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CPR II Exam 1 > Chapter 12/Lecture 8: Arrhythmia, SCD, HTN, Cardiac Valve Dz, Cardiomyopathy, Pericardial Dz, Cardiac Tumors, Transplantation > Flashcards

Chapter 12/Lecture 8: Arrhythmia, SCD, HTN, Cardiac Valve Dz, Cardiomyopathy, Pericardial Dz, Cardiac Tumors, Transplantation Flashcards

1
Q

SA node damage by ischemic injury leads to what?

A

Sick sinus syndrome —> Bradycardia

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2
Q

Irritated atrial myocytes which depolarize independently and sporadically (atrial dilation) lead to variable transmission through which node and cause what?

A

AV node –> Atrial Fibrillation

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3
Q

What is the most common inherited arrhythmogenic disease?

A

Long QT syndrome

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4
Q

Patients w/ long QT syndrome commonly present how?

A

With stress-induced syncope or sudden cardiac death

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5
Q

What are 4 genes implicated in long QT syndrome?

A
  • KCNQ1
  • KCNH2
  • SCN5A
  • CAV3
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6
Q

Which inherited arrhythmogenic disease presents with syncope or SCD during rest or sleep or after large meals?

A

Brugada syndrome

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7
Q

What is the leading cause of SCD?

A

Coronary artery disease

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8
Q

The mechanism leading to SCD is most often due to what?

A

Lethal arrhythmia (i.e., asystole or ventricular fibrillation) arising from ischemia-induced myocardial irritability

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9
Q

80-90% of pt’s who suffer SCD but are successfully resuscitated do not show what?

A

Enzymatic or ECG evidence of myocardial necrosis

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10
Q

In structurally normal hearts, arrhythmias are more often due to what?

A

Mutations in ion channels that cause aberrant repolarization or depolarization

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11
Q

What are the 2 criteria for the diagnosis of systemic (left-sided) hypertensive heart disease?

A

1) LV hypertrophy (usually concentric) in the absence of other cardiovascular pathology
2) Clinical hx or pathologic evidence of HTN in other organs (i.e., kidney)

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12
Q

In Systemic (left-sided) HHD as the LV wall continues to increase in thickness what associated morphological changes occur?

Enlargement of?

A

↑ interstitial CT –> stiffness = impaired diastolic filling –> LEFT ATRIAL ENLARGEMENT

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13
Q

In many pt’s systemic HHD comes to attention due to what signs/sx’s?

A
  • New atrial fibrillation induced by left atrial enlargement
  • Progressive CHF
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14
Q

What are some of the potential long term complications associated with Systemic (left-sided) HHD?

Risk factors for what?

A
  • Development of IHD
  • Renal damage or cerebrovascular stroke
  • Progressive CHF or SCD
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15
Q

Isolated pulmonary (right-sided) HHD (cor pulmonale) arises in the setting of what?

A

Pulmonary HTN

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16
Q

What is the most common cause of pulmomary HTN (cause of isolated right-sided HHD)?

A

Left-sided heart disease

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17
Q

What are the 2 typical causes of chronic cor pulmonale (right-sided HHD)?

A
  • Chronic parenchymal disease (ie emphysema)
  • Primary pulmonary HTN
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18
Q

Acute cor pulmonale (right-sided HHD) may follow what?

A

Massive pulmonary embolism

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19
Q

What are the morphological changes seen in the right-side of the heart in the setting of acute vs. chronic cor pulmonale?

A
  • Acute = marked RV DILATION, but WITHOUT hypertrophy
  • Chronic = RV wall THICKENS
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20
Q

What are 5 diseases affecting the pulmonary parenchyma which predispose to cor pulmonale?

A
  • COPD
  • Diffuse pulmonary interstitial fibrosis
  • Pneumoconioses
  • CF
  • Bronchiectasis
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21
Q

Stenosis is failure of a valve to _______ completely, which impedes _______ flow.

A

Stenosis is failure of a valve to open completely, which impedes forward flow.

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22
Q

Insufficiency is failure of a valve to _______ completely, which allows _______ flow.

A

Insufficiency is failure of a valve to close completely, which allows reverse flow.

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23
Q

Chronic stenosis may cause what type of overload hypertophy vs. chronic insufficiency?

A
  • Chronic stenosis = cause pressure overload hypertrophy
  • Chronic insufficiency = cause volume overload hypertrophy

*Both leading to CHF

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24
Q

What are the 4 most frequent causes of the major functional valvular lesions?

A
  • Aortic stenosis
  • Aortic insufficiency
  • Mitral stenosis
  • Mitral insufficiency
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25
Q

What is the major etiology causing Mitral Stenosis?

A

Postinflammatory scarring (rheumatic heart disease)

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26
Q

What are the 3 major etiologies causing Aortic Stenosis?

A
  • Postinflammatiory scarring (rheumatic heart disease)
  • Senile calcific aortic stenosis
  • Calcification of congenitally deformed valve
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27
Q

What are 4 causes of abnormalities of leaflets and commissures leading to mitral regurgitation?

A
  • Postinflammatory scarring
  • Infective endocarditis
  • Mitral valve prolapse
  • Drugs (i.e., fen-phen)
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28
Q

What is the major etiology responsible for abnormalities of leaflets and commissures leading to Aortic Regurgitation?

A

Postinflammatory scarring (rheumatic heart disease)

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29
Q

Abnormalities of the tensor apparatus leading to Aortic Regurgitation may be caused by what 4 etiologies?

A
  • Syphilitic aortitis
  • Ankylosing spondylitis
  • Rheumatoid arthritis
  • Marfan Syndrome
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30
Q

When is the typical onset for calcific aortic stenosis and what is it due to?

A
  • Manifests at 60-80 yo
  • “Wear and tear” assoc. w/ chronic HTN, hyperlipidemia, and inflammation
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31
Q

Why does calcific aortic stenosis of congenital bicuspid valves have an accelerated clinical course and come to clinical attention sooner than normal vavles?

A

Bicuspid valves incur greater mechanical stress

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32
Q

In calcific valvular degneration the affected valves contain what kind of cells, which do what?

A

Osteoblast-like cells –> synthesize bone matrix and promote deposition of Ca2+ salts

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33
Q

What is the morphological hallmark of nonrheumatic, calcific aortic stenosis (involving either tricuspid or bicuspid valves)?

A

Mounded calcified masses in aortic cusps, which protrude and prevent complete opening of valve

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34
Q

In contrast to rheumatic (and congenital) aortic stenosis, what are 2 major differences seen in nonrheumatic, calcific aortic stenosis?

A
  • Commissural fusion is NOT usually seen
  • Mitral valve = normal
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35
Q

What are 3 major sx’s that may mark the onset of cardiac decompensation associated w/ Calcific Aortic Stenosis?

A
  • Angina
  • CHF
  • Syncope
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36
Q

Which ventricle is affected in Calcific Aortic Stenosis due to the increased pressure and what is seen?

A

Concentric LV hypertrophy

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37
Q

What is the prognosis and treatment for Calcific Aortic Stenosis?

A
  • Poor prognosis
  • Tx requires surgical valve replacement
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38
Q

SOB and cough 2’ to pulmonary congestion may be a feature of which type of calcific valvular degeneration?

A

Calcific Aortic Stenosis

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39
Q

Congenital bicuspid aortic valve (BAV) may have a genetic association due to loss of function mutations in which gene?

A

NOTCH1 on cr. 9

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40
Q

If present, which site on the cusp is a major site of calcific deposits in those with congenital bicuspid aortic valves (BAV)?

A

Midline raphe

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41
Q

Although bicuspid aortic valve (BAV) is usually asymptomatic early in life, what are some of the late complications which may arise?

A
  • Aortic stenosis and regurgitation
  • Infective endocarditis
  • Aortic dilation and/or dissection
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42
Q

As opposed to the predominantly cuspal involvement in aortic valve calcification, where do calcific deposits occur in the mitral valve?

A

In the fibrous annulus

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43
Q

What is the gross morphology of the calcific deposits in mitral annular calcification?

A

Irregular, stony hard, occassionaly ulcerated nodules

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44
Q

Calcific nodules seen in mitral annular calcification may provide a site for what complications?

Pt’s are at greater risk for what?

A
  • Thrombus formation, these pt’s have ↑ risk of embolic stroke
  • Infective endocarditis
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45
Q

Mitral annular calcification is most common in what sex and at what age?

Also in pt’s with what underlying complication?

A
  • Women >60 yo
  • Pt’s w/ mitral valve prolapse
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46
Q

Mitral valve prolapse has a higher incidence in what gender?

A

Females (7:1)

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47
Q

Mitral Valve Prolapse is often discovered incidentally by hearing what during ausculation?

A

Mid systolic click sometimes followed by mid-to-late systolic murmur

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48
Q

What occurs to the valve leaflets in Mitral Valve Prolapse?

A

“Floppy” leaflets balloon back into the LA during systole

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49
Q

Which heritable disorder of CT is associated with Mitral Valve Prolapse?

A

Marfan Syndrome

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50
Q

The leaflets in Mitral Valve Prolapse become thickened and rubbery due to what?

A

Proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption

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51
Q

The key histo change in the tissue seen in Mitral Valve Prolapse is thickening of which layer and deposition of what?

A

Spongiosa layer w/ deposition of mucoid (myxomatous) material

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52
Q

2’ changes reflecting the stresses and tissue injury incident to the billowing leaflets in mitral valve prolapse include thicking of what 3 structures?

A
  • Fibrous thickening of valve leaflets
  • Linear fibrous thickening of LV endocardial surface
  • Thickening of the mural endocardium of the LV or LA
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53
Q

Majority of patients with Mitral Valve Prolapse are asymptomatic, but a small minority may develop which 4 serious complications?

A
  1. Infective endocarditis
  2. Mitral insufficiency
  3. Stroke or thromboembolism
  4. Arrhythmias
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54
Q

How can the diagnosis of mitral valve prolapse be made?

A
  • Auscultation
  • Confirmed w/ Echocardiography
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55
Q

What is the most common cause for mitral valve surgery in the US?

A

Mitral Valve Prolapse

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56
Q

Rheumatic heart disease is virtually the only cause of what cardiac disorder?

A

Mitral Stenosis

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57
Q

The pathogenesis of Rheumatic Fever involves host immune responses to what?

A

Streptococcal M proteins cross reacting with cardiac (among other) self-antigens

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58
Q

What are the distinctive lesions found in the heart during acute RF, and what do these lesions consist of?

A
  • Aschoff bodies
  • Consisting of: T lymphocytes, plasma cells, and plump activated macrophages called Anitschkow cells
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59
Q

Which cells are pathognomonic for RF?

A

Anitschkow cells (aka caterpillar cells)

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60
Q

During acute RF, diffuse inflammation and Aschoff bodies may be found in which layers of the heart, resulting in?

A

Pericarditis, myocarditis, or endocarditis = Pancarditis

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61
Q

Inflammation of the endocardium and the left-sides valves seen in acute RF results in what type of necrosis?

What is seen overlying these necrotic foci?

A
  • Fibrinoid necrosis within the cusps of tendinous cords
  • Overlying is vegetations called verrucae
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62
Q

Subendothelial lesions seen in acute RF can induce irregular thickenings in the left atrium, known as what?

A

MacCallum plaques

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63
Q

What are the cardinal anatomic changes seen in the leaflet and tendinous cords of the mitral valve with chronic RHD?

A

- Leaflet thickening + commissural fusion and shortening

- Thickening and fusion of the tendinous cords

- Results in MITRAL STENOSIS

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64
Q

In rheumatic mitral stenosis, calcification and fibrous bridging across the valvular commissures create a stenoses named what?

A

Fish mouth or “buttonhole” stenoses

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65
Q

With tight mitral stenosis seen in RHD what compensatory changes occur in the left atrium and it may harbor what?

A

Left atrium DILATES and may harbor mural thrombi that can embolize

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66
Q

With chronic RHD, long-standing congestive changes in the lungs may induce what changes and over time lead to hypertrophy of what?

A

Pulmonary vascular and parenchymal changes; over time lead to right ventricular hypertrophy

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67
Q

What is the JONES criteria for establishing diagnosis of RF?

A
  • J = joints; migratory polyarthritis of large joints
  • O = heart; pancarditis
  • N = nodules; subcutaneous
  • E = erythema marginatum
  • S = sydenham chorea (involuntary rapid, purposless movements)
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68
Q

Acute RF appears how soon after a group A strep infection and most often in which pt population?

A
  • 10 days to 6 weeks
  • Most often in children btw ages 5-15
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69
Q

Which 2 antibodies to streptococcal enzymes may be detected in the sera of pt with RF?

A
  • Anti-streptolysin O
  • Anti-DNase B
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70
Q

What are the 2 predominant clinical manifestations and features of each in RF?

Which is more common in affected adults?

A
  • Carditis = pericardial friction rubs, tachycardia, and arrhythmias
  • Migratory polyarthritis = more common adults
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71
Q

After an initial attack of RF there is an increased vulnerability to what?

A

Reactivation of the dz w/ subsequent pharyngeal infections and the same manifestations are likely to appear

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72
Q

Pt’s with chronic RHD are may potentially suffer from what 3 consequences?

A

1) Atrial Fibrillation
2) Thromboembolic complications
3) Infective endocarditis

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73
Q

Infective endocarditis is an infection of valves and endocardium, characterized by the formation of what hallmark feature?

A

Vegetations composed of thrombotic debris and organisms, associated with underying tissue destruction

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74
Q

How does acute infective endocarditis differ from subacute infective endocarditis in the type of organism involved?

A
  • Acute IE = infection by highly virulent bacteria (i.e., S. aureus)
  • -* Subacute IE = infection w/ lower virulence bacteria (i.e., Viridians strep)
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75
Q

How does the treatment for acute infective endocarditis differ from subacute?

A
  • Acute requires surgery in addition to Abx
  • Subacute can be cured w/ Abx alone
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76
Q

What are 5 predisposing conditions which increase the risk of developing infective endocarditis?

A
  • RH
  • Mitral valve prolapse
  • Degenerative calcific valvular stenosis
  • Bicuspid aortic valves (w/ or w/o calcification)
  • Artificial (prosthetic) valves
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77
Q

Which organism is most often responsible for infective endocarditis of native but previously damaged or abnormal valves?

A

Streptococcus viridians

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78
Q

Which bacteria is responsible for a majority of the mortality associated with infective endocarditis and is common in IV drug abusers?

A

S. aureus

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79
Q

Which bacteria is most often the culprit of infectious endocarditis in those with prosthetic valves?

A

Coagulase-neg. staph (S. epidermidis)

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80
Q

Which organisms make up the HACEK group which are sometimes implicated in infective endocarditis?

A
  • Hemophilus
  • Actinobacillus
  • Cardiobacterium
  • Eikenella

- Kingella

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81
Q

The most important among the risk factors for infective endocarditis are those that can cause microorganisms to do what?

A

Seeding into blood stream (bacteremia or fungemia) –> infections elsewhere, dental/surgical procedures, contaminated needles

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82
Q

Which valves are most commonly infected during infective endocarditis?

A

LEFT sided = Aortic and Mitral

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83
Q

Valves of which side of the heart are most commonly infected in IV drug users with infective endocarditis?

A

Valves of the right heart

84
Q

Vegetations seen in infective endocarditis can occasionally erode into the underlying myocardium and produce what?

A

Ring abscess

85
Q

Vegetations of IE are prone to embolization and abscess development from the infected embolic fragments can lead to what complications?

A
  • Septic infarcts
  • Mycotic aneursyms

- Pulmonary embolism (if right side valve infected)

86
Q

Microscopically, the vegetations of subacute IE typically exhibit what that is indicative of healing?

With time what else is seen?

A
  • Granulation tissue at their bases
  • With time = fibrosis, calcification, and chronic inflammatory infiltrate
87
Q

What is the clinical presentation (signs/sx’s) of infective endocarditis?

What may be heard upon auscultation in left-sided IE?

A
  • Rapidly developing fever + Chills
  • Weakness + Malaise
  • Left sided IE = MURMUR
88
Q

Which renal complication may occur within first few weeks of the onset of infective endocarditis?

A

Glomerulonephritis

89
Q

Early dx/tx of infective endocarditis has nearly eliminated some previously common immunologic phenomena of long-standing IE, such as what (list 4 of them)?

A
  • Splinter or subungal hemorrhages
  • Janeway lesions = nontender lesions on the palms or soles
  • Osler nodules = subcutaneous nodules in the pulp of digits
  • Roth spots = retinal hemorrhages in the eyes
90
Q

What is the etiology for each of these different forms of vegetative endocarditis from left to right?

A
  • RHD
  • IE
  • Nonbacterial thrombotic endocarditis (NBTE)
  • Libman-sacks endocarditis (LSE)
91
Q

Which type of endocarditis is characterized by deposition of small sterile vegetations along the lines of closure of the leaflets or cusps of cardiac valves?

A

Nonbacterial Thrombotic Endocarditis (NBTE)

92
Q

Although not invasive or inflammatory, NBTE can be a source of what?

A

Systemic emboli producing infarcts in brain, heart, or elsewhere

93
Q

NBTE is often encountered in which patients and is seen occuring concomitantly with what underlying conditions?

A
  • Debilitated pt’s such as those w/ cancer or sepsis
  • Occurs w/ DVT’s, pulmonary emboli, or findings of hypercoagulable state
94
Q

There is a striking association of NBTE with what malignancies?

A

Mucinous adenocarcinomas –> Trousseau syndrome

95
Q

Endocardial trauma, as from an indwelling catheter, is a well-recognized predisposing condition for what type of endocarditis?

A

NBTE

96
Q

Which type of endocarditis used to be a common findings in SLE pt’s until the use of steroids?

A

Libman-Sacks disease

97
Q

What is the morphology of the lesions like in Libman-Sacks endocarditis associated with SLE?

Which valves are most often involved?

A
  • Small, single or multiple, sterile, pink vegetations w/ warty (verrucous) appearance on either or both sides of valve leaflets
  • Mitral > Aortic
98
Q

Histologically how do the vegetations in Libman-Sack endocarditis appear?

Vegetations in this setting are often associated with intense?

A
  • Fine, granular, fibrinous eosinophilic material w/ cellular debris
  • Associated with intense vasculitis –> fibrinoid necrosis of valve
99
Q

Thrombotic heart valve lesions with sterile vegetations or rare fibrous thickening can occur in the setting of what disease that induces a hypercoagulable state?

A

Antiphospholipid syndrome

100
Q

Using the mnemonic CARCinoid, what are the manifestations of carcinoid syndrome?

A
  • Cutaneous flushing and dermatitis
  • Asthmatic wheezing (bronchoconstriction)
  • Right-sided valvular heart lesions
  • Cramping and diarrhea
101
Q

Cardiac lesions of carcinoid syndrome ususally only occur after there is a massive burden where?

A

Hepatic metastatic burden

102
Q

Which area of the heart is most often affected in Carcinoid Heart Disease?

A

RIGHT-sided endocardium and valves

103
Q

Urinary excretion of what correlates with the severity of the cardiac lesions in carcinoid heart disease?

A

5-HIAA

104
Q

What are the distinctive morphological features of the cardiac lesions seen in carcinoid heart disease?

Composed of smooth m. cells and sparse collagen fibers embedded in what?

A

- Glistening white intimal plaque-like thickening of the endocardial surfaces of the cardiac chambers and valve leaflets

  • Embedded in an acid mucopolysaccharide-rich matrix material
105
Q

What is the major complication associated with the use of mechanical prosthetic valves?

A

Thromboembolism –> thrombotic occlusion of the prosthesis or emboli released from thrombi formed on the valve

106
Q

Due to the major risk of thromboembolism associated with mechanical prosthetic valves, what long-term therapy must be given?

A

Long-term anti-coagulation tx

107
Q

Which type of prosthetic valve (mechanical or bioprostheses) almost always undergoes structural deterioration?

A

Almost ALL bioprostheses eventually become incompetent due to calcification and/or tearing

108
Q

Pt’s with mechanical prosthetic valves must be on long-term anticoagulant therapy to prevent thromboembolism, but this puts them at a risk of what complication?

A

Hemorrhagic stroke

109
Q

Infective endocarditis is a potentially serious complication associated with what type of prosthetic valve (mechanical or bioprostheses)?

A

Both :)

110
Q

Although the right side of the heart is most often affected by carcinoid tumors, how may the left side become involved?

A
  • Atrial or septal defects and right-to-left flow
  • Elicited by pulmonary carcinoid tumors
111
Q

The mechanism of heart failure in dilated cardiomyopathy (DCM) is an impairment in what?

A

Contractility (systolic dysfunction)

112
Q

The mechanism of heart failure in hypertrophic and restrictive cardiomyopathy is an impairment in what?

A

Compliance (diastolic dysfunction)

113
Q

Familial cases of dilated cardiomyopathy are linked to mutations in what gene?

Major inheritance pattern?

A
  • Mutations in TTN
  • Autosomal dominant
114
Q

X-linked forms of DCM may be due to mutations in which membrane-associated protein that is also seen mutated in the most common skeletal myopathies (i.e., Duchenne and Becker muscular dystrophies)?

A

Dystrophin

115
Q

Alcohol abuse is strongly associated with what cardiomyopathy?

What is the toxic agent(s)?

A
  • Dilated cardiomyopathy
  • Alcohol and acetaldehyde are directly toxic to myocardium
116
Q

Myocarditis can progress to what type of cardiomyopathy and is often associated with what virus?

A
  • Dilated cardiomyopthy
  • Coxsackie B
117
Q

Familial cases of DCM are due to mutations of genes encoding proteins of what 4 important cellular components/proteins?

A
  • Cytoskeleton
  • Sarcomere
  • Mitochondria
  • Nuclear envelope
118
Q

Which cardiotoxic drugs/substances are implicated in dilated cardiomyopathy?

A
  • Doxorubicin (chemotherapy drug)
  • Cobalt
119
Q

Pregnancy-associated HTN, volume overload, and nutritional deficiency may cause what type of cardiomyopathy?

When during pregnancy does it occur?

A
  • Special form of DCM = peripartum cardiomyopathy
  • Occurs late in pregnancy or up to few month post-partum
120
Q

What is the most common cardiac manifestation associated with iron-overload often seen in hereditary hemochromatosis or from multiple transfusions?

A

Dilated cardiomyopathy

121
Q

What are some of the underlying causes of supraphysiologic stress which can lead to DCM?

A
  • Persistent tachycardia, hyperthyroidism (ie Graves)
  • Fetuses of insulin-dependent diabetic mothers
  • Excess catecholamines –> pheochromocytomas, COCAINE, or vasopressors such as dopamine
  • Emotional duress –> takotsubo cardiomyopathy (aka “broken heart syndrome”)
122
Q

What are the common gross morphological features of DCM?

Which type of thrombi are common and valvular alterations?

A
  • Dilation of ALL chambers (enlarged, heavy, and flabby)
  • Mural thrombi are common
  • NO primary valvular alterations; functional regurgitation due to dilation may be present
123
Q

Takotsubo cardiomyopathy (aka “broken heart syndrome”) is due to the release of what?

A

Excess catecholamines following extreme emotional/physio. stress

124
Q

Dilated cardiomyopathy typically manifests during what ages?

Presents with signs/sx’s of what?

A
  • Age 20-50 yo
  • Slowly progressive signs/sx’s of CHF –> dyspnea, easy fatigability, and poor exertional capacity
125
Q

What serious complications are associated with dilated cardiomyopathy?

A
  • Thrombus 2’ to stasis –> embolism (stroke)
  • Arrhythmias –> sudden cardiac death
126
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) shows what characteristic gross morphology of the right ventricle?

A

Severely thinned wall, accompanied by extensive fatty infiltration and fibrosis

127
Q

Arrhythmogenic right ventricular cardiomyopathy leads to failure of what and is associated with what rhythm disturbances?

A
  • Right-ventricular failure
  • Ventricular tachycardia or fibrillation —> sudden death
128
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) has what inheritance pattern?

A

Autosomal dominant w/ variable penetrance

129
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a component of what syndrome?

What is seen in this disease?

Due to what mutation?

A
  • Naxos syndrome
  • Characterized by ARVC + hyperkeratosis of plantar palmar skin surfaces
  • Mutations in desmosome-associated protein plakoglobin
130
Q

Which type of cardiomyopathy has a 100% genetic cause?

A

Hypertrophic cardiomyopathy

131
Q

Is arrhythmogenic right ventricular cardiomyopathy (ARVC) considered inflammatory or non-inflammatory?

A

NON-inflammatory

132
Q

What is the most common cause of sudden, unexplained death in young athletes?

A

Hypertrophic Cardiomyopathy

133
Q

Which phase of the cardiac cycle is dysfunctional in Hypertrophic Cardiomyopathy?

A

Diastolic dysfunction

134
Q

How is the gross morphology and contractility of hypertrophic cardiomyopathy different from dilated cardiomyopathy?

A
  • Heart is thick-walled, heavy, and HYPERcontracting in HCM
  • Compared to flabby + HYPOcontracting heart in DCM
135
Q

Mutations in genes encoding which functional cellular proteins is most often implicated in Hypertrophic Cardiomyopathy?

Which is most common?

A

Sarcomeric proteins –> β-myosin heavy chain (most common)

136
Q

In hypertrophic cardiomyopathy, the poorly compliant left ventricular myocardium leads to abnormal diastolic filling and can lead to intermittent what?

A

Ventricular outflow obstruction

137
Q

Which cardiomyopathy is mostly associated with abnormal cytoskeletal proteins and can be conceptualized as a disease of abnormal force generation, force transmisson, or myocyte signaling?

A

Dilated Cardiomyopathy

138
Q

What is the essential morphological feature of Hypertrophic Cardiomyopathy?

A

Massive myocardial hypertrophy, usually W/O ventricular dilation

139
Q

In classic hypertrophic cardiomyopathy what is the disproportionate thickening that is seen?

A

Ventricular septum relative to left ventricle free wall, termed asymmetric septal hypertrophy

140
Q

What are the 3 most important histologic features of hypertrophic cardiomyopathy?

A
  1. Massive myocyte hypertrophy
  2. Haphazard disarray of bundles of myocytes = Myofiber disarray
  3. Interstitial and replacement fibrosis
141
Q

Central abnormality of hypertrophic cardiomyopathy is reduced ________ due to impaired diastolic filling

A

Stroke volume

142
Q

Due to compromised cardiac output and increased pulmonary congestion what type of dyspnea is seen pt’s with HCM?

What is heard on auscultation?

A
  • Exertional dyspnea
  • Harsh systolic ejection murmur on auscultation
143
Q

Due to the massive hypertrophy, high LV chamber pressure, and frequently thick-walled intramural arteries seen in HCM, there is often focal what?

A

Focal myocardial ischemia

144
Q

What are the major clinical problems associated with HCM?

A
  • Atrial fibrillation
  • Mural thrombus –> emboli (stroke)
  • Cardiac failure, ventricular arrhythmias and sudden death
145
Q

Reducing septal myocardial mass in HCM may be of some benefit and can be accomplished surgically or through carefully controlled septal infarction using what?

A

Catheter-based infusion of alcohol

146
Q

Restrictive cardiomyopathy is characterized by a primary decrease in the compliance of what, resulting in what impairment?

A

Decreased ventricular compliance = impaired ventricular filling during diastole

147
Q

What are 5 distinct diseases/processes affecting the myocardium which are associated with Restrictive Cardiomyopathy?

A
  • Radiation fibrosis
  • Amyloidosis
  • Sarcoidosis
  • Metastatic tumors
  • Inborn errors of metabolism
148
Q

What is the gross morphology of the ventricles and myocardium in Restrictive Cardiomyopathy?

What type of dilation is common?

A
  • Ventricles = normal sized
  • Myocardium = firm and noncompliant
  • BI-ATRIAL dilation is common
149
Q

Which restrictive condition is principally a disease of children and young adults in Africa and other tropical areas, characterized by fibrosis of the ventricular endocardium and subendocardium, often involving the atrial and mitral valve?

A

Endomyocardial fibrosis

150
Q

Loeffler endomyocarditis results in endomyocardial fibrosis, with large mural thrombi, and what systemic manifestations?

A
  • Peripheral eosinophilia
  • Eosinophilic infiltration in multiple organs
151
Q

Which toxic product released by eosinophils initiates endomyocardial necrosis –> scarring, thrombosis and organization of the thrombus in Loeffler Endomyocarditis?

A

Major basic protein

152
Q

Many pt’s with Loeffler Endomyocarditis have what type of underlying disorder?

Associated w/ chromosomal rearrangements involving what GF?

A
  • Myeloproliferative disorder
  • PDGFR-α or -β genes
153
Q

Which uncommon heart disease is most often seen in the first 2 years of life and is characterized by fibroelastic thickening of the LV endocardium?

A

Endocardial fibroelastosis

154
Q

Endocardial fibroelastosis may represent a common morphological end-point due to what 2 insults?

A
  • Viral infections (intrauterine exposure to mumps)
  • Mutations in gene for tafazzin
155
Q

What is the most commom cause of Myocarditis in the US?

A

Viral infections –> Coxsackie viruses A and B

156
Q

Inflammatory cytokines produced in response to myocardial injury causing myocardial dysfunction that is out of proportion to the degree of actual myocyte damage is characteristic of?

A

Myocarditis

157
Q

Most common helminthic disease associated with myocarditis?

A

Trichinella spiralis = Trichinosis

158
Q

Non-infectious causes of myocarditis are due to what conditions?

A
  • Hypersensitivity –> Post-strep (RF), SLE, drug hypersensitivity, and transplant rejection
  • Idiopathic –> Giant cell myocarditis
159
Q

What type of infiltrates are seen in Hypersensitivity Myocarditis?

A

Perivascular, composed of lymphocytes, macrophages, and high proportion of eosinophils

160
Q

Giant-cell myocarditis is characterized by widespread inflammatory infiltrates composed of?

A

Multinucleate giant cells + lymphocytes, eosinophils, plasma cells, and macrophages

161
Q

What is the distinct morphology of the myocarditis of Chagas disease?

A

Parasitization of scattered myofibers by trypanosomes w/ mixed inflammatory infiltrate (neutrophils, lymphocytes, macrophages, and some eosinophils)

162
Q

Clinical features of myocarditis can mimic what?

Late complication?

A
  • Can mimic acute MI
  • Late complication = Dilated Cardiomyopathy
163
Q

Which chemotherapeutic drugs are cardiotoxic and can cause myocardial disease?

A

Anthracyclines: doxorubicin and daunorubicin

164
Q

Amyloidosis results from the extracellular accumulation of protein fibrils which form?

A

Insoluble β-pleated sheets

165
Q

Amyloidosis of the heart can appear as a consequence of what 2 underlying conditions?

A
  • Systemic amyloidosis = myeloma or inflammation-assoc.
  • Restricted to heart of older pt’s w/ senile cardiac amyloidosis
166
Q

In senile cardiac amyloidosis the deposits are largely composed of what protein?

Normal function of this protein?

A

Transthyretin = transports thyroxin and retinol-binding protein

167
Q

Cardiac amyloidosis most frequently causes what type of cardiomyopathy when deposits are in the interstitium?

A

Restrictive cardiomyopathy

168
Q

Small, semitranslucent nodules resembling wax drippings seen on the atrial endocardial surface is characteristic of?

A

Cardiac amyloidosis

169
Q

How can the hyaline eosinophilic deposits of amyloid in the interstitium, conduction tissue, valves, endocardium, pericardium, and intramural coronary arteries be distinguished from other deposits?

A

Congo red stain –> apple-green birefringence

170
Q

Acute, rapidly developing fluid collections of 200-300 mL in the pericardial sac can cause what fatal complication?

A

Cardiac Tamponade

171
Q

Serous pericarditis is characteristically produced by what 5 non-infectious inflammatory diseases?

A
  • Rheumatic fever
  • SLE
  • Scleroderma
  • Tumors
  • Uremia
172
Q

What are the most frequent types of pericarditis?

A

Fibrinous and serofibrinous pericarditis

173
Q

What are the most common causes of Fibrinous and Serofibrinous pericarditis?

A
  • Acute MI
  • Postinfarction (Dressler) syndrome
  • Uremia
  • Chest radiation
  • RF, SLE, and trauma
174
Q

What are the common sx’s of fibrinous pericarditis?

Upon auscultation what’s heard?

A
  • Pain that is sharp, pleuritic, and position dependent
  • Fever
  • LOUD pericardial friction rub = most striking clinical finding
175
Q

Purulent or suppurative pericarditis reflecting an active infection is most often a result of microbial invasion via what 4 routes?

A
  • Direct extension from: empyema, lobar pneumonia, mediastinal infections, or ext. of ring abscess thru myocardium
  • Seeding from the blood
  • Lymphatic extension
  • Direct introduction during cardiotomy
176
Q

The intense inflammatory rxn of purulent or suppurative pericarditis eventually causes scarring and commonly leads to what?

A

Constrictive pericarditis

177
Q

The active phase of purulent/suppurative pericarditis can resemble that of fibrinous, but the sx’s differ how?

A

Marked systemic sx’s —> Spiking fevers and rigors

178
Q

Hemorrhagic pericarditis is most commonly caused by the spread of what?

A

Malignant neoplasm to the pericardial space

179
Q

Caseous pericarditis is of what origin until proven otherwise?

A

Tuberculosis

180
Q

In chronic/healing pericarditis, fibrosis in the form of mesh-like stringy adhesions completely obliterates the pericardial sac and is known as?

Effect on cardiac function?

A
  • Adhesive pericarditis
  • NO effect on cardiac function
181
Q

Adhesive mediastinopericarditis may follow infectious pericarditis, previous cardiac surgery, or mediastinal irradiation leading to what clinical findings/problems?

A
  • Strains cardiac function
  • Systolic retraction of rib cage and diaphragm
  • Pulsus paradoxus = ↓ systolic pressure upon inhalation
  • Increased cardiac workload may cause severe cardiac hypertrophy and dilation
182
Q

What are 3 signs of constrictive pericarditis?

A
  1. Distant or muffled heart sounds
  2. Elevated jugular venous pressure
  3. Peripheral edema
183
Q

What is the most common cardiac manifestation seen in Rheumatoid Arthritis?

May also see what in the myocardium, endocardium, valves, and aortic root?

A

- Fibrinous pericarditis

- Granulomatous rheumatoid nodules resembling the subcutaneous nodules

184
Q

Rheumatoid valvulitis can lead to what morphological changes of the valves?

A

Marked fibrous thickening + 2’ calcification of aortic valve cusps

185
Q

Myxomas may grow as what 2 distinct types of lesions?

Most often occur where in the heart?

A
  • Sessile or pedunculated
  • 90% in the ATRIA, most often LEFT-side; most common in fossa ovalis in the atrial septum
186
Q

Familial syndromes associated with myxomas are associated with what 2 genes and what are the associated syndromes?

A
  • GNAS1 encoding subunit of Gsα = McCune-Albright syndrome
  • PRKAR1A encoding subunit of cAMP-dependent kinase = Carney complex
187
Q

What is the clinical significance of the pedunculated form of Myxoma’s?

A
  • Often mobile and cause intermittent obstruction of AV valve during systole
  • May exert “wrecking ball” effect, damaging valve leaflets
188
Q

Major clinical manifestations of Myxomas are due to what and include?

A
  • Valvular “ball-valve” obstruction
  • Embolization
  • Constitutional sx’s = fever and malaise
189
Q

Which cytokine elabortated by Myxomas is responsible for the consititutional sx’s, such as fever and malaise?

A

IL-6

190
Q

Histologically myxomas are composed of what cells?

Which peculiar structures are characteritics findings?

A
  • Stellate or globular myxoma cells
  • Peculiar vessel-like or gland-like structures
191
Q

3 most common locations of lipomas in the heart?

A
  • Left ventricle
  • Right atrium
  • Atrial septum
192
Q

Which benign neoplasm of the heart is described as being “sea-anemone-like” lesions most often identified at autopsy, but may embolize and become clinically important?

A

Papillary Fibroelastoma

193
Q

Papillary fibroelastomas are usually found on what in the heart?

How do they appear morphologically?

A
  • 80% found on valves –> ventricular surface of semilunar valves
  • Distinctive cluster of hairlike projections up to 1 cm in length
194
Q

What is the most frequent primary tumor of the pediatric heart and is commonly discovered at what age?

A

Rhabdomyomas; discovered in first years of life

195
Q

50% of Rhabdomyomas are associated with mutations in what genes and disease?

A

TSC1 and TSC2 –> Tuberous Sclerosis

196
Q

What is the characteristic gross and histologic morphology of Rhabdomyomas?

Involve which part of the heart most often?

A
  • Gray-white masses; usually multiple and involve ventricle
  • Composed of bizarre, enlarged myocytes
  • “Spider” cells - thin strands of cytoplasm that stretch from nucleus to the surface membrane
197
Q

Rhabdomyomas are typically discovered due to what complication?

Prognosis?

A
  • Obstruction of valvular orifice or cardiac chamber
  • Often regress spontaneously
198
Q

The most frequent metastatic tumors involving the heart include what 4 types?

A
  • Carcinomas of the lungs and breast
  • Melanomas
  • Leukemias
  • Lymphomas
199
Q

Tumors in what 2 locations most often reach the heart by venous extension?

A
  • Renal cell carcinoma
  • Hepatic cell carcinoma
200
Q

What are 3 direct consequnces/effects on the heart caused by noncardiac neoplasms?

A
  • Pericardial and myocardial metastasis
  • Large vessel obstruction (i.e., Superior Vena Cava Syndrome)
  • Pulmonary tumor emboli
201
Q

What are 4 indirect consequences/effects on cardiac function produced by noncardiac neoplasms?

A
  • Nonbacterial thrombotic endocarditisi
  • Carcinoid heart disease
  • Pheochromocytoma-associated heart disease
  • Myeloma-associated amyloidosis
202
Q

Clinical sx’s associated with noncardiac neoplasms is most often associated with pericardial spread, which can cause what 2 complications?

A
  • Symptomatic pericardial effusions
  • Mass-effect sufficient enough to restrict cardiac filling
203
Q

What is the major complication associated with cardiac transplantation?

A

Allograft rejections; either cellular or Ab-mediated

204
Q

What is the single most important long-term limitation for cardiac transplantation?

A

Allograft arteriopathy = late, progressive, diffusely stenosing intimal proliferation

205
Q

Allograft arteriography in a cardiac transplant is a problem because it can lead to what complications?

A
  • Silent MI (transplant pt hearts are denervated, so no angina experienced)
  • Progressive CHF
  • Sudden cardiac death
206
Q

Which malignancy may arise in cardiac transplant recipient due to chronic T-cell immunosuppression?

A

EBV-associated B-cell lymphoma

CPR II Exam 1 (25 decks)

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