Track 7: Valvular general approach and guidelines Flashcards
Stages of valvular heart disease
Patient with risk factors for development of VHD
Stage A
Patient with progressive VHD (mild to moderate severity and asx
Stage B
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
Stage C1
Stage C2
What is the difference between VHD stage C1 and stage C2
Both have severe VHD and are asx
C1 LV and RV remain compensated
C2 decompensation of LV and RV
What is the difference between VHD stage C and stage D
Stage C are asx severe
Stage D are sx severe
Patients who have developed sxs as a result of severe VHD
Stage D
Outline the stages of VHD A-D with one line descriptors
A: At risk
B: Progressive
C: Asx severe
D: Symptomatic severe
Key TTE measurements for stenotic lesions
- Max velocity
- Mean gradient
- Valve area
Key TTE measurements for regurgitant lesions
Calculation of regurgitant orifice area, volume, and fraction
Color doppler imaging
Surveillance TTE in progressive (Stage B) AS
Surveillance TTE in severe asx (Stage C1) AS
- 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)
Surveillance TTE in progressive (Stage B) AR
Surveillance TTE in Severe asx (Stage C1) AR
- Every 3-5 years (mild severity)
- Every 1-2 years (moderate severity)
-C1: Every 6-12 months
- C1, dilating LV: more frequently
Surveillance TTE in progressive (Stage B) MS
Surveillance TTE in severe asx (Stage C1) MS
- 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)
Surveillance TTE in progressive (Stage B) MR
Surveillance TTE in severe asx (Stage C1) MR
- Every 3-5 years (mild severity)
- Every 1-2 years (moderate severity)
-C1: every 6-12 months
-C1, dilating LV: more frequently
Risk of developing IE is highest in what populations?
- Prosthetic valve
- Prior IE
- Congenital heart disease with residual flow disturbance
VKA verus DOAC in concomitant VHD and AF
VKA:
- Rheumatic MS
- Mechanical valve
- Bioprosthetic valve < 3 months ago
DOAC alternative:
- Bioprosthetic ≥ 3 months ago
- Native VHD (excluding rheumatic MS)
Postoperative AF after VHD intervention is associated with increased stroke and mortality irrespective of
CHA2DS2VASc score
MC complication early after surgical valve replacement is
Postoperative AF
Prevalence and timeline of postoperative AF after surgical valve replacement
Occurs in up to 1/3 of patients within 3 months of surgery
Name some of the possible complications after valve replacement surgery (8)
- # 1 postoperative AF
- Stroke
- Vascular and bleeding complications
- Pericarditis
- Heart block requiring temporary or permanent pacing (especially after AVR)
- HF
- Renal dysfunction
- Infection
Name some of the possible complications after transcatheter valvular intervention (5)
- Permanent pacing need
- Paravalvular leak
- Stroke
- Vascular complications
- Residual valve dysfunction
Hemodynamic severity for AS is best calculated by
- Transaortic max velocity
- Mean pressure gradient
Stage A AS
**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
Stage B AS
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
Stage C1 AS
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
Severe versus very severe AS
Severe: Vmax ≥ 4 m/s, mean gradient ≥ 40 mmHg
Very severe: Vmax ≥ 5 m/s, mean gradient ≥ 60 mmHg
Stage C2 AS
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
Stage D1 AS
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
Stage D2 AS
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%
Stage D3 AS
*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%
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
Blood pressure
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?
Dobutamine stress test with echocardiographic or invasive hemodynamic measurements
What factor may cause measurements of AS severity to be underestimated
If the patient is hypertensive
(systemic hypertension imposes a second pressure load on the LV)
Medial therapy for AS stage A, stage B, stage C
GDMT HTN management (ACE/ARB if tolerated)
Class I
Calcific AS medical therapy
Statin
Class I
After TAVI, what med may reduce long0term risk of all cause mortality 2b
ACE/ARB
Statin role in calcific AS
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)
Name the 5 class I indications for AVR
Name the 4 2a indications
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
Most common presenting initial sx of AS
Exertional dyspnea or decreased exercise tolerance
Severe asx AS (stage C)
If Vmax ≥ 4.0 m/s or mean pressure gradient ≥ 40 mmHg, when is mean onset of symptoms
2-5 years
Age and AVR recommendations (2a)
< 50 yo and no contraindication to anticoagulation, mechanical reasonable
50-65 shared decision making
> 65 yo bioprosthetic reasonable
Likelihood of aortic bioprosthetic structural deterioration at 15-20 years based on age
>65
<50
40
20
> 65 yo, <10%
< 50 yo, 22%
40 yo, 30%
20 yo, 50%
Severe AS
< 65 yo
Life expectancy > 20 years
SAVR
Severe AS
65-80 yo
No anatomic contraindication to transfemoral access
TAVI or SAVR
Symptomatic severe AS
> 80 yo OR life expectancy < 10 years
TAVI
Asx severe AS
LVEF < 50%
≤ 80 yo
TAVI or SAVR
Asx severe AS
Abnormal exercise test, very severe AS, rapid progression, or elevated BNP
SAVR recommended over TAVI
Age < 65
SAVR or TAVI
SAVR
Name some of the benefits associated with TAVI and with SAVR
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
Name some causes of acute AR
- Endocarditis
- Aortic dissection
- Iatrogenic
- Blunt chest trauma
Tx plan for acute severe MR
- 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)
Describe the role of beta blockers in acute severe AR
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)
MC causes of chronic AR
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
At risk of AR
BAV, AV sclerosis, disease of aortic sinuses or ascending aorta, hx of rheumatic fever or known rheumatic heart disease, IE
Stage A
Define mild AR
- 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
Define moderate AR
- 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
Define severe AR
- 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
Outline difference between asymptomatic severe AR stage C1 and stage C2
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)
For severe AR, what are the key values for EF and LVESD
EF < 55%
LVESD > 50 mm
Medical therapy in chronic AR
- 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
Name the 3 class I indications for AVR (in chronic AR)
Class 2a indications?
- Symptomatic severe AR (stage D) (regardless of LVSF)
- Asx severe AR and LVEF ≤ 55% (stage C2)
- 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
Severe AR
Generally replacement or repair?
Replacement
LVSF important determinant of survival and functional status after AVR for AR, outcomes are optimal when surgery performed before LVEF decreases below
55%
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
LVESD
(left ventricular end systolic dimensions)
> 55 mm (or >25mm/m2 if indexed for body size) = severe
Explain the limitations to TAVI in chronic AR
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
Prevalence of BAV
.5-2.0%
3:1 male to female predominance
What 2 commonly co-occurring conditions need to be evaluated in patients with BAV
- Aortic aneurysm
- Coarctation of aorta
(monitor for development of AR and AS too)
Why is surveillance in pt with BAV s/p AVR necessary after AVR
Studies demonstrate that the aorta may continue to dilate even after AVR
Class I recommendation of BAV intervention
2a?
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
Discuss TAVI and BAV
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
Define stage C MS (asx severe MS)
- 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
Define severe MS
- mitral valve area ≤ 1.5 cm2
- transmitral mean gradient > 5-10 mmhg
What classic feature is seen during diastole in MS
diastolic doming
Why is heart rate important to take into account when assessing MS by TTE
Higher heart rate will result in overestimation of stenosis severity (when evaluating mean gradient)
Estimated RVSP is obtained from
TR velocity
Medical therapy with rheumatic MS
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
Rheumatic MS and AF, discuss rhythm control
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
Class I indications for rheumatic MS intervention
- 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
- 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
Name some causes of acute MR
*IE causing leaflet perforation or chordal rupture
*Spontaneous chordal rupture (myxomatous MV disease)
*Rupture of papillary muscle (STEMI, inferior)
Temporary bridge therapy in acute MR
- Vasodilator to reduce impedance of aortic flow (sodium nitroprusside or nicardipine)
- IABP
In evaluating chronic MR, what is the first step in classification?
Primary or Secondary
What is the MC cause of primary MR in high income countries?
MVP
LV dysfunction in MR when EF <
60%
MR. Repair or replacement preferred?
Repair
Define stage B (progressive MR)
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
Define severe MR
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)
Medical therapy in primary MR
GDMT for LV systolic dysfunction or systemic HTN Best evidence for BB
No convincing evidence that vasodilator therapy reduces MR severity
Why is a higher cut off for “normal” LVEF used in MR?
B/c loading conditions in MR allow continued late ejection into a lower impedance LA
2 major categories of chronic secondary MR
ischemic
nonischemic
Definition of severe secondary MR
Same as for primary
ERO ≥ .4 cm2 and regurgitant volume ≥ 60 mL
Name one good prognostic factor surrounding ischemic secondary MR
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
COAPT
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
Medical therapy for secondary MR
GDMT as indicated
Class 2a recommendations for intervention in secondary MR
- 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
- severe secondary MR, mitral valve surgery reasonable when CABG is undertaken
If surgery pursued for secondary MR, generally repair or replacement?
replacement
Most cases of significant TR are
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)
Name some sxs associated with severe TR
fatigue, abdominal bloating, peripheral edema, end organ damage (hepatic failure, renal failure
Define severe TR
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
Medical therapy in severe TR 2a
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)
Define mixed valve disease
- Stenosis and regurgitation of a single vale
- Stenosis or regurgitation of 2 separate valves
Repeat imaging for bioprosthetic surgical valves and bioprosthetic transcatheter valves
Surgical:
5 years
10 years
Then annually
Transcathete
Annually
Name some of the causes you should be considering for prosthetic valve failure
Infective endocarditis
Rupture of valve cusp
Thromboembolic event (especially for mechanical, INR levels?)
Prosthesis-patient mismatch
Functional stenosis of repaired valve
Imaging to evaluate prosthetic valve dysfunction?
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
TAVI based imaging protocols
TTE before discharge, at 30 days, at 1 year, routine annual
Define valve pannus
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
Name some of the mechanisms behind the need for lifelong VKA with mechanical valve
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
INR goals mechanical mitral and aortic
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)
Anticoagulation after TAVI
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
General guideline for VKA bridging
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)
Reversal agent for VKA
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
Reversal for DOAC (anti Xa agents)
Andexanet alfa
Asx young man with a diastolic murmur most likely has
bicuspid aortic valve
Middle aged man with loud systolic murmur, decreased exercise tolerance likely has
MVP, MR
Echocardiography is recommended for any murmur
(1) associated with cardiac symptoms
(2) grade 3 or louder systolic murmur
(3) any diastolic murmur
Systolic murmurs are caused by
- 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)
Diastolic murmurs are caused by
- Regurgitation of a semilunar valve (aortic or pulmonic)
- Stenosis of an atrioventricular valve (mitral or tricuspid)
Inspiration has what effect on right sided murmurs
right sided murmur increase in loudness with inspiration
Murmur of AS radiating to the apex in some (often elderly) patients
Gallavardin phenomenon
Absence or reduced S2 (aortic closure sound) is a relatively sensitive and specific finding for
severe AS
Bounding carotid artery impulse
Rhythmic bobbing of the head
severe AR
Large v wave
Severe TR
Delayed carotid upstroke
severe AS
*But note not sensitive finding b/c carotid pulsations may be brisk if concurrent increased vessel stiffness or AR
CMR role in valvular heart disease
- 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
CT role in valvular heart disease
- 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)
Role of stress testing in VHD (3)
- ETT to eval exercise capacity, BP response, sxs (especially when functional status unclear)
- Low dose dobutamine SEH for eval of AS severity when concurrent LV dysfunction present
- Bicycle or treadmill stress testing with TTE eval of pulmonary pressures (with MV disease and exertional sxs despite only moderate disease at rest)
Explain the reasoning behind dobutamine SEH in the evaluation of low output low gradient AS
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
Pt presents for TTE to evaluate AS. Found to be fairly hypertensive. Should you proceed?
HTN can result in underestimation of AS severity
If possible adjust meds and wait until pt is normotensive to perform testing
Discuss LV dysfunction and VHD
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
