Congenital defect

Thursday, October 29, 2015

7:42 PM
 
1. What is epidemiology of congenital heart defect?
 Occur during week 3-8 (organogenesis)
 Seen in 1% of live births
 Most diseases are sporadic
 Most common congenital heart defect is VSD
 
2. If there's a left-right shunt in heart, which direction does it initially present? Why does it
reverse?
 Early shunt is left to right due to reduced resistance in pulmonary circulation.
 Shunt later becomes right to left - pulmonary circulation increases resulting in pulmonary HTN
and hypertrophy of pulmonary vessels
 
3. What is Eisenmenger syndrome (aka tardive cyanosis)?
 Serious hypoxemia caused by reversal of left-to-right shunt is called Eisenmenger syndrome.
 It can be present during atrial septal defect, VSD or patent ductous arteriosus
 
4. What are presentation of Eisenmenger syndrome?
 Right ventricular hypertrophy
 Polycythemia vera (increased RBC to combat hypoxemia)
 Clubbing, cyanosis

VSD
1. What's most common congenital heart defect? What is it associated with (HY)?
 Ventricular septal defect
 It's associated with fetal alcohol syndrome

2. How does it present?

 Early on, the shunt is left to right, later on it becomes right to left.
 
 3. How is it treated?
 Small defects close spontaneously. Surgery for large defects.
 
ASD
1. What are types of atrial septal defects?
 Ostium secundum (most common) - hole between atria. Ostium is primitive membrane that
divides heart to left and right sides.
 Ostium primum (aka endocardial cushion defect) -
o ASD + valve defect + defect in intraventricular wall.
o Endocardial cushion - junction of atrial septum, ventricular septum, tricuspid and mitral
valves.
o Most associated heart defect with Down's syndrome
 Sinus venosus

Fig: osteum primum (left), osteum secundum (middle and right)

 
2. What's ASD presentation? What's an important complication?
 Split S2 sound: due to increased blood in right heart, pulmonic valve closes late.
 Paradoxical emboli are important complication - ex - DVT emboli will go to brain instead of
lungs
 
PDA
1. What is patent ductous arteriosus? What's it associated with?
 Failure of ductous arteriorus to close after birth.
 Associated with congenital rubella
 Presents with left to right shunt between aorta and pulmonary artery. Later on, the shunt
becomes right to left due to pulmonary HTN and hypertrophy of pulmonary vessels

 
 2. What's it's presentation?
 Asymptomatic at birth but has 'machine-like murmur'
 May lead to Eisenmenger syndrome results in lower extremity cyanosis (because ductus
arteriosus happen after upper extremity branching)
 
3. What's it's treatment?
 Indomethacin - decreased PGE. PGE kEEEps PDA open.
 
Tetralogy of fallot
1. What is tetralogy of fallot?
 Stenosis of right ventricular outflow tract
 Right ventricular hypertrophy
 VSD
 Aorta that overrides the VSD
 Right to left shunt. Almost all others are left to right in the beginning.

 
2. What's it's presentation?
 Early cyanosis due to right-to-left shunt (more stenting = more cyanosis)
 Usually after exercise, pt squat to increase pulmonary blood flow (squatting increases systemic
resistance)
 Boot shaped heart on X-ray
 Fig: boot shaped heart indicating tetralogy of falot
 
Transposition of great vessels
1. What is transposition of great vessels?
 Aorta arises from right ventricle and pulmonary artery arises from left ventricle. Right side
does systemic circulation and left side does pulmonary curculation
 Left and right sided blood never mix (early cyanosis)

 
2. What's it's presentation? What's it associated with? How do you treat?
 Presentation:
o Early cyanosis (right and left sided blood don't mix)
o Right ventricle hypertrophy and atrophy of left ventricle
 Treatment:
o Create a shunt after birth is required for survival
o Administer PGE (PGE kEEEps PDA open)
 Association:
o Maternal diabetes
 
Truncus arteriosus
1. What is truncus arteriosus?
 It's when a single large vessel arises from both ventricles. (truncus fails to divide to aorta and
pulmonary artery)
 Presentation:
o Early cyanosis

 
Tricuspid atresia (atresia means fail to form a tube)
1. What's tricuspid atresia? How does it present?
 It's failure of development of orifice of tricuspid valve.
 Presentation:
o Hypoplastic right ventricle (ASD and VSD often present)
o Early cyanosis
 Association:
o ASD alone or ASD + VSD

 
Coarctation of aorta
1. What's coarctation of aorta? What are two types?
 Coarctation of aorta is narrowing of aorta
  Infantile type Adult type

Anatomy Narrowing is after aortic arc but before PDA Narrowing is after aortic arch (not
associated with PDA; if PDA present, it's
infantile type)

Associatio Associated with PDA and Turner syndrome (one X, no Y) Associated with bicuspid aortic valve (HY
n (HY)

Presentati Presents as lower extremity cyanosis in infants, often at  Presents as HTN in upper extremitties
on birth - due to coarctation, lower extremity isn't supplied and hypotension with weak pulse in
by LV but by RV. Upper extremities are fine because LV lower extremities; often discovered in
supplies there adulthood
 Collateral circulation across intercosta
arteries causes engorged artieries and
notching on ribs on X-ray (HY)
    

 
 
Ischemic heart disease
Thursday, September 10, 2015
7:43 PM
 
 Infarction - tissue necrosis due to lack of oxygen
 Ischemia - inadequate blood supply to an organ
 Hypoxemia - (PaO2 < 60mm Hg)
 Early MI - <55 year for men and <45 for women
 3 most common cause of chest pain in outpatient setting: GERD, anxiety, costochondral
tenderness
 Pain with MI is usually described as pressure - elephant sitting on lung. Pleuritic chest pain is
more sharp
 ST depression in AVR lead is more specific for pericarditis
 
 What is most common cause of ischemic heart disease?
 Artherosclerosis of coronary arteries
 Risk factors same as risk factor for artherosclerosis - age, sex, race, smoking, HTN, diabetes
 
How long does a ischemia last before irreversible injury to cardiac myocytes occur?
20 minutes
Angina (reversible injury to cardiac myocytes)
 Describe Stable angina. What type of damage is suffered by the cells?
 Chest pain develops with physical or emotional stress
 Caused due to >70% stenosis of coronary arteries
 Myocytes undergo reversible injury during stable angina (HY)
 
  What is presentation of stable angina? What is seen on EKG?
 Chest pain <20 mins that radiates to left arm or jaw. If > 20 minutes, it causes myocardial
infarction (irreversible damage to myocytes)
 Diaphoresis, SOB
 Pain relieved by rest or nitroglycerin
 EKG shows ST segment depression - because subendocardial ischemia is seen as ST depression.
Stable angina causes subendocardial ischemia because blood vessels travel in epicardium and
endocardium is last part to receive blood.
 
 Describe unstable angina.
 Chest pain occurs at rest (that's why called unstable)
 It's due to rupture of artherosclerotic plaque with thrombosis and incomplete occlusion of
coronary artery (rupture usually occurs at neck of plaque)
 Myocytes undergo reversible injury
 
 What is presentation of unstable angina? What is seen on EKG?
 Relieved by nitroglycerin (venodialation reduces the work heart has to do)
 High risk of progression to MI because the thrombus can grow.
 ST depression on EKG - same reason as stable angina
 

Fig - unstable angina in coronary artery. Note the dark thrombus. The thrombus has high
chance of growing and leading to MI.
 
 What is prinzmetal angina?
 Vasospasm that completely clamps coronary artery - leads to transmural ischemia
 Chest pain irrespective of physical/emotional exertion
 Myocytes undergo reversible injury
 
 What is presentation of prinzmetal angina?
 ST segment elevation - as coronary artery completely clamps down, we get transmural
ischemia. Transmural ischemia presents at ST elevation.
 Relieved by NG or calcium channel blockers
 
Myocardial infarction (irreversible injury to cardiac myocytes)
 What is MI? What are it's causes?
 Necrosis of cardiac myocytes (irreversible injury)
  Main cause - rupture of artherosclerotic plaque with thrombosis and complete occlusion of
coronary artery
 Other causes - coronary artery vasospasm, emboli, vasculitis (ex - kawasaki disease)
 
 What are clinical features of MI?
 Severe crushing chest pain (>20 minutes - cells die after this time)
 Diaphoresis, SOB
 Symptoms not relieved by nitroglycerin
 Mostly involve left ventricle. Right atria and ventricles are usually spared
 
 What are key arteries involved in MI?
 LAD (most common) - leads to infraction of anterior wall of LV and anterior interventriclular
septum
 Right coronary artery (2nd common) - infraction of posterior wall of LV and posterior
interventricular septum
 Left circumflex artery - infraction of lateral wall of LV
 
 Describe initial phase of MI.
 Subendocardial necrosis involving <50% of myocardial thickness
 ST depression (recall subendocardial infraction leads to ST depression and transmrural
infraction leads to ST elevation)
 
 What are lab enzyme tests of MI?
 Hallmark of irreversible damage to cell is membrane leak. So, cardiac enzymes will leak.
 Troponin I - most sensitive and specific marker
o Rises 2-4hrs post infraction
o Peaks at 24 hrs
o Returns to normal 7-10 days
 CK-MB - useful for detecting reinfarction
o Rises 4-6 hrs after infraction
o Peaks at 24 hrs
o Returns to normal by 72 hours
 
 What is treatment of MI?
 MONA (morphine, oxygen, nitrates, asprin)
 ACEi (decreases blood volume due to low aldo, and reduces peripheral vasoconstriction
(afterload))
 Beta blocker (slow heart rate and reduce risk of arrhythmia)
 Definitive treatment:
o Fibrinolysis or angioplasty
 Complications: contraction band necrosis and repurfusion injury (reperfusion
injury occurs due to free radical damage by neutorphils and oxygen.
 Fig - the box shows necrotic myocytes (no nuclei) and the circles show contraction band
necrosis
 
 Describe time frame of MI (HY)
Time Microscopic Gross change Complication
change

<4 hrs none none  Cardiogenic shock

 CHF
 Arrhythmia

4-24 hrs Coagulative Dark discoloration  Arrhythmia (it doesn't happen post 24 hrs
necrosis because the conduction system is already
damaged and necrosis occurs < 1 day. So if
arrhythmia don't happen by then, it won't
happen.

1-3 days Inflammation Yellow pallor  Fibrinous pericarditis (chest pain with friction
(Neutrophil) rub)- only occurs with transmural infraction

 
 

3 day - 1 Macrophages Yellow pallor  Rupture of ventricular free wall (cardiac

week tamponade), papillary muscle (mitral regurg)
or interventricular septum (shock)

1-3 Granulation Red border (blood vessels)  

 weeks tissue with emerging from edge of infract
fibroblasts,
collagen and
blood vessels

Months Fibrosis White scar  Aneurysm

 Mural thrombosis
 Dressler syndrome (autoimmune pericarditis)
(HY)

 Arrhythmia doesn't happen post 24 hrs because the conduction system is already damaged
and necrosis occurs < 1 day.
 Fibrinous pericarditis only occur with transmural infaract
 Papillary muscles are fed by right coronary artery
 Dressler syndrome - inflammation of pericardium and exposure of pericardial antigen can
cause autoimmune attack to pericardium
 
<1 day 1 day - 1 week 1 week- 1 month >1 month

Coagulative necrosis First neutrophils and then Granulation tissue Scar tissue
macrophage

 Dark discoloration of  Yellow pallor  Red border surrounding  White

heart yellow pallor scar
 

Fig - coagulative necrosis of heart showing dark discoloration (<1 day)

 
Fig- yellow pallor of heart post MI (1 day - 1 week)
 

Fig - fibrinous pericarditis (fibrin exudate during neutrophil rich stage (day 1-3 post MI) rubs
when hear contracts producing and characteristic friction rub). Only see during transmural
infraction
 

Fig - 1-3 weeks post MI. The yellow pallor is central area of necrosis (granulation tissue?)
surrounded by emerging blood vessels from edge of infaract
 
 Fig - Months after MI (white scar tissue)
 

Fig - layers of heart muscle

 
 What is sudden cardiac death? What is it's etiology
 Unexpected death due to cardiac disease with no symptom or death <1 hr after symptom arise
 Cause : ventricular arrhythmia
 Etiology:
o Severe artherosclerosis (90% of cases)
o Less common: cardiomyopathy, mitral valve prolapse, cocaine abuse
 
 What is chronic ischemic heart disease?
 Poor myocardial function due to chronic ischemic damage (with or without infraction)
 Can progress to congestive heart failure
 
  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Congestive heart failure (CHF)
Friday, October 30, 2015
12:54 AM
 
1. What is division of CHF?
 Left sided failure
 Right sided failure
 
2. Differentiate right and left sided CHF.
  Left sided failure Right sided failure

Causes  HTN  Most common cause

 Dilated cardiomyopathy is left sided failure
 MI  Left-to-right shunt
 Restrictive cardiomyopathy  Chronic lung disease
(cor pulmonale)
 Presentatio  Presentation based on pulmonary congestion and  Jugular venous
n pulmonary edema distension
 Dyspnea, paroxysmal nocturnal dyspnea (increased  Painful
venous return while lying flat), orthopnea (SOB hepatosplenomegaly
while flat), crackles in lung with characterstic
 Hemosiderin laden macrophage in lung (aka heart 'nutmeg liver'
failure cells) - pulmonary capillaries burst due to  Cardiac cirrhosis
backing up  Pitting edema

   Decreased flow to kidney activates RAS which leads  

to fluid retention and worsens CHF

Treatment ACE inhibitors  

 

 
 
 
Valvular disorders
Thursday, October 29, 2015
11:52 PM
 
Acute rheumatic fever
1. What is pathogenesis of actue rheumatic fever?
 It's a systemic complication of group A strep which presents 2-3 weeks after streptococcal
pharyngitis
 Bacterial M protein mimics human protein and autoantibodies are generated.
 
2. How is acute rheumatic fever diagnosed?
 Diagnosis is based on evidence of group A strep infection (elevated ASO or anti-DNAse B titer) +
major (JONES) or minor criterea
 Minor criteria
o Fever and elevated ESR (non-specific)
 Major criteria (JONES)
o Joint (migratory polyarthritis) - swelling in pain in large joints (wrist, knee, ankle) that
resolve in days and move to another large joint
o O (pancarditis)
 Endocarditis - Mitral valve is most commonly affected. See small vegetations along
line of closure that lead to regurgitation
  Myocarditis - Aschoff bodies seen (focal area of chronic inflammation). Presence of
Anitschkow cells (reactive histiocytes with slender, wavy nucleus), fibrinoid
material and giant cells. (myocarditis most common cause of death)
 Pericarditis - friction rub and chest pain
o Subcutaneous Nodules
o Erythema marginatum - nonpruritic rash with erythematous border commonly on trunk
and limbs
o Sydenham chorea

3. What is most common cause of death in acute rheumatic fever?

 Myocarditis
 
4. What is prognosis of acute rheumatic fever?
 Acute attack usually resolvs but may progress to chronic rheumatic heart disease
 Repeat exposure with group A strep increases chance of rheumatic heat disease
 
Chronic rheumatic fever
1. What's presentation of chronic rheumatic fever?
 Mitral valve is most commonly affected, aortic valve is no. 2; other valves rarely affected
 Mitral valve - classic fish mouth appearancedue to stenosis (valve can't open well)
 Aortic valve - fusion of commissures
 
2. What's a complication of chronic rheumatic fever?
 Infective endocarditis

 
Aortic stenosis
1. What are some causes of aortic stenosis?
 Normal wear and tear of valve
 Bicuspid aortic valve (speeds up wear and tear)
 Chronic rheumatic fever
 
 2. What is its presentation?
 Presents in late adulthood (>60 years)
 Crescendo-decrescendo murmur with systolic ejection click (click is when the valve opens?)
 
3. How do you distinguish stenosis from chronic rheumatic fever vs normal wear and tear?
 In chronic rheumatic fever, there is fusion of commissures of aortic valves. Also, we see mitral
stenosis.
 
4. What are complications of aortic stenosis?
 Concentric left ventricular hypertrophy - may progress to cardiac failure
 Angina with syncope with exercise (decreased perfusion of heart and brain)
 Microangiopathic hemolytic anemia (see schistocytes)
 
5. How do you treat aortic stenosis?
 Valve replacement
 
Aortic regurgitation
1. What are causes of aortic regurgitation?
 Isolated aortic root dilation (most common cause)
 Aortic dissection, Syphillis (causes aortic root dilation)
 Valve damage, ex - infective endocarditis
 
2. What are clinical features of aortic regurgitation?
 Increased pulse pressure (water-hammer pulse) - diastolic pressure is low due to regurgitation,
systolic pressure increases due to increased stroke volume (pulse pressure is difference
between systolic and diastolic pressures)
 LV dilation and eccentric hypertrophy due to volume overload
 
3. What is treatment of aortic regurgitation?
 Valve replacement once LV dysfunction develops
 
Mitral valve prolapse
1. What is mitral valve prolapse? What are some etiologies?
 Mitral valve prolapse is ballooning of mitral valve into left atrium during systole
 It occurs due to myxoid degenration of valve making it floppy
 Etiologies:
o Marfan syndrome
o Ehlers-Danlos syndrome
 
2. What is presentation of mitral valve prolapse?
 Mostly asymptomatic
 Mid-systolic click followed by regurgitation murmur
 Murmur is softer with squatting (increased systemic resistance decreases left ventricular
emptying)
 
3. What are complications?
 Rare but infective endocarditis, arrhythmia and severe mitral regurg
 
4. What is treatment of mitral valve prolapse?
 Valve replacement
 
Mitral regurgitation
 1. What are some causes of mitral regurgitation?
 Complication of mitral prolapse
 LV dilation
 Infective endocarditis
 Acute rheumatic fever - vegetation on valve edge prevent smooth closing
 Papillary muscle rupture after MI
 
2. What is presentation of mitral regurgitation?
 Holosystolic "blowing" murmur; lower when squatting (increased systemic resistance
decreases LV emptying) and expiration (increases blood return to LV)
 Volume overload and left sided failure
 
Mitral stenosis
1. What are some causes of mitral stenosis?
 Chronic rheumatic valve disease most common cause
 
2. What are presentations of mitral stenosis?
 Opening snap followed by diastolic rumble
 Volume overload with dilation of left atrium:
o Pulmonary congestion with edema and alveolar hemorrhage
o Pulmonary HTN and eventual right sided heart failure
o A-fib with mural thrombus
 
 
 
Endocarditis
Sunday, September 6, 2015
8:20 PM
 
1. What is endocarditis?
 Inflammation of endocardium (mostly valves) usually due to bacterial infection.
 
Pathogen    

1 S. viridans Most common cause of Subacute endocarditis (small

endocarditis; dental procedure vegetations)

2 S. aureus Most common cause of Acute endocarditis (large vegetati

endocarditis in IV drug users

3 S. epidermidis Key organism to cause  

endocarditis of prosthetic valves

4 Strep bovis Cause endocarditis in pt with  

colorectal carcinoma (HY)

5 HAECK organism Hemophilus, Actinobacillus, Cause endocarditis with negative

Cardiobacterium, Eikenella, culture (because pathogens diffic
Kingella grow)

6 Nonbacterial Occurs if pt is hypercoagulable or  

thrombotic endocarditis has adenocarcinoma
 7 Libman-Sacks Sterile vegetations on both side Associated with lupus
endocarditis of mitral valve

8 Coxiella burnetti Most common cause of culture -  

ve endocarditis
1. Describe endocarditis due to S. viridans.
 Most common cause of endocarditis.
 Low virulence pthogen; therefore mainly infects previously damaged valves
 Results in small vegetations that don't destroy valves (therefore called subacute endocarditis)
 
3. Describe pathogenesis of endocarditis due to S. viridans.
 Damaged endocardial surface develops thrombotic vegetations
 During transient bacteremia (ex - dental procedure), bacteria can be trapped in these
vegetations
 
4. Describe endocarditis due to S. aureus.
 Most common cause of endocarditis in IV drug abusers
 High virulence organism; can infect normal valves (mainly tricuspid)
 Vegetations are large and destroy valve (called acute endocarditis)
 

Fig - staph aureus endocarditis

 
5. Describe clinical presentation of endocarditis. (FOR JANE)
 Fever
 Murmur
 Janeway lesion - mainly on palm and sole (painless)
 Osler nodules (hurts - ouch!) - mainly on finger and toes (painful)
 Roth nodules
 Hemolytic anemia (usually microcytic)
 Nailbed splinter hemorrhage
 Emboli
  

Fig - roth nodules (retinal hemorrhage); osler and roth nodules are immunologic.
 
Endocarditis may lead to glomerulonephritis and positive Rheumatic factor.
 
6. How does endocarditis lead to low blood iron.
 Acute phase reactant proteins are made (hepsidin being one major one). Hepsidin traps iron in
storage site. This leads to high ferritin. Also, bone marrow takes iron from blood because
hepsidin is trapping iron in storage site. That’s how serum iron decreases.
 
7. Describe nonbacterial thrombotic endocarditis.
 It is sterile vegetation seen on valves during hypercoagulable state or underlying
adenocarcinoma.
 These vegetations occur on bicuspid valves along lines of closure and lead to mitral regurg
 
8. Describe Libman-Sacks endocarditis.
 Sterile vegetations on both side of mitral valve - leads to mitral regurg
 Associated with lupus (HY)
 
9. Describe diagnosis of endocarditis.
 Surface Echo - 60% sensitive
 Transesophageal echo - 90% sensitive
 
 Endocarditis leads more often regurg of valves rather than stenosis
 If valve vegetation is >1cm, consider surgery of valves
 
 
Cardiomyopathy
Sunday, September 6, 2015
9:19 PM
 
1. Describe dialated cardiomyopathy.
  Most common type of cardiomyopathy
 Leads to systolic dysfunction (heart can't contract very well)
 Complications:
o mitral and tricuspid regurg
o Arrhythmia (heart's conduction system is stretched up)
 
2. What are some causes of dialated cardiomyopathy?
 Idiopathic in most cases
 Mutation - they are autosomal dominant
 Myocarditis - coxcakie virus most common pathogen
 EtOH abuse (HY)
 Drugs - doxorubicin, cocaine
 Pregnancy (HY) - occurs in 3rd trimester or soon after birth
 

Fig - myocarditis; notice the presence of lymphocytes. Most common cause is coxcakie virus;
acutely, it can cause death; in chronic cases, it can cause dialated cardiomyopathy
 
3. What is treatment for dialated cardiomyopathy?
 Nothing; pt need transplant
 
Hypertrophic cardiomyopathy
4. Describe hypertrophic cardiomyopathy.
 Massive hypertrophy of left ventricle
 Most common cause (HY): due to autosomal dominant mutations in sarcomere proteins
 
5. What are its clinical presentation?
 Diastolic dysfunction (heart doesn't fill well)
 Sudden death in young athletes due to ventricular arrhythmias.
 Syncope with exercise
 Biopsy (HY):
o Myofiber hypertrophy with disarray
 Fig - myofiber hypertrophy and disarray (fibers oriented in different directions)common
in hypertrophic cardiomyopathy
 
Restrictive cardiomyopathy
6. What is restrictive cardiomyopathy and it's causes?
 Diastolic dysfunction
 Causes
o Amyloidosis
o Sarcoidosis
o Hemochromatosis
o Endocardial fibroelastosis (in kids) - there's fibrosis and elastosis in endocardium
o Loeffler syndrome - eosinophilic inflammation of endocardium and myocardium
 
7. What is EKG finding of restrictive cardiomyopathy?
 Low voltage EKG
 Diminished QRS amplitudes
 
 
 
 
Cardiac tumors
Friday, October 30, 2015
12:40 AM
 
Myxoma Rhabdomyoma Metastasis

Most common cardiac tumor in Most common cardiac Most common cardiac tumor
adults tumor in children

Benign mesenchymal tumor with Benign hamartoma of  

abundant ground substance in cardiac muscle
histology

Pedunculated mass in left atrium Usually seen in ventricle Most commonly affects
pericardium and seen as
pericardial effusion
 
 

  Associated with tuberous Breast, lung carcinoma,

sclerosis melanoma and lymphoma
common source of metastasis
Myxoma
1. What is most common primary cardiac tumor in adults?
 Myxoma
 
2. What type of tumor is myxoma?
 Benign mesenchymal tumor with abundant ground substance in histology
 
2. What is its presentation?
 Pedunculated mass in left atrium that can obstruct mitral valve (syncope)
 

Fig: biopsy (abundant ground substance) and autopsy of myxoma

 
Rhabomyoma
1. What is most common primary cardiac tumor in children?
 Rhabdomyoma
 
2. What kind of tumor is rhabdomyoma?
 Benign hamartoma of cardiac muscle
 Usually seen in ventricle
 
2. What is it associated with?
 Tuberous sclerosis (a genetic disorder that causes non-malignant tumors in many different
organs, primarily in the brain, eyes, heart, kidney, skin and lungs. Common presentation:
seizures, developmental delay, intellectual disability and autism)
 
 Fig: rhabdomyoma
 
Metastasis
1. What is most common type of cardiac tumor?
 Metastasis (more common than primary tumors)
 
2. What are common sites of metastasis?
 Breast, lung carcinoma, melanoma and lymphoma
 
3. What is its most common presentation?
 Most commonly affects pericardium and seen as pericardial effusion