its seen during late pregnancy or soon (weeks to months) after childbirth
What characterizes myocarditis leading to dilated cardiomyopathy?
characterized by a lymphocytic infiltrate in the myocardium
What does dilated cardiomyopathy from myocarditis result in?
chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.
What is the treatment for dilated cardiomyopathy?
heart transplant.
What is hypertrophic cardiomyopathy?
Massive hypertrophy of the left ventricle
What is hypertrophic cardiomyopathy usually due to?
genetic mutations in sarcomere proteins; most common form is autosomal dominant
What are the clinical features for hypertrophic cardiomyopathy?
- Decreased cardiac output 2. Sudden death due to ventricular arrhythmias 3. Syncope with exercise
How does hypertrophic cardiomyopathy lead to syncope with exercise?
Subaortic hypertrophy of the ventricular septum results in functional aortic stenosis
What is a common cause of sudden death in young athletes?
hypertrophic cardiomyopathy
In hypertrophic cardiomyopathy what does the decreased cardiac output lead to?
Left ventricular hypertrophy leads to diastolic dysfunction (ventricle cannot fill).
In hypertrophic cardiomyopathy, what does biopsy show?
myofiber hypertrophy with disarray
What is restrictive cardiomyopathy?
Decreased compliance of the ventricular endomyocardium that restricts filling during diastole
What are the causes of restrictive cardiomyopathy?
amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis (in children), and Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia).
What does restrictive cardiomyopathy present as?
congestive heart failure;
What is the classic finding in restrictive cardiomyopathy?
low-voltage EKG with diminished QRS amplitude.
What are the cardiac tumors?
Myxoma, rhabdomyoma
What is myoxma?
Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology
What is the most common primary cardiac tumor in adults?
myxoma
What does myxoma usually form?
a pedunculated mass in the left atrium
What does the pedunculated mass in the left atrium due to myxoma cause?
syncope due to obstruction of the mitral valve
What is rhabdomyoma?
Benign hamartoma of cardiac muscle
What is the most common primary cardiac tumor in children?
rhabdomyoma
What is rhabdomyoma associated with?
Tuberous sclerosis
Where does rhabdomyoma usually arise?
in the ventricle
Which type of tumors are more common in the heart?
Metastatic tumors more than primary tumors
What does common metastases to the heart include?
breast and lung carcinoma, melanoma, and lymphoma
What does metastatic tumors in the heart most commonly involve? What does this result in?
the pericardium, resulting in a pericardial effusion
