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Mayo Cardiology Core Competencies > Track 7: Valvular general approach and guidelines > Flashcards

Track 7: Valvular general approach and guidelines Flashcards

1
Q

Stages of valvular heart disease

A
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2
Q

Patient with risk factors for development of VHD

A

Stage A

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3
Q

Patient with progressive VHD (mild to moderate severity and asx

A

Stage B

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4
Q

Asx patient with severe VHD in whom the LV or RV remains compensated

Asx patient with severe VHD with decompensation of the LV or RV

A

Stage C1

Stage C2

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5
Q

What is the difference between VHD stage C1 and stage C2

A

Both have severe VHD and are asx
C1 LV and RV remain compensated
C2 decompensation of LV and RV

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6
Q

What is the difference between VHD stage C and stage D

A

Stage C are asx severe
Stage D are sx severe

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7
Q

Patients who have developed sxs as a result of severe VHD

A

Stage D

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8
Q

Outline the stages of VHD A-D with one line descriptors

A

A: At risk
B: Progressive
C: Asx severe
D: Symptomatic severe

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9
Q

Key TTE measurements for stenotic lesions

A
  • Max velocity
  • Mean gradient
  • Valve area
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10
Q

Key TTE measurements for regurgitant lesions

A

Calculation of regurgitant orifice area, volume, and fraction
Color doppler imaging

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11
Q

Surveillance TTE in progressive (Stage B) AS

Surveillance TTE in severe asx (Stage C1) AS

A
  • Every 3-5 years (mild severity, Vmax 2.0-2.9 m/s)
  • Every 1-2 years (moderate severity, Vmax 3.0-3.9 m/s)
  • C1: Every 6-12 months (Vmax ≥ 4 m/s)
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12
Q

Surveillance TTE in progressive (Stage B) AR

Surveillance TTE in Severe asx (Stage C1) AR

A
  • Every 3-5 years (mild severity)
  • Every 1-2 years (moderate severity)

-C1: Every 6-12 months
- C1, dilating LV: more frequently

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13
Q

Surveillance TTE in progressive (Stage B) MS

Surveillance TTE in severe asx (Stage C1) MS

A
  • Every 3-5 years (MV area > 1.5cm2)

-C1: Every 1-2 years (MV area 1.0-1.5 cm2)
-C1: Every year (MV area < 1.0 cm2)

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14
Q

Surveillance TTE in progressive (Stage B) MR

Surveillance TTE in severe asx (Stage C1) MR

A
  • Every 3-5 years (mild severity)
  • Every 1-2 years (moderate severity)

-C1: every 6-12 months
-C1, dilating LV: more frequently

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15
Q

Risk of developing IE is highest in what populations?

A
  • Prosthetic valve
  • Prior IE
  • Congenital heart disease with residual flow disturbance
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16
Q

VKA verus DOAC in concomitant VHD and AF

A

VKA:
- Rheumatic MS
- Mechanical valve
- Bioprosthetic valve < 3 months ago

DOAC alternative:
- Bioprosthetic ≥ 3 months ago
- Native VHD (excluding rheumatic MS)

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17
Q

Postoperative AF after VHD intervention is associated with increased stroke and mortality irrespective of

A

CHA2DS2VASc score

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18
Q

MC complication early after surgical valve replacement is

A

Postoperative AF

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19
Q

Prevalence and timeline of postoperative AF after surgical valve replacement

A

Occurs in up to 1/3 of patients within 3 months of surgery

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20
Q

Name some of the possible complications after valve replacement surgery (8)

A
  • # 1 postoperative AF
  • Stroke
  • Vascular and bleeding complications
  • Pericarditis
  • Heart block requiring temporary or permanent pacing (especially after AVR)
  • HF
  • Renal dysfunction
  • Infection
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21
Q

Name some of the possible complications after transcatheter valvular intervention (5)

A
  • Permanent pacing need
  • Paravalvular leak
  • Stroke
  • Vascular complications
  • Residual valve dysfunction
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22
Q

Hemodynamic severity for AS is best calculated by

A
  • Transaortic max velocity
  • Mean pressure gradient
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23
Q

Stage A AS

A

**At risk of AS **

  • BAV, other congenital valve anomaly, aortic valve sclerosis
  • Aortic Vmax <2 m/s, normal leaflet motion
  • No hemodynamic consequences
  • No sxs
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24
Q

Stage B AS

A

Progressive AS

  • Mild-mod leaflet calcification/fibrosis of bicuspid or trileaflet valve w/ some reduction in systolic motion OR rheumatic valve changes with comissural fusion
  • Mild AS: Aortic vmax 2.0-2.9 m/s or mean gradient < 20 mmHg
  • Moderate AS: Aortic Vmax 3.0-3.9 m/s or mean gradient 20-39 mmHg
  • Early LV diastolic dysfunction may be present
  • Normal LVEF
  • Asx
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25
Q

Stage C1 AS

A

Asx severe AS

  • Severe leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet opening
  • Vmax ≥ 4 m/s or mean gradient ≥ 40
  • AVA typically ≤ 1.0 cm2
  • Very severe AS if Vmax ≥ 5 m/s or mean gradient ≥ 60 mmHg
  • LV diastolic dysfunction
  • Mild LVH
  • Normal LVEF
  • Asx
    *Exercising testing reasonable to confirm sx status
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26
Q

Severe versus very severe AS

A

Severe: Vmax ≥ 4 m/s, mean gradient ≥ 40 mmHg

Very severe: Vmax ≥ 5 m/s, mean gradient ≥ 60 mmHg

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27
Q

Stage C2 AS

A

Asx severe AS with LV systolic dysfunction

  • Severe leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet opening
  • V max ≥ 4 m/s or mean gradient ≥ 40 mmHg
    AVA typically ≤ 1 cm2
  • LVEF < 50%
  • Asx
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28
Q

Stage D1 AS

A

Symptomatic severe high-gradient AS

  • Severe leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet opening
  • Vmax ≥ 4 m/s, mean gradient ≥ 40 mmHg, AVA typically ≤ 1 cm2 (may be larger w/ mixed AS/AR)
  • LV diastolic dysfunction, LVH, pulmonary hypertension possible
  • DOE, HF, angina, syncope, presyncope
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29
Q

Stage D2 AS

A

Symptomatic severe low-flow, low-gradient AS with reduced LVEF

  • Severe leaflet calcification/fibrosis with severely reduced leaflet motion
  • AVA ≤ 1.0 cm2, V max < 4 m/s, mean gradient < 40 mmHg
  • Dubotamine stress TTE shows AVA < 1.0 cm2, with v max ≥ 4 m/s at any flow rate
  • LV diastolic dysfunction, LVH, LVEF < 50%
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30
Q

Stage D3 AS

A

*Symptomatic severe low-gradient AS with normal LVEF or paradoxical low-flow severe AS**

  • Severe leaflet calcification/fibrosis with severely reduced leaflet motion
  • AVA ≤ 1.0 cm2, V max < 4 m/s, mean gradient < 40 mmHg
    AND
  • Stroke volume index < 35 mL
  • Increased LV wall thickness, small LV chamber with low stroke volume, restrictive diastolic filling, LVEF ≥ 50%
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31
Q

Stage D3 (suspected low flow, low gradient severe AS with normal LVEF), optimization of what should be achieved before further workup to assess AS?
Class I

A

Blood pressure

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32
Q

Stage D2 AS (low flow, low gradient, severe AS w/ reduced LVEF).
What test can be performed to help further define severity/assess contractile reserve?

A

Dobutamine stress test with echocardiographic or invasive hemodynamic measurements

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33
Q

What factor may cause measurements of AS severity to be underestimated

A

If the patient is hypertensive
(systemic hypertension imposes a second pressure load on the LV)

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34
Q

Medial therapy for AS stage A, stage B, stage C

A

GDMT HTN management (ACE/ARB if tolerated)
Class I

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35
Q

Calcific AS medical therapy

A

Statin
Class I

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36
Q

After TAVI, what med may reduce long0term risk of all cause mortality 2b

A

ACE/ARB

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37
Q

Statin role in calcific AS

A

Concurrent CAD common. All should be screened and treated for HLD (no data to support prevention of progression of AS but may reduce ischemic events)

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38
Q

Name the 5 class I indications for AVR

Name the 4 2a indications

A

Class I
- Stage D1 (Symptomatic severe high gradient AS)
- Stage C2 (Axs, severe AS, LVEF < 50%)
- Stage C1 (Asx severe) AND undergoing cardiac surgery
- Stage D2 (Symptomatic low flow, low gradient severe AS w/ reduced LVEF)
- Stage D3 (Symptomatic low flow, low gradient severe AS w/ normal LVEF) IF AS most likely cause of sxs

2a
- Stage C1 (asx severe) and low surgical risk, reasonable when an exercise test demonstrates decreased tolerance or a fall in systolic BP ≥ 10 mmHg from baseline to peak exercise
- Asx with very severe AS (Vmax ≥ 5 m/s) and low surgical risk
- Stage C1 (asx, severe) and low surgical risk, when BNP is > 3x normal
- Stage C1 (asx, severe) and low surgical risk, AVR reasonable when serial testing shows increase in Vmax ≥ .3m/s per year

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39
Q

Most common presenting initial sx of AS

A

Exertional dyspnea or decreased exercise tolerance

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40
Q

Severe asx AS (stage C)
If Vmax ≥ 4.0 m/s or mean pressure gradient ≥ 40 mmHg, when is mean onset of symptoms

A

2-5 years

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41
Q

Age and AVR recommendations (2a)

A

< 50 yo and no contraindication to anticoagulation, mechanical reasonable

50-65 shared decision making

> 65 yo bioprosthetic reasonable

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42
Q

Likelihood of aortic bioprosthetic structural deterioration at 15-20 years based on age
>65
<50
40
20

A

> 65 yo, <10%

< 50 yo, 22%

40 yo, 30%

20 yo, 50%

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43
Q

Severe AS
< 65 yo
Life expectancy > 20 years

A

SAVR

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44
Q

Severe AS
65-80 yo
No anatomic contraindication to transfemoral access

A

TAVI or SAVR

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45
Q

Symptomatic severe AS
> 80 yo OR life expectancy < 10 years

A

TAVI

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46
Q

Asx severe AS
LVEF < 50%
≤ 80 yo

A

TAVI or SAVR

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47
Q

Asx severe AS
Abnormal exercise test, very severe AS, rapid progression, or elevated BNP

A

SAVR recommended over TAVI

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48
Q

Age < 65
SAVR or TAVI

A

SAVR

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49
Q

Name some of the benefits associated with TAVI and with SAVR

A

TAVI
- Slightly lower mortality rate
- Lower risk of stroke
- Shorter hospital length of stay
- More rapid return to normal activities
- Lower risk of transient or permanent AF
- Less bleeding
- Less pain
*downside to TAVI, durability of transcatheter valves beyond 5-6 years is not yet known

SAVR
- Lower risk or paravalvular leak
- Less need for valve reintervention
- Less need for permanent pacemaker

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50
Q

Name some causes of acute AR

A
  • Endocarditis
  • Aortic dissection
  • Iatrogenic
  • Blunt chest trauma
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51
Q

Tx plan for acute severe MR

A
  • Medical therapy to reduce afterload (nitroprusside)
  • Ultimately surgery
    *IABP contraindicated
    *BB to be used with extreme caution (may be beneficial if d/t dissection but in any other acute cause of AR they will block the compensatory tachycardia and prolong diastolic period and therefore degree of regurgitation and could precipitate a marked reduction in blood pressure)
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52
Q

Describe the role of beta blockers in acute severe AR

A

BB to be used with extreme caution (may be beneficial if d/t dissection but in any other acute cause of AR they will block the compensatory tachycardia and prolong diastolic period and therefore degree of regurgitation and could precipitate a marked reduction in blood pressure)

53
Q

MC causes of chronic AR

A

BAV disease
- Primary diseases of the ascending aorta or the sinuses of Valsalva

  • (rheumatic heart disease in low-middle income countries)
  • Calcific disease regurgitation often accompanies AS but degree of AR is usually mild to mod
54
Q

At risk of AR
BAV, AV sclerosis, disease of aortic sinuses or ascending aorta, hx of rheumatic fever or known rheumatic heart disease, IE

A

Stage A

55
Q

Define mild AR

A
  • Jet width < 25% of LVOT
  • Vena contacta < .3 cm
  • Regurgitant volume < 30 mL/beat
  • Regurgitant fraction < 30%
  • ERO < .1 cm2
  • Angiography grade 1
  • Normal LV systolic function
  • Normal LV volume or mild LV dilation
56
Q

Define moderate AR

A
  • Jet width 25-64% of LVOT
  • Vena contracta .3-.6 cm
  • Regurgitant volume 30-59 mL/beat
  • Regurgitant fraction 30%-49%
  • ERO .1-.29 cm2
  • Angiography grade 2
  • Normal LV systolic function
  • Normal LV volume or mild LV dilation
57
Q

Define severe AR

A
  • Jet width ≥ 65% of LVOT
  • Vena contracta > .6 cm
  • Holodiastolic flow reversal in proximal abdominal aorta
  • Regurgitant volume ≥ 60 mL/beat
  • Regurgitant fraction ≥ 50%
  • ERO ≥ .3 cm2
  • Angiography garde 3 to 4
  • Evidence of LV dilation
58
Q

Outline difference between asymptomatic severe AR stage C1 and stage C2

A

C1: Normal LVEF (>55%) and mild to moverate LV dilation (LVESD < 50 mm)

C2: Abnormal LV systolic function and depressed LVEF (≤ 55%), severe LV dilation (LVESD >50 mm or indexed LVESD > 25 mm/m2)

59
Q

For severe AR, what are the key values for EF and LVESD

A

EF < 55%
LVESD > 50 mm

60
Q

Medical therapy in chronic AR

A
  • In asx with chronic AR (stages B and C), tx HTN if SBP > 140 mmHg
  • Severe AR w/ sxs and/or LV systolic dysfunction (stages C2 and D) but a prohibitive surgical risk, GDMT for reduced LVEF with ACE/ARB and/or sacubitril/valsartan
61
Q

Name the 3 class I indications for AVR (in chronic AR)

Class 2a indications?

A
  1. Symptomatic severe AR (stage D) (regardless of LVSF)
  2. Asx severe AR and LVEF ≤ 55% (stage C2)
  3. Severe AR (stage C or stage D) and undergoing cardiac surgery for other indication

2a
- asx severe AR and LVEF > 55%, reasonable when LV severely enlarged LVESD > 50 mm or indexed LVESD > 25 mm/m2)
- Moderate AR (stage B) and undergoing cardiac or aortic surgery for other indications

62
Q

Severe AR
Generally replacement or repair?

A

Replacement

63
Q

LVSF important determinant of survival and functional status after AVR for AR, outcomes are optimal when surgery performed before LVEF decreases below

A

55%

64
Q

Measurement to assess AR
Reflects severity of the LV volume overload and degree of LV systolic shortening
Often an indicator of LV systolic dysfunction and degree of LV remodeling

A

LVESD
(left ventricular end systolic dimensions)

> 55 mm (or >25mm/m2 if indexed for body size) = severe

65
Q

Explain the limitations to TAVI in chronic AR

A

TAVI for isolated chronic AR is challenging d/t dilation of the aortic annulus and aortic root, lack of sufficient leaflet calcification

Risks: transcatheter valve migration, significant paravalvular leak

66
Q

Prevalence of BAV

A

.5-2.0%
3:1 male to female predominance

67
Q

What 2 commonly co-occurring conditions need to be evaluated in patients with BAV

A
  • Aortic aneurysm
  • Coarctation of aorta

(monitor for development of AR and AS too)

68
Q

Why is surveillance in pt with BAV s/p AVR necessary after AVR

A

Studies demonstrate that the aorta may continue to dilate even after AVR

69
Q

Class I recommendation of BAV intervention

2a?

A

I
Asx or sx pt with BAV and diameter of aortic sinus or ascending aorta > 5.5 cm, operative intervention to replace aortic sinuses and ascending aorta recommended

2a
- asx BAV, diameter of aortic sinuses or asc ao 5-5.5cm and additional risk factors for dissection (family hx, aortic growth rate >.5cm/yr, ao coarctation)
- BAV with indications for SAVR and diameter of aortic sinuses or asc ao ≥ 4.5cm

70
Q

Discuss TAVI and BAV

A

Recent data suggests with use of newer generation prosthetic valves the rate of paravalvular leak is no different in patients with BAV than in patients with trileaflet aortic valve, need more RCTs

71
Q

Define stage C MS (asx severe MS)

A
  • Rheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets
  • Planimetered MV area ≤ 1.5cm2
    -Mitral valve area ≤1.5 cm2
  • Diastolic pressure half time ≥ 150 ms
  • Severe LA enlargement
  • Elevated PASP > 50 mmHg
72
Q

Define severe MS

A
  • mitral valve area ≤ 1.5 cm2
  • transmitral mean gradient > 5-10 mmhg
73
Q

What classic feature is seen during diastole in MS

A

diastolic doming

74
Q

Why is heart rate important to take into account when assessing MS by TTE

A

Higher heart rate will result in overestimation of stenosis severity (when evaluating mean gradient)

75
Q

Estimated RVSP is obtained from

A

TR velocity

76
Q

Medical therapy with rheumatic MS

A

I
- Rheumatic MS + AF or prior embolic event or LA thrombus, VKA indicated

2a
- Rheumatic MS and AF w/ RVR, heart rate control can be beneficial
- Rheumatic MS in NSR with symptomatic resting or exertional sinus tachycardia, heart rate control can be beneficial to manage sxs

VKA anticoagulation if limited + Rate control

77
Q

Rheumatic MS and AF, discuss rhythm control

A

Rhythm control difficult to achieve in rheumatic MS d/t rheumatic process itself, progressive fibrosis and enlargement of the atria, fibrosis of the internodal and interatrial tracts, damage to the sinoatrial node

78
Q

Class I indications for rheumatic MS intervention

A
  1. Symptomatic (NYHA II, III, IV) w/ severe rheumatic MS (MV area ≤ 1.5 cm2, stage D) and favorable valve morphology w/ less than moderate (2+) MR in absence of LA thrombus, PMBC recommended
  2. Severely symptomatic (NYHA class III or IV) with severe rheumatic MS (MV area ≤ 1.5 cm2, stage D) who are not candidates for PMBC OR failed prior PMBC OR require other cardiac procedure OR no access to PMBC, mitral valve surgery (repair, commissurotomy, or valve replacement indicated
79
Q

Name some causes of acute MR

A

*IE causing leaflet perforation or chordal rupture
*Spontaneous chordal rupture (myxomatous MV disease)
*Rupture of papillary muscle (STEMI, inferior)

80
Q

Temporary bridge therapy in acute MR

A
  • Vasodilator to reduce impedance of aortic flow (sodium nitroprusside or nicardipine)
  • IABP
81
Q

In evaluating chronic MR, what is the first step in classification?

A

Primary or Secondary

82
Q

What is the MC cause of primary MR in high income countries?

A

MVP

83
Q

LV dysfunction in MR when EF <

A

60%

84
Q

MR. Repair or replacement preferred?

A

Repair

85
Q

Define stage B (progressive MR)

A

Central jet MR 20-40% LA or late systolic eccentric jet MR
Vena contracta < .7 cm
Regurgitant volume < 60 mL
Regurgitant fraction < 50%
ERO < .4 cm2
Angiographic grade 1+ to 2+

Mild LA enlargement
No LV enlargement
Normal pulmonary pressures

86
Q

Define severe MR

A

Central jet MR > 40% LA or holosystolic eccentric jet MR
Vena contracta ≥ .7 cm
Regurgitant volume ≥ 60 mL
Regurgitant fraction ≥ 50%
ERO ≥ .4 cm2
Angiographic 3+ to 4+

Mod-severe LAE
LV enlargement
Pulmonary HTN

(C1: LVEF >60% and LVESD < 40mm, C2: LVEF ≤ 60% and/or LVESD ≥ 40 mm)

87
Q

Medical therapy in primary MR

A

GDMT for LV systolic dysfunction or systemic HTN Best evidence for BB

No convincing evidence that vasodilator therapy reduces MR severity

88
Q

Why is a higher cut off for “normal” LVEF used in MR?

A

B/c loading conditions in MR allow continued late ejection into a lower impedance LA

89
Q

2 major categories of chronic secondary MR

A

ischemic
nonischemic

90
Q

Definition of severe secondary MR

A

Same as for primary

ERO ≥ .4 cm2 and regurgitant volume ≥ 60 mL

91
Q

Name one good prognostic factor surrounding ischemic secondary MR

A

Ischemic MR lends itself to possibility of revascularization and potential improvement in LV function if CAD has led to large areas of hibernating viable myocardium

92
Q

COAPT

A

Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional MR
(trial of patients with secondary MR and HF)

Improvement in survival, hospitalization, sxs, quality of life

93
Q

Medical therapy for secondary MR

A

GDMT as indicated

94
Q

Class 2a recommendations for intervention in secondary MR

A
  1. chronic severe secondary MR, LVEF <50%, persistent NYHA class II, III, or IV while on optimal GDMT, TEER is reasonable if with underlying appropriate anatomy with LVEF between 20-50%, LVESD ≤ 70 mm, and PASP ≤ 70 mmHg
  2. severe secondary MR, mitral valve surgery reasonable when CABG is undertaken
95
Q

If surgery pursued for secondary MR, generally repair or replacement?

A

replacement

96
Q

Most cases of significant TR are

A

secondary and related to tricuspid annular dilation, leaflet tethering in the setting of RV remodeling d/t pressure or volume overload (pulmonary hypertension or dilated cardiomyopathies)

97
Q

Name some sxs associated with severe TR

A

fatigue, abdominal bloating, peripheral edema, end organ damage (hepatic failure, renal failure

98
Q

Define severe TR

A

Central Jet ≥ 50% RA
Vena contracta width ≥ .7cm
ERO .4 cm2
Regurgitant volume ≥ 45 mL
Dense continuous wave signal with triangular shape
Hepatic vein systolic flow reversal

Dilated RV and RA
Elevated RA with “c-V” wave

99
Q

Medical therapy in severe TR 2a

A

Diuretics (loop +/- aldosterone antagonists)

If right sided HF attributable to severe secondary TR- tx primary cause of HF (ie pulmonary vasodilators to reduce elevated artery pressures, GDMT for HFrEF, rhythm control of AF)

100
Q

Define mixed valve disease

A
  1. Stenosis and regurgitation of a single vale
  2. Stenosis or regurgitation of 2 separate valves
101
Q

Repeat imaging for bioprosthetic surgical valves and bioprosthetic transcatheter valves

A

Surgical:
5 years
10 years
Then annually

Transcathete
Annually

102
Q

Name some of the causes you should be considering for prosthetic valve failure

A

Infective endocarditis
Rupture of valve cusp
Thromboembolic event (especially for mechanical, INR levels?)
Prosthesis-patient mismatch
Functional stenosis of repaired valve

103
Q

Imaging to evaluate prosthetic valve dysfunction?

A

TTE ok to start with

Likely TEE will be needed:
LA side of prosthetic MV is obscured by acoustic shadowing in TTE
Posterior aspect of valve for prosthetic aortic is shadowed in TTE

Mechanical: fluoroscopy o CT imaging

104
Q

TAVI based imaging protocols

A

TTE before discharge, at 30 days, at 1 year, routine annual

105
Q

Define valve pannus

A

a non-immune inflammatory reaction of the body to the valve prosthesis, a proliferation of fibroelastic tissue and collagen, with a starting point in the suture area and subacute or chronic centripetal evolution

106
Q

Name some of the mechanisms behind the need for lifelong VKA with mechanical valve

A

increased thrombogenicity of intravascular prosthetic material, impose abnormal flow conditions with zones of low flow within their components as well as areas of high shear stress, can cause platelet activation that leads to valve thrombosis and embolic events

107
Q

INR goals mechanical mitral and aortic

A

Mitral: 2.5-3.5
Aortic: 2.0-3.0 (unless high risk then 2.5-3.5, high risk: AF, prior emboli, hypercoagulable state, older gen prosthesis)
*On-X aotic valve, INR 1.5-2.0 + AAA 81 mg (INR 2.5 fo first 3 months + ASA 81)

108
Q

Anticoagulation after TAVI

A

Still in the works
initially DAPT advised, but now seems ASA alone works too
Maybe some role for VKA shortly after in higher risk patients, may help decrease incidence of leaflet thrombosis

109
Q

General guideline for VKA bridging

A

When deemed necessary, stop VKA 3-4 days prior to planned procedure
Restart post op as soon as risk allows (generally 24 hours)
Bridge with UFH or Lovenox when INR falls below therapeutic thresholds (ie 2.0 or 2.5) , usually 36-48 hours before surgery
Bridge therapy stopped prior to procedure; 4-6 hours prior (UFH) or 12 hours prior (Lovenox)

110
Q

Reversal agent for VKA

A

Pro-thrombin complex concentrate (II, VII, IX, X) (onset 5-15 minutes, duration 12-24 hours)
FFP (onset 1-4 hours, duration < 6 hours)
Vitamin K

111
Q

Reversal for DOAC (anti Xa agents)

A

Andexanet alfa

112
Q

Asx young man with a diastolic murmur most likely has

A

bicuspid aortic valve

113
Q

Middle aged man with loud systolic murmur, decreased exercise tolerance likely has

A

MVP, MR

114
Q

Echocardiography is recommended for any murmur

A

(1) associated with cardiac symptoms
(2) grade 3 or louder systolic murmur
(3) any diastolic murmur

115
Q

Systolic murmurs are caused by

A
  • Stenosis of a semilunar valve (aortic or pulmonic)
  • Regurgitation of an atrioventricular valve (mitral or tricuspid)
    *Other abnormal systolic cardiac flows (ie ventricular septal defect, hyperdynamic LV, etc)
116
Q

Diastolic murmurs are caused by

A
  • Regurgitation of a semilunar valve (aortic or pulmonic)
  • Stenosis of an atrioventricular valve (mitral or tricuspid)
117
Q

Inspiration has what effect on right sided murmurs

A

right sided murmur increase in loudness with inspiration

118
Q

Murmur of AS radiating to the apex in some (often elderly) patients

A

Gallavardin phenomenon

119
Q

Absence or reduced S2 (aortic closure sound) is a relatively sensitive and specific finding for

A

severe AS

120
Q

Bounding carotid artery impulse
Rhythmic bobbing of the head

A

severe AR

121
Q

Large v wave

A

Severe TR

122
Q

Delayed carotid upstroke

A

severe AS
*But note not sensitive finding b/c carotid pulsations may be brisk if concurrent increased vessel stiffness or AR

123
Q

CMR role in valvular heart disease

A
  • More accurate and reproducible measurements for LV volumes and EF
  • Allows for quantitation of AR and MR (can be helpful if echo is non-diagnostic or when degree of LV dilation seems out of proportion to regurgitant severity)
  • Less helpful for AS, underestimates max velocity
124
Q

CT role in valvular heart disease

A
  • Aortic dilation evaluation
  • Prosthetic valve dysfunction (allows accurate visualization of mechanical leaflet occluder motion and detection of thrombus or pannus)
  • Endocarditis (visualize full extent of aortic or ventricular pseudoaneurysms)
125
Q

Role of stress testing in VHD (3)

A
  1. ETT to eval exercise capacity, BP response, sxs (especially when functional status unclear)
  2. Low dose dobutamine SEH for eval of AS severity when concurrent LV dysfunction present
  3. Bicycle or treadmill stress testing with TTE eval of pulmonary pressures (with MV disease and exertional sxs despite only moderate disease at rest)
126
Q

Explain the reasoning behind dobutamine SEH in the evaluation of low output low gradient AS

A

If true severe AS, with stress EF will increase, but AV will remain stenotic and AVA will remain the same as at rest

If “psuedo severe”, moderate AS, with stress the EF will increase and the transaortic SV “push” the aortic leaflets to open more, increase in AVA

127
Q

Pt presents for TTE to evaluate AS. Found to be fairly hypertensive. Should you proceed?

A

HTN can result in underestimation of AS severity
If possible adjust meds and wait until pt is normotensive to perform testing

128
Q

Discuss LV dysfunction and VHD

A

LV dysfunction is an indication for intervention
But need to be smart about, other factors could lead to LV dysfunction. Careful history and exam
Is degree of dysfunction expected with extent of valvular disease?
Special note in elderly patients with calcific valve disease, underlying amyloid should be considered

Mayo Cardiology Core Competencies (14 decks)

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