Ch283 Aortic Valve Disease Flashcards
(89 cards)
1
Q
Dominant cause of valvular heart disease in developing and low-income countries
A
Rheumatic fever
2
Q
T or F: Prevalence of valvular heart disease increases with age for both men and women.
A
True
3
Q
T or F: 80% of adult patients with symptomatic, valvular AS are female.
A
False.
MALE
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
5
Q
Conditions linked to development of calcific AS
A
- Vascular atherosclerosis
- Genetic polymorphisms (vitamin D receptor)
- Estrogen receptor in postmenopausal women
- Interleukin 10
- Apolipoprotein E4
- Familial
6
Q
Thickening and calcification of leaflets not severe enough to cause obstruction
A
Aortic valve sclerosis
7
Q
Most common congenital heart valve defect with 2-4:1 male-to-female predominance
A
Bicuspid aortic valve (BAV)
8
Q
Gene associated with the development of bicuspid aortic valve
A
NOTCH1 gene
9
Q
Causes of obstruction to left ventricular outflow
A
- Valvular AS
- Hypertrophic obstructive cardiomyopathy
- Discrete fibromuscular/membranous subaortic stenosis
- Supravalvular AS
Cardiac examination and 2D echo differentiates these
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)
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
12
Q
3 Cardinal symptoms of AS
A
- Exertional dyspnea
- Angina pectoris
- Syncope
13
Q
T or F: Orthopnea, PND and pulmonary edema occur during advanced stages of AS
A
True
14
Q
Physical finding in AS wherein the carotid arterial pulse rises slowly to a delayed peak
A
Pulsus parvus et tardus
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
16
Q
Etiologies of aortic stenosis
A
- Congenital (bicuspid, unicuspid)
- Degenerative calcific
- Rheumatic fever
- Radiation
17
Q
T or F: Fixed splitting of S2 is a cardiac finding in AS
A
False
Paradoxical splitting of S2
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
19
Q
Characteristics of the mumur in AS
A
- Low pitched
- Rough and rasping
- Loudest at the base of heart, most commonly in 2nd right ICS
- Atleast grade III/VI
20
Q
ECG findings that can be present in patients with AS
A
- LV hypertrophy
- ST segment depression
- T wave inversion (LV strain) in leads I, AVL, left precordial leads
21
Q
TTE key findings in AS
A
Thickening, calcification, reduced systolic opening of valve leaflets and LV hypertrophy
22
Q
Severity of AS according to aortic valve area
A
Severe AS: <1cm2
Moderate AS: 1 - 1.5cm2
Mild AS: 1.5 - 2cm2
23
Q
Uses of 2D echo in AS
A
- Identifying coexisting valvular abnormalities
- Differentiating valvular AS from other forms of LV ouflow obstruction
- Measurement of aortic root and proximal ascending aortic dimensions
24
Q
Chest Xray findings in AS
A
- May show no or little overall cardiac enlargement initially
- Rounding of cardiac apex in frontal projection and slight backward displacement in lateral view
- LV enlargement
- Pulmonary congestion
- Enlargement of LA, PA, right heart chambers
- Dilated proximal ascending aorta along the upper right heart border in frontal view
25
Role of catheterization in AS
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
26
Indication of coronary angiography in AS
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)
27
Death in AS
1. In severe AS: 7th-8th decades
2. Symptomatic px <4 years
3. Among with valvular AS : sudden death
28
Annual reduction in valve area, annual increase in peak jet velocity, and mean valve gradient in calcific AS
Annual reduction in valve area: 0.1cm2
Annual increase in peak jet velocity : 0.3meter/s
Mean valve gradient : 7mmHg
29
Medical treatment for AS
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
30
Indication for operation in AS
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)
31
Operation for aneurysm disease
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)
32
Operation for asymptomatic moderate or severe AS
For those that needs coronary artery bypass grafting surgery for which aortic valve replacement (AVR) should also be done
33
Relative indications for AVR in asymptomatic patients
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
34
T or F: Age is a contraindication to AVR for AS
False
Age alone not a contraindication
35
10 year survival rate of alder adult patients with AVR
60%
36
Complications of AVR
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
Involves replacement of the diseased aortic valve with autologous pulmonic valve and implantation of a homograft in the native pulmonic position
Ross procedure
Use has declined in US due to technical complexity of procedure and complications
38
Procedure preferable to operation in many children and young adults with congenital, noncalcific AS
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
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
Transcatheter aortic valve replacement (TAVR)
40
Preferred route for TAVR
Transfemoral route
Others: Trans-LV apical, subclavian, carotid, ascending aortic routes
41
T or F: 1 and 2 year survival rates are higher with TAVR compared with medical therapy (including PABV).
True
42
Complications of TAVR
1. Early hazard for stroke
| 2. Higher incidence of postprocedural, paravalvular AR (risk factor for mortality)
43
Etiologies of Aortic Regurgitation
Primary valve disease
Primary aortic root disease
Aortitis
Hypertension
44
Causes of AR in primary valve disease
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
Causes of AR in primary aortic root disease (aortic annular dilation)
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
T or F: Total stroke volume ejected by LV is increased in patients with AR.
True
47
Changes in LV in patients with AR
Dilation with eccentric hypertrophy
Allow LV to eject larger stroke volume without requiring any increase in relative shortening of each myofibril
48
Hemodynamic compensation for AR
Increase in LV end-diastolic volume (increased preload)
49
T or F: In AR, deterioriation of LV function precedes the development of symptoms
True
50
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.
True
Until the adaptive measures fail, where LV function deteriorates, end-diastolic volume rises further and SV and EF decline
51
On autopsy, hearts of these patients may be among the largest encountered, weighing >1000g
AR
52
State in which the LV preload and afterload are both increased
Chronic AR
53
Gradient from aorta to LV that drives the AR flow and falls during diastole
Reverse pressure gradient
54
Cause of myocardial ischemia in AR
Increased oxygen demand due to LV dilation and hypertrophy
Reduced blood and oxygen supply
55
T or F: 3/4 of patients with pure and predominant valvular AR are men
True
56
T or F: Among patients with primary valvular AR associated with mitral valve disease, most patients are women
True
57
The first symptom of diminished cardiac reserve
Exertional dyspnea
58
T or F: Anginal chest pain is uncommon in patients with severe AR
False
Anginal chest pain even in the absence of CAD may occur i patients with severe AR, even in younger patients
59
Arterial pulse in AR described as rapidly rising "water-hammer" pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole
Corrigan's pulse
60
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
Quincke's pulse
61
Booming "pistol-shot" heard over the femoral arteries
Traube's sign
62
To-and-fro murmur audible if the femoral artery is lightly compressed with a stet
Duroziez's sign
63
Characteristic of LV impulse in patients with chronic severe AR
Heaving and displaced laterally and inferiorly
64
T or F: Diastolic thrill in AR may be palpable along the left sternal border in thin-chested individuals
True
65
T or F: Prominent systolic thrill in AR may be palpable in suprasternal notch and transmitted upward along the carotid arteries
True
66
Auscultation in severe AR
1. aortic valve closure (A2) is usually absent
| 2. systolic ejection sound audible in patients with BAV dse with occ S4
67
Murmur of chronic AR
1. High pitched
2. Blowing
3. Decrescendo
4. Diastolic
5. Heard best in 3rd intercostal space along the left sternal border
68
Maneuver to listen to the murmur of AR
Heard best with diaphragm of stethoscope
Patient sitting up, leaning forward, with breath held in forced expiration
69
LOCATION of mumur in AR caused by primary valvular disease
Diastolic murmur usually louder along the LEFT STERNAL BORDER than the right
70
ETIOLOGY of AR if murmur is heard best along the RIGHT sternal border
Aneurysmal dilation of the aortic root
71
Description of mumur in AR suggesting eversion of aortic cusp vibrating in regurgitant stream
"cooing" or musical diastolic murmur
72
T or F: Mid-systolic ejection murmur is possible in isolated AR.
True
Heard best at base of heart and transmitted along the carotid arteries. Quite loud.
73
Third murmur heard in patients with severe AR described as soft, low-pitched rumbling mid-to-late diastolic murmur
Austin Flint murmur
74
ECG findings in AR
1. LVH
2. ST segment depression
3. T wave inversions (I, AVL, V5, V6)
75
Characteristic finding for AR in 2D echo
Rapid, high-frequency diastolic fluttering of the anterior mitral leaflet produced by the impact of the regurgitant jet
76
Use of 2D ehco for AR
1. Determines the cause of AR
2. Detect dilation of aortic annulus and root
3. Aortic dissection
4. Primary leaflet pathology
77
Cornerstone of longitudinal follow-up and allows for the early detection of changes in LV size and/or function
Surveillance transthoracic echocardiography
78
Drugs used in treatment of acute severe AR
1. IV diuretics
| 2. Vasodilators (sodium nitroprusside)
79
T or F: Operation is indicated urgently in acute severe AR
True
Surgery is the treatment of choice usually necessary within 24h of diagnosis
80
Procedure contraindicated in acute severe AR
Intraaortic balloon counterpulsation
81
Drug avoided so as not to reduce the CO further or slow the heart rate, thus allowing more time for diastolic filling of LV
Beta blockers
82
Drugs for chronic aortic regurgitation
1. Diuretics
| 2. Vasodilators (ACE inhibitors, dihydropyridine calcium channel blockers, hydralazine)
83
Target systolic BP for AR
<140mmHg
Systolic BP should be controlled
84
Excellent first choice of antihypertensive agent in AR
Vasodilators
85
Retard the rate of aortic root enlargement in young patients with Marfan's syndorme and aortic root dilation
Beta blockers
| ARB (Losartan)
86
Guide in the proper timing of surgery in AR
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
In chronic severe AR, when should follow-up and noninvasive testing with echocardiography be done?
6 to 12-month intervals
88
T or F: Operation in AR should be urgent once detected even on asymptomatic patients.
False
Can be deferred as long as the patient both remains asymptomatic and retains normal LV function without severe chamber dilation
89
Indicated for the treatment of severe AR in symptomatic patients irrespectvie of LV function
AVR
