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Block 9 Week 1 Meg > Fung: Cardiovascular System > Flashcards

Fung: Cardiovascular System Flashcards

1
Q

Which ventricle is thicker, right or left?

A

left ventricle

**1.3-1.5cm vs 0.3-0.5cm (right ventricle)

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2
Q

T/F: Males’ hearts have greater mass than female hearts by about 50gm

A

True

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3
Q

Describe the three layers of the heart tissue

A
  1. Intima (endocardium lined by endothelial cells)
  2. media (myocardium made up of smooth muscle cells)
  3. adventitia (epicardium)
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4
Q

What are some features of cardiac muscle?

A

striated
centrally located nuclei
intercalated discs

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5
Q

Describe blood flow through the heart beginning with deoxygenated blood entering the right atrium via the superior vena cava.

A

superior vena cava –> right atrium –> tricuspid valve –> right ventricle –> pulmonary circulation (picks up O2) –> enters left atrium –> through mitral valve to left ventricle –> out the aortic valve and aorta to the systemic circulation

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6
Q

What connects the papillary muscles to the mitral and tricuspid valves?

A

chordae tendinae

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7
Q

Describe the pathway of electrical conduction through the heart

A

SA node –> AV node –> Bundle of HIS –> Purkinje fibers

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8
Q

Which arteries are responsible for supplying blood to the heart tissue itself?

A

the right and left coronary arteries come off of the aorta to supply the cardiac tissue with nutrients; the left coronary artery divides immediately into the left circumflex artery and the left anterior descending artery. The right coronary artery does not divide immediately, but then does diverge into the right marginal artery and the posterior descending artery

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9
Q

What are the three main components of vascular structure?

A

endothelial cells
smooth muscle cells
extracellular matrix

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10
Q

What are some functions of the vascular endothelial cells?

A 
maintain non-thrombotic state
modulate vascular resistance
metabolize hormones
regulate inflammation
regulate cell growth
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11
Q

What are some functions of vascular smooth muscle cells?

A

proliferate when stimulated
synthesize collagen, elastin, proteoglycans
increase growth factors and cytokines

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12
Q

What makes up the extracellular matrix of the blood vessels?

A

elastin
collagen
GAGs

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13
Q

In which vessels, arteries or veins, is there a thicker media layer?

A

arteries handle blood under a lot more pressure, so they have a much thicker media

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14
Q

In what layer of the blood vessel is the vasa vasorum located? What does it do?

A

in the adventitia - it’s the blood supply for the blood vessels themselves

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15
Q

How are muscular arteries different from elastic arteries?

A

muscular arteries have less elastin and require less recoil; muscular arteries have an internal (between intima and media) and external elastic lamina (between media and adventitia)

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16
Q

How do veins differ from arteries?

A

they are not as thick (thinner media)
they move blood via contraction of skeletal muscle
contain valves
no adventitia

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17
Q

Three types of arteries?

A 
elastic arteries (ex: aorta, brachiocephalic)
muscular arteries (ex: radial, femoral)
arterioles
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18
Q

Cadiovascular disease can be caused by six different mechanisms. Name as many as you can.

A 
failure of the pump
obstruction to flow
regurgitant flow
shunted flow
disorders of cardiac conduction
rupture of heart or major blood vessel
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19
Q

The stereotypical response in cardiovascular disease involves loss or dysfunction of (blank) which stimulates (blank) cell growth and ECM deposition leading to (blank)

A

endothelial cells; smooth muscle cells; intimal thickening

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20
Q

Explain how the juxtaglomerular apparatus of the kidney regulates blood pressure

A

The juxtaglomerular apparatus is located near the renal glomerulus; it senses how much blood is passing through the kidney. When it senses low blood pressure, the kidney releases RENIN. Renin causes angiotensinogen to be converted to angiotensin I in the liver. Ang I is converted to Ang II in the lungs, which causes the adrenal gland to release aldosterone. Aldosterone causes increased resorption of Na+ which increases blood volume.

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21
Q

What is released from the heart in response to high blood pressure?

A

atrial natriuretic peptide

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22
Q

What is normal blood pressure? What BP, systolic and diastolic, is considered prehypertension? What BP is considered malignant hypertension?

A

120/80mgHg
120/80 - 140/90mgHg
200/120mmHg

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23
Q

What is essential hypertension? What can cause it?

A

hypertension with no real known cause; 90% of HTN is essential hypertension

single gene defects, polymorphisms, vascular problems (structural changes), environmental factors (obesity, stress, diet)

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24
Q

10% of hypertension is secondary hypertension. What kinds of things can cause secondary hypertension?

A

renal disease (renal artery stenosis)
endocrine problems
cardiovascular problems
neurologic problems

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25
Q

What is hyaline arteriosclerosis? In what disease state does it occur?

A

Hyaline arteriosclerosis occurs in essential benign hypertension and diabetes. It is the deposition of protein into the vessel walls of arterioles, which creates pink hyaline. Causes end organ ischemia, glomerular scarring, and can cause chronic renal failure when it presents around the arterioles in the kidney.

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26
Q

What is hyperplastic arteriosclerosis? What disease state is it associated with?

A

Hyperplastic arteriosclerosis is associated with malignant hypertension. It is the proliferation of smooth muscle cells around the arterioles, especially those of the kidney. Forms onion-like appearance.

**Can cause end organ ischemia.
Causes flea-bitten appearance of kidney.

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27
Q

What makes up an atheroma? What can happen when atheromas protrude into the vessel lumen?

A

So, an atheroma is a mass or plaque of degenerative tissue in the tunica intima of blood vessels; obstruction of blood flow, rupture of vessel wall, formation of aneurysm

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28
Q

Consist of raised lesions with a soft, yellow, core of lipid covered with a fibrous cap

A

atherosclerotic plaque

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29
Q

What are two main causes of endothelial dysfunction leading to atherosclerosis?

A
  1. hemodynamic disturbances - plaques occur in areas of disturbed, turbulent flow, like ostia of exiting vessels or branch points of vessles
  2. hyperlipidemia - most plaques are made up of cholesterol and cholesterol esters; lowering serum cholesterol can decrease rate of atherosclerosis
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30
Q

What happens to smooth muscle cells in the media during arthersclerosis?

A

these cells migrate into the intima and begin proliferating due to chemokines and growth factors produces

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31
Q

What are some non-modifiable risks for atherosclerosis?

What are some modifiable risks?

A 
age
gender (females more protected)
genetics (ex: familial hypercholesterolemia);
hyperlipidemia
hypertension
smokers
diabetes
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32
Q

a chronic inflammatory and healing response to arterial wall and endothelial injury

A

atherosclerosis

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33
Q

List some of the pathologic events in formation of atheromas

A

endothelial injury
lipid accumulation in intima
monocyte adhesion and formation of foam cells (LDL eaten by macrophages)
smooth muscle cell recruitment to intima
smooth muscle cell proliferation, and ECM deposition

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34
Q

How does a fatty streak become an atheroma?

A

endothelial cell injury, lipids accumulate, lipids are oxidized and eaten by macrophages to form foam cells, T cell recruited, smooth muscle cells also recruited, ECM deposited, etc.
Becomes a mature atheroma when it develops a fibrous cap.

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35
Q

What are some major consequences of atherosclerosis?

A

Myocardial infarction (plaque rupture with thrombosis)
Cerebral infarction
Aortic aneurysms (weakening of vessel wall)
Stenosis of medium sized vessels –> Peripheral vascular disease (claudication), angina, ischemic bowel disease

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36
Q

How do atheromas evolve?

A

they undergo acute plaque changes; for example, an atheroma with a weak fibrous cap can rupture and release its thrombogenic contents. Or, the atheromas can grow so much that they almost completely occlude the vessel

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37
Q

an imbalance between the supply and demand of the heart for oxygenated blood; frequently referred to as coronary artery disease

A

myocardial ischemia

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38
Q

What causes ischemic heart disease?

A

> 90% obstructive atherosclerotic lesions in the coronary arteries
coronary emoboli
blockage of coronary arteries
severe hypotension

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39
Q

Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis

A

angina pectoris

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40
Q

What is stable angina? What causes it? What can relieve this type of angina?

A

it is chest pain following physical activity, emotional excitement, or increased cardiac workload; it is caused by an imbalance or perfusion relative to oxygen demand; relieved by rest or vasodilators

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41
Q

What causes prinzmetal angina? What can relieve this type of angina?

A

coronary artery spasm that is NOT related to physical activity, heart rate, or blood pressure

ex: cocaine abuse

can be relieved by vasodilators or Ca+ channel blockers

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42
Q

What is unstable angina? What is it caused by?

A

a pattern of increasingly frequent pain of prolonged duration that occurs even a low levels of activity or at rest; caused by acute plaque change with superimposed thrombosis/embolism or vasospasm

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43
Q

This type of angina is seen in artery occlusion of 90% or greater and is a warning sign of impending acute MI

A

unstable angina

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44
Q

Death of cardiac muscle due to prolonged severe ischemia

A

myocardial infarction

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45
Q

What is the typical sequence of an MI? What happens first?

A

acute change of an atheromatous plaque exposes the thrombogenic contents; platelets adhere to the exposed plaque and degranulate; tissue factor activates the coag cascade which adds to the bulk of the thrombus; eventually, the thrombus completely occludes the lumen of the vessel

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46
Q

What are some things that can cause an MI NOT related to coronary vascular pathology?

A

vasospasm due to cocaine or platelets aggregating
emboli
ischemia without atherosclerosis or thrombus formation (ex: vasculitis, severe hypotension or amyloid deposition)

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47
Q

How long is heart tissue viable after an MI? In other words, what is the time period for “reversible injury” during an MI?

A

for 20-30 minutes of ischemia, the injury is reversible; after this time period, myocytes begin necrosing and necrosis will be complete within 6 hours

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48
Q

Myocardial ischemia proceeds from the (blank) outward

A

endocardium

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49
Q

Necrosis involves the full thickness
Associated with chronic atherosclerosis, acute plaque change
ST elevation infarcts

A

transmural infarction

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50
Q

Necrosis limited to inner 1/3 of ventricular wall
Due to any reduction in coronary flow
Non-ST elevation infarcts

A

subendocardial infarction

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51
Q

If the left anterior descending artery is occluded, which portions of the heart may become ischemic?

A

apex
anterior wall of left ventricle
anterior 2/3 of ventricular septum

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52
Q

If the right coronary artery is occluded, what portions of the heart may become ischemic?

A

posterior 1/3 of septum
right ventricle wall
posterobasal wall of left ventricle

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53
Q

If the left circumflex artery is occluded, what portion of the heart may become ischemic?

A

left ventricular myocardium

54
Q

What will you see histologically 1-2 days after an MI?
After 3-4 days?
1-2 weeks?
Long term?

A

coagulated necrosis;
recruitment of acute inflammatory cells;
granulation tissue with macrophages eating up dead tissue;
remote scar (infarcted tissue that has scarred)

55
Q

What are some clinical signs of ischemic heart disease?

A

rapid, weak pulse
diaphoresis (sweating)
dyspnea
**can be asymptomatic

56
Q

How many hours after an MI will myoglobin levels rise in the blood? When will they peak? In what other muscle type is myoglobin found?

A

0-2 hrs;
6-8 hrs;
also found in skeletal muscle

57
Q

How many hours after an MI will CK-MB levels rise? When will they peak? Is CK-MB sensitive or specific? Where else can CK-MB be found?

A

2-4 hours;
24 hours;
sensitive, but not specific;
some skeletal muscle, too

58
Q

How many hours after an MI will troponin levels rise? When will they peak? Are troponins sensitive or specific? How many days after an MI will they remain present in the blood?

A

2-4 hours;
48 hours;
sensitive and specific;
persist for 7-10 days after the MI

59
Q

How to treat an acute MI?

A 
aspirin
heparin
oxygen
nitrates (vasodilation)
beta blockers
ACE inhibitors
reperfusion
60
Q

Rescues ischemic myocardium and limits infarct size

A

reperfusion

61
Q

What are some mechanisms of reperfusion?

A

thrombolysis
angioplasty
stent placement
coronary artery bypass graft

62
Q

What adverse consequences can reperfusion cause?

A

arrhythmias
myocardial hemorrhage with contraction bands
irreversible cell damage on top of the original injury
microvascular injury
prolonged ischemic dysfunction

63
Q

Progressive heart failure as a consequence of ischemic myocardial damage
Also referred as ischemic cardiomyopathy
Appears due to function decompensation of hypertrophied noninfarcted myocardium

A

chronic ischemic heart disease

64
Q

So what causes chronic ischemic heart disease?

A

hypertrophied myocardium which is not totally functional

65
Q

Caused by a lethal arrhythmia that is normally triggered by myocardial ischemia

A

sudden cardiac death

ex: asystole or V fib

66
Q

What are some things that can cause sudden cardiac death that are NON-atherosclerotic?

A 
congenital abnormalities
aortic valve stenosis
mitral valve prolapse
cardiomyopathies
drug abuse
hereditary or acquired arrhythmias
67
Q

What is heart failure?

A

when the heart is unable to pump enough blood to meet the demands of the tissue; when the heart can only pump blood sufficiently at elevated filling pressures

68
Q

What types of things can cause heart failure?

A

valve disease
long term hypertension
ischemic heart disease with MI
fluid overload

69
Q

Compare forward heart failure and backward heart failure

A

forward: decreased cardiac output and tissue perfusion
backward: pooling of blood in the venous system (pulmonary/peripheral edema)

70
Q

What are 3 adaptive mechanisms for heart failure?

A
  1. Frank Starling: dilation and increased filling pressure increases contractility
  2. ventricular remodeling: hypertrophy with or without dilation
  3. neurohormonal mechisms: ex: norepi to increase HR, renin-angiotensin-aldosterone to increase BP, release of atrial natriutetic peptide to adjust filling volumes
71
Q

What is this?

dilation and increased filling pressure increases contractility

A

Frank-starling mechanism

72
Q

Increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size

A

hypertrophy

**myocytes increase in protein synthesis, mitochondria, and size of nucleus

73
Q

Two types of overload hypertrophy? How are they different?

A

pressure overload and volume overload; with pressure overload, you will get sarcomeres increased in parallel to the long axes of cells; with volume overload, you will get dilation of the ventricle and ventricular wall may become thicker

74
Q

T/F: The molecular and cellular changes in hypertrophied hearts that initially mediate enhanced function may themselves contribute to the development of heart failure

A

True

**these compensatory mechanisms will work initially, but will eventually fail

75
Q

What four things can cause left sided heart failure?

A

Ischemic heart disease
Hypertension
Aortic and valvular diseases
Myocardial diseases

76
Q

Compare systolic failure to diastolic failure

A

systolic failure: insufficient cardiac output (pump failure)

vs.

diastolic failure: stiff ventricle can’t increase its output and can’t fill appropriately

77
Q

What causes the symptoms of left sided heart failure?

A

congestion in the pulmonary circulation
stasis of blood in left chambers
hypoperfusion of tissues

78
Q

What are the symptoms of left sided heart failure?

A 
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
79
Q

What causes right sided heart failure?

A

left sided heart failure

or pulmonary hypertension or disease

80
Q

Symptoms of right sided heart failure?

A 
Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites 
Abnormal mental function
Renal failure
81
Q

How do you treat heart failure?

A

diuretics to remove congestion
renin-angiotensin-aldosterone blockers to decrease blood volume
beta blockers to lower adrenergic tone

82
Q

Results from sustained increased hypertension that causes pressure overload and ventricular hypertrophy

A

hypertensive heart disease

**can be left sided or right sided

83
Q

Left ventricular hypertrophy without any other cardiovascular pathology
History or pathologic evidence of hypertension

A

systemic hypertensive heart disease

84
Q

Characterized by right ventricular hypertrophy and dilation

Can be acute (pulmonary embolism) or chronic

A

pulmonary hypertensive heart disease

85
Q

What are the AV valves?

A

the mitral (left atrium/ventricle) and tricuspid (right atrium/ventricle) valves

86
Q

What are the semilunar valves?

A

aortic and pulmonary valves

87
Q

Failure of a valve to open completely, which impedes flow

Leads to pressure overload

A

stenosis

88
Q

Failure of a valve to close completely, allowing reversed flow
Leads to volume overload

A

Insufficiency/regurgitation

89
Q

What can cause mitral valve stenosis?

A

rheumatic heart disease

90
Q

What can cause mitral regurgitation?

A 
rheumatic heart disease
infective endocarditis
mitral valve prolapse
drugs
rupture of papillary muscle
papillary muscle dysfunction
rupture of chordae tendinae
LVD
calcification
91
Q

What can cause aortic stenosis?

A

Rheumatic heart disease
Senile calcifications
Calcification of a congenitally deformed valve

92
Q

What can cause aortic regurgitation?

A 
Rheumatic heart disease
Infective endocarditis
Marfan syndrome
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
Rheumatoid arthritis
Marfan syndrome
93
Q

Due to normal wear and tear
Normally presents in the seventh to ninth decades of life
Obstruction results in pressure overload and LVH

A

calcific aortic stenosis

94
Q

Most frequent congenital cardiovascular malformation
Due to normal wear and tear
Presents in the fifth to seventh decades of life

A

calcific stenosis of congenitally BICUSPID aortic valve

**should have 3 cusps

95
Q

Calcifications in the peripheral fibrous ring

Does not affect valvular function or become clinically important

A

mitral annular calcification

96
Q

What is mitral valve prolapse? How does it present clinically?

A

Occurs when mitral valve leaflets become floppy and prolapse into the left atrium during systole
most patients are asymptomatic and may present with a mid-systolic click

97
Q

Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis
Acute rheumatic carditis is a frequent consequence

A

rheumatic fever

98
Q

What are the clinical features of rheumatic heart disease?

A 
migratory polyarthritis of large joints
pancarditis (Aschoff bodies, Anitschkow cells)
subcutaneous nodules
sydenham chorea (dancing movements)
skin miscoloring
99
Q

Acute rheumatic heart disease is characterized by (blank) and (blank) in the valves

A

Aschoff bodies; vegetations

100
Q 
A deforming fibrotic valvular disease
Only cause of mitral stenosis
Other valves can be involved
Aschoff bodies not identified
Mitral valve shows
Leaflet thickening
Commissural fusion and shortening
Thickening and fusion of tendinous cords
A

Chronic rheumatic heart disease

101
Q

Serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe
Vegetations composed of thrombotic debris and organisms
Acute or subacute forms

A

infective endocarditis

**fever, sepsis, vegetations

102
Q

Previously normal heart valve infected by a highly virulent organism
Necrotizing, ulcerative, destructive lesions
Difficult to cure with antibiotics

A

infective endocarditis

**valves are not very vascular so antibiotics difficult

103
Q

Insidious infections of deformed valves by organisms of lower virulence
Less destructive lesion
Cures produced with antibiotics

A

subacute endocarditis

104
Q

What organism is the most common cause of endocarditis and is likely to infect previously damaged or abnormal valves?
Which organism is likely to infect healthy valves, and is seen in IV drug users?
Which organism is likely to infect prosthetic valves?

A

S. viridans; S. aureus; S. epidermis

105
Q

Characterized by deposition of small sterile thrombi on the leaflets of cardiac valves
Vegetations are thrombi that do not invade or elicit an inflammatory reaction
May be the source of systemic thrombi
Occurs in patients with cancer (mucinous adenocarcinoma), sepsis or hypercoagulable state

A

Non-bacterial thrombotic endocarditis

106
Q

Non-infected (sterile) vegetations caused by
non-bacterial thrombotic endocarditis

Ex: Libman-Sacks endocarditis (SLE)

A

non-infective endocarditis

107
Q

Patients have systemic lupus erythematosus
Vegetations located
mitral and tricuspid valves
Valvular endocardium
Chords
Mural endocardium of the atria
Vegetations composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies
Intense valvulitis with fibrinoid necrosis of the valve

A

Libman-Sacks disease

**no major destructive lesions

108
Q

Characterized by progressive cardiac dilation and contractile dysfunction

A

dilated cardiomyopathy

109
Q

Characterized by myocardial hypertrophy, poorly compliant LV myocardium leading to abnormal diastolic filling and intermittent ventricular outflow obstruction
Leading cause of unexplained left ventricular hypertrophy

A

hypertrophic cardiomyopathy

**you may also see thickened interventricular wall

110
Q

Characterized by primary decreased ventricular compliance resulting in impaired filling during diastole

A

restrictive cardiomyopathy

111
Q

How does a dilated cardiomyopathy cause impairment? What can cause it?

A

impairs contractility and causes systolic dysfunction (heart is dilated and cannot contract normally); idiopathic, genetics, myocarditis, alcohol abuse, drugs, pregnancy/childbirth, chronic anemia, medications

**the most common form of cardiomyopathy

112
Q

How does hypertrophic cardiomyopathy cause impairment? What causes it? What are some symptoms?

A

causes decreased compliance due to massive hypertrophy of the left ventricle (can’t fill the same way that a normal heart would fill) - diastolic dysfunction

autosomal dominant gene mutations!!!

decreased CO, sudden cardiac death, syncope with exercise

113
Q

How does restrictive cardiomyopathy cause impairment? What can cause it?

A

decreased compliance, stiff ventricle (diastolic dysfunction); idiopathic, amyloidosis, sarcoidosis, radiation induced, fibrosis

114
Q

Inherited (autosomal dominant, variable penetrance) disease of the cardiac muscle
Right ventricular wall is severely thinned
Disease is related to defective cell adhesion proteins in the desmosomes that link adjacent myocytes

A

Arrhythmogenic right ventricular cardiomyopathy

115
Q

Infectious or inflammatory processes that cause myocardial injury

A

myocarditis

116
Q

What is the leading cause of infectious myocarditis?

A

viruses: Coxsackie A/B

**can also be caused by viruses, bacteria, fungus, protozoa, helminths

117
Q

What can cause immune-mediated myocarditis?

A

post-viral
post-strep
SLE
drug hypersensitivity

118
Q

What pathological things can fill up the pericardial space leading to pericardial disease?

A

serous fluid (pericardial effusion)
blood (hemopericardium)
puss (purulent pericarditis)

119
Q

What are some types of acute pericarditis?

A 
serous
fibrinous/serofibrinous (most common)
purulent
hemorrhagic
caseous
120
Q

What are two types of chronic pericarditis?

A

adhesive

constrictive

121
Q

Type of acute pericarditis produced by non-infectious inflammatory diseases; mild lymphocytic infiltrate in the epipericardial fat

A

serous pericarditis

122
Q

Most frequent type of acute pericarditis; causes a loud pericardial friction rub; composed of serous fluid + fibrinous exudate

A

fibrinous/serofibrinous pericarditis

123
Q

Caused by invasion of microbes into the pericardial space by
Direct extension
Seeding from the blood
Lymphatic extension
Introduction during cardiotomy
Acute inflammatory reaction that can produce a mediastinopericarditis
Organization and scarring usual outcome with constrictive pericarditis

A

acute purulent pericarditis

124
Q

Blood with a fibrinous or suppurative effusion
Most commonly caused by a metastatic malignant neoplasm
Also found in TB and bacterial infections and post-cardiac surgery

A

hemorrhagic acute pericarditis

125
Q

Rare
Almost always due to TB by direct spread, but sometimes fungus
Leads to a disabling, fibrocalcific, chronic constrictive pericarditis

A

caseous acute pericarditis

126
Q

Follow infectious pericarditis, cardiac surgery, radiation

Pericardial sac is obliterated and pericardium adheres to surrounding structures

A

adhesive mediastinopericarditis

**pericardium may become adhered to the chest wall, causing pain with each breath

127
Q

Heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
Mimic restrictive cardiomyopathy
Heart sounds are muffled or distant

A

constrictive pericarditis

128
Q

Most common primary cardiac tumor in adults
Benign neoplasm with abnormalities of chr 12 & 17
Arise from primitive multipotent mesenchymal cells
Most often in the left atria (forms a pedunculated mass), but can arise in any chamber
10% associated with Carney complex

A

myxoma

129
Q

Where do myxomas most often occur in the heart?

A

in the atria

130
Q

Most frequent primary tumor in children
Associated with tuberous sclerosis
Considered hamartomas of cardiac muscle
Usually arises in the ventricle

A

rhabdomyoma

131
Q

Benign tumor of mature adipose tissue

Most often located in the LV, RA or atrial septum

A

lipoma

Block 9 Week 1 Meg (9 decks)

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