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HPIM Cardio > Ch283 Aortic Valve Disease > Flashcards

Ch283 Aortic Valve Disease Flashcards

1
Q

Dominant cause of valvular heart disease in developing and low-income countries

A

Rheumatic fever

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2
Q

T or F: Prevalence of valvular heart disease increases with age for both men and women.

A

True

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3
Q

T or F: 80% of adult patients with symptomatic, valvular AS are female.

A

False.

MALE

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4
Q

In adults, due to degenerative calcification of the aortic cusps; however occurs most commonly on congenital disease (bicuspid aortic valve), chronic (trileaflet) deterioration, or prev rheumatic inflammation

A

Aortic stenosis

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5
Q

Conditions linked to development of calcific AS

A
  1. Vascular atherosclerosis
  2. Genetic polymorphisms (vitamin D receptor)
  3. Estrogen receptor in postmenopausal women
  4. Interleukin 10
  5. Apolipoprotein E4
  6. Familial
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6
Q

Thickening and calcification of leaflets not severe enough to cause obstruction

A

Aortic valve sclerosis

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7
Q

Most common congenital heart valve defect with 2-4:1 male-to-female predominance

A

Bicuspid aortic valve (BAV)

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8
Q

Gene associated with the development of bicuspid aortic valve

A

NOTCH1 gene

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9
Q

Causes of obstruction to left ventricular outflow

A
  1. Valvular AS
  2. Hypertrophic obstructive cardiomyopathy
  3. Discrete fibromuscular/membranous subaortic stenosis
  4. Supravalvular AS

Cardiac examination and 2D echo differentiates these

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10
Q

Defines severe obstruction to LV outflow

A

Mean systolic pressure gradient >40mmHg with normal CO or

An effective aortic orifice area of approx <1 cm2 (approx <0.6cm2/m2 bsa in normal sized adult)

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11
Q

T or F: Severe AS may exist for many years without producing any symptoms.

A

True

Due to the ability of the hypertrophied LV to generate the elevated intraventricular pressures required to maintain a normal stroke volume

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12
Q

3 Cardinal symptoms of AS

A
  1. Exertional dyspnea
  2. Angina pectoris
  3. Syncope
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13
Q

T or F: Orthopnea, PND and pulmonary edema occur during advanced stages of AS

A

True

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14
Q

Physical finding in AS wherein the carotid arterial pulse rises slowly to a delayed peak

A

Pulsus parvus et tardus

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15
Q

T or F: A systolic thrill may be present in AS at the base of the heart to the right of sternum when leaning forward or in suprasternal notch

A

True

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16
Q

Etiologies of aortic stenosis

A
  1. Congenital (bicuspid, unicuspid)
  2. Degenerative calcific
  3. Rheumatic fever
  4. Radiation
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17
Q

T or F: Fixed splitting of S2 is a cardiac finding in AS

A

False

Paradoxical splitting of S2

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18
Q

Murmur of AS

A

Ejection (mid) systolic murmur that commences shortly after S1, increases in intensity to reach a peak toward the middle ejection, and ends just before aortic valve closure

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19
Q

Characteristics of the mumur in AS

A
  1. Low pitched
  2. Rough and rasping
  3. Loudest at the base of heart, most commonly in 2nd right ICS
  4. Atleast grade III/VI
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20
Q

ECG findings that can be present in patients with AS

A
  1. LV hypertrophy
  2. ST segment depression
  3. T wave inversion (LV strain) in leads I, AVL, left precordial leads
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21
Q

TTE key findings in AS

A

Thickening, calcification, reduced systolic opening of valve leaflets and LV hypertrophy

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22
Q

Severity of AS according to aortic valve area

A

Severe AS: <1cm2
Moderate AS: 1 - 1.5cm2
Mild AS: 1.5 - 2cm2

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23
Q

Uses of 2D echo in AS

A
  1. Identifying coexisting valvular abnormalities
  2. Differentiating valvular AS from other forms of LV ouflow obstruction
  3. Measurement of aortic root and proximal ascending aortic dimensions
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24
Q

Chest Xray findings in AS

A
  1. May show no or little overall cardiac enlargement initially
  2. Rounding of cardiac apex in frontal projection and slight backward displacement in lateral view
  3. LV enlargement
  4. Pulmonary congestion
  5. Enlargement of LA, PA, right heart chambers
  6. Dilated proximal ascending aorta along the upper right heart border in frontal view
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25
Q

Role of catheterization in AS

A

General: Not frequently done but can be useful when there is discrepancy between the clinical and noninvasive findings

  1. Patients with multivalvular disease in whom the role played by each valvular deformity should be defined to aid planning of operative treatment
  2. Young, asymptomatic patients with noncalcific congenital AS to define severity of obstruction to LV outflow because operation or percutaneous aortic balloon valvuloplasty (PABV) may be indicated
  3. Patients in whom it is suspected that the obstruction to LV outflow may not be at the level of the aortic valve but rather sub or supravalvular level
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26
Q

Indication of coronary angiography in AS

A

To screen for CAD in appropriate patients with severe AS who are being considered for surgery.

(Incidence of CAD needing bypass grafting exceeds 50% during aortic valve replacement)

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27
Q

Death in AS

A
  1. In severe AS: 7th-8th decades
  2. Symptomatic px <4 years
  3. Among with valvular AS : sudden death
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28
Q

Annual reduction in valve area, annual increase in peak jet velocity, and mean valve gradient in calcific AS

A

Annual reduction in valve area: 0.1cm2
Annual increase in peak jet velocity : 0.3meter/s
Mean valve gradient : 7mmHg

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29
Q

Medical treatment for AS

A
  1. Severe AS: strenous physical activity and competitive sports should be avoided, even if asymptomatic
  2. Beta blockers and ACE inhibitors as treatment for HPN or CAD asymptomatic px with preserved LV systolic funtion
  3. Nitroglycerin for angina
  4. HMG-COA reductase inhibitors for degenerative calcific AS as treatment and prevention of ASCVD events
  5. Endocarditis prophylaxis only for AS patients with prior history of endocarditis
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30
Q

Indication for operation in AS

A
  1. Severe AS (valve area: <1cm2 or 0.6cm2/m2 bsa) who are symptomatic [CLASS 1 indication]
  2. Exhibit LV systolic dysfunction (EF <50%)
  3. BAV disease
  4. Aneurysmal root or ascending aorta (maximal dimension >5.5cm)
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31
Q

Operation for aneurysm disease

A

Recommended at smaller aortic diameters (4.5-5.0cm) for px with family history of aortic catastrophe and those who exhibit rapid aneurysm growth (>0.5cm/year)

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32
Q

Operation for asymptomatic moderate or severe AS

A

For those that needs coronary artery bypass grafting surgery for which aortic valve replacement (AVR) should also be done

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33
Q

Relative indications for AVR in asymptomatic patients

A
  1. Abnormal response to treadmill exercise
  2. Rapid progression of AS
  3. Very severe AS (aortic vlave jet velocity >5 meter/s or mean gradient >60mmHg and low operative risk
  4. Excessive LV hypertrophy in absence of systemic hypertension
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34
Q

T or F: Age is a contraindication to AVR for AS

A

False

Age alone not a contraindication

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35
Q

10 year survival rate of alder adult patients with AVR

A

60%

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36
Q

Complications of AVR

A
  1. Primary valve failure : Re-replacement occurring in 30% of bioprosthetic valves in 10 years
  2. Hemorrhagic complications : In mechanical prostheses as consequence of vitamin K antagonists
37
Q

Involves replacement of the diseased aortic valve with autologous pulmonic valve and implantation of a homograft in the native pulmonic position

A

Ross procedure

Use has declined in US due to technical complexity of procedure and complications

38
Q

Procedure preferable to operation in many children and young adults with congenital, noncalcific AS

A

Percutaneous aortic balloon valvuloplasty (PABV)

Not for calcific AS : Due to very high restenosis rate (80% in 1 year)

Done routinely as part of the TAVR procedure

39
Q

Treatment of AS in prohibitive or high-surgical risk adult patients using one of two available systems, a balloon expandable valve and self expanding valve, both of which incorporate a pericardial prosthesis

A

Transcatheter aortic valve replacement (TAVR)

40
Q

Preferred route for TAVR

A

Transfemoral route

Others: Trans-LV apical, subclavian, carotid, ascending aortic routes

41
Q

T or F: 1 and 2 year survival rates are higher with TAVR compared with medical therapy (including PABV).

42
Q

Complications of TAVR

A
  1. Early hazard for stroke

2. Higher incidence of postprocedural, paravalvular AR (risk factor for mortality)

43
Q

Etiologies of Aortic Regurgitation

A

Primary valve disease
Primary aortic root disease
Aortitis
Hypertension

44
Q

Causes of AR in primary valve disease

A
  1. Rheumatic in origin
  2. Congenital defects
  3. Infective endocarditis
  4. Syphilis / Ankylosing spondylitis
  5. Traumatic rupture or avulsion of aortic cusp (Uncommon but most frequent serious lesion)
45
Q

Causes of AR in primary aortic root disease (aortic annular dilation)

A
  1. Medial degeneration of ascending aorta (Marfan syndrome)
  2. idiopathic
  3. annuloaortic ectasia
  4. osteogenesis imperfecta
  5. severe, chronic HPN
  6. aortic dissection
  7. Syphilis / Ankylosing spondylitis
46
Q

T or F: Total stroke volume ejected by LV is increased in patients with AR.

47
Q

Changes in LV in patients with AR

A

Dilation with eccentric hypertrophy

Allow LV to eject larger stroke volume without requiring any increase in relative shortening of each myofibril

48
Q

Hemodynamic compensation for AR

A

Increase in LV end-diastolic volume (increased preload)

49
Q

T or F: In AR, deterioriation of LV function precedes the development of symptoms

50
Q

T or F: Severe AR may occur with normal effective forward stroke volume and normal LVEF together with elevated LV end-diastolic pressure and volume.

A

True

Until the adaptive measures fail, where LV function deteriorates, end-diastolic volume rises further and SV and EF decline

51
Q

On autopsy, hearts of these patients may be among the largest encountered, weighing >1000g

52
Q

State in which the LV preload and afterload are both increased

A

Chronic AR

53
Q

Gradient from aorta to LV that drives the AR flow and falls during diastole

A

Reverse pressure gradient

54
Q

Cause of myocardial ischemia in AR

A

Increased oxygen demand due to LV dilation and hypertrophy

Reduced blood and oxygen supply

55
Q

T or F: 3/4 of patients with pure and predominant valvular AR are men

56
Q

T or F: Among patients with primary valvular AR associated with mitral valve disease, most patients are women

57
Q

The first symptom of diminished cardiac reserve

A

Exertional dyspnea

58
Q

T or F: Anginal chest pain is uncommon in patients with severe AR

A

False

Anginal chest pain even in the absence of CAD may occur i patients with severe AR, even in younger patients

59
Q

Arterial pulse in AR described as rapidly rising “water-hammer” pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole

A

Corrigan’s pulse

60
Q

Capillary pulsation, an alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail

A

Quincke’s pulse

61
Q

Booming “pistol-shot” heard over the femoral arteries

A

Traube’s sign

62
Q

To-and-fro murmur audible if the femoral artery is lightly compressed with a stet

A

Duroziez’s sign

63
Q

Characteristic of LV impulse in patients with chronic severe AR

A

Heaving and displaced laterally and inferiorly

64
Q

T or F: Diastolic thrill in AR may be palpable along the left sternal border in thin-chested individuals

65
Q

T or F: Prominent systolic thrill in AR may be palpable in suprasternal notch and transmitted upward along the carotid arteries

66
Q

Auscultation in severe AR

A
  1. aortic valve closure (A2) is usually absent

2. systolic ejection sound audible in patients with BAV dse with occ S4

67
Q

Murmur of chronic AR

A
  1. High pitched
  2. Blowing
  3. Decrescendo
  4. Diastolic
  5. Heard best in 3rd intercostal space along the left sternal border
68
Q

Maneuver to listen to the murmur of AR

A

Heard best with diaphragm of stethoscope

Patient sitting up, leaning forward, with breath held in forced expiration

69
Q

LOCATION of mumur in AR caused by primary valvular disease

A

Diastolic murmur usually louder along the LEFT STERNAL BORDER than the right

70
Q

ETIOLOGY of AR if murmur is heard best along the RIGHT sternal border

A

Aneurysmal dilation of the aortic root

71
Q

Description of mumur in AR suggesting eversion of aortic cusp vibrating in regurgitant stream

A

“cooing” or musical diastolic murmur

72
Q

T or F: Mid-systolic ejection murmur is possible in isolated AR.

A

True

Heard best at base of heart and transmitted along the carotid arteries. Quite loud.

73
Q

Third murmur heard in patients with severe AR described as soft, low-pitched rumbling mid-to-late diastolic murmur

A

Austin Flint murmur

74
Q

ECG findings in AR

A
  1. LVH
  2. ST segment depression
  3. T wave inversions (I, AVL, V5, V6)
75
Q

Characteristic finding for AR in 2D echo

A

Rapid, high-frequency diastolic fluttering of the anterior mitral leaflet produced by the impact of the regurgitant jet

76
Q

Use of 2D ehco for AR

A
  1. Determines the cause of AR
  2. Detect dilation of aortic annulus and root
  3. Aortic dissection
  4. Primary leaflet pathology
77
Q

Cornerstone of longitudinal follow-up and allows for the early detection of changes in LV size and/or function

A

Surveillance transthoracic echocardiography

78
Q

Drugs used in treatment of acute severe AR

A
  1. IV diuretics

2. Vasodilators (sodium nitroprusside)

79
Q

T or F: Operation is indicated urgently in acute severe AR

A

True

Surgery is the treatment of choice usually necessary within 24h of diagnosis

80
Q

Procedure contraindicated in acute severe AR

A

Intraaortic balloon counterpulsation

81
Q

Drug avoided so as not to reduce the CO further or slow the heart rate, thus allowing more time for diastolic filling of LV

A

Beta blockers

82
Q

Drugs for chronic aortic regurgitation

A
  1. Diuretics

2. Vasodilators (ACE inhibitors, dihydropyridine calcium channel blockers, hydralazine)

83
Q

Target systolic BP for AR

A

<140mmHg

Systolic BP should be controlled

84
Q

Excellent first choice of antihypertensive agent in AR

A

Vasodilators

85
Q

Retard the rate of aortic root enlargement in young patients with Marfan’s syndorme and aortic root dilation

A

Beta blockers

ARB (Losartan)

86
Q

Guide in the proper timing of surgery in AR

A
  1. Patients with chronic severe AR usually do not become symptomatic until AFTER the development of myocardial dysfunction
  2. When delayed too long (>1 year from onset of symptoms or LV dysfunction), surgical treatment often does not restore normal LV function
87
Q

In chronic severe AR, when should follow-up and noninvasive testing with echocardiography be done?

A

6 to 12-month intervals

88
Q

T or F: Operation in AR should be urgent once detected even on asymptomatic patients.

A

False

Can be deferred as long as the patient both remains asymptomatic and retains normal LV function without severe chamber dilation

89
Q

Indicated for the treatment of severe AR in symptomatic patients irrespectvie of LV function

HPIM Cardio (10 decks)

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