AHA Guidelines - Valve 2020 Flashcards
1
Q
What is the aorto-mitral curtain?
A
Where the anterior mitral leaflet unionizes with the L-non commissure of the aortic valve.
2
Q
Where is the AV node in relation to the mitral valve?
A
immediately adjacent to the R fibrous trigone (near A3/posteromedial commissure/P3); beware placing sutures here
3
Q
Describe the posterior leaflet of the mitral valve?
A
occupies 2/3 of mitral annulus, free edge is scalloped, quadrangular in shape; scallops are anterolateral (P1), middle (P2), posteromedial (P3)
4
Q
Describe papillary muscles of mitral valve
A
Anterolateral has 1 muscle body, but dual blood supply (LAD, Cx).
Posteromedial has 2 muscle bodies, but single blood supply (Cx or R coronary) - this is the one most prone to ischemia and can be part of the pathogenesis of ischemic MR.
5
Q
What are the anatomic limits of the aorto-mitral curtain?
A
right (confluence of mitral, tricuspid, and noncoronary cusp of aortic + membranous septum) and left (fibrous continuity of the aortic and mitral valves) fibrous trigone
6
Q
Which mitral leaflet is more prone to dilating and causing MR? Why?
A
Posterior - annular tissue is thinnest and not attached to the fibrous skeleton of the heart.
7
Q
First line imaging to eval MV disease?
A
TTE.
TEE is used for further refinement and surgical planning.
8
Q
What is the Wilkins echo score used for?
A
ID which patients may benefit from valvotomy vs MV replacement.
Takes into account: leaflet mobility, subvalvular involvement, leaflet thickening, and degree of calcification.
4 grades per category.
> 8 indicates more severe anatomic disease and a higher risk of suboptimal outcome from PMBC (suboptimal = MVA <1, LA pressure >10, <25% improvement in MVA).
9
Q
For MR, which TTE and TEE views allow for eval of the 6 scallops?
A
TTE parasternal.
TEE transgastric.
10
Q
When is cardiac cath used in workup for MV disease?
A
Pts older than 40 (up to 25% have disease w/o symptoms).
LV and RV ventriculography can also assess severity of disease.
11
Q
Describe incidence/prevalence of rheumatic MS.
A
Incidence low in high-income countries. Slowly declining in low and mid income countries.
Rheumatic MS cases are 80% women.
High prevalence areas tend to present at earlier ages - teens to 30s.
Low prevalence regions usually present 50-70 yrs.
12
Q
What is mild/progressive MS in terms of objective measurement?
A
MV area > 1.5 cm2. Diastolic pressure half-time <150ms.
13
Q
When is MS considered severe by valve hemodynamics?
A
MV area < 1.5 cm2. Or diastolic half-time 150 ms or >.
14
Q
What is the pathophysiology of nonrheumatic calcific MS?
A
Calcification of the mitral annulus that extends into the leaflets, resulting in narrowing of the annulus and rigidity of the leaflets.
15
Q
What is the primary cause of MS?
A
Rheumatic disease.
16
Q
How are the stages of MS defined?
A
Symptoms, valve anatomy, valve hemodynamics, and consequences of obstruction as it relates to the LA and pulm circulation.
*Of note, the trans-mitral mean pressure gradient should be obtained to further understand hemodynamic effect of stenosis, but b/c of variability w/ heart rate and forward flow, it is NOT part of the severity criteria (>10 mm Hg was previous “severe” cutoff).
17
Q
What are the pertinent hemodynamic consequences of severe MS?
A
Hemodynamic consequences are measured in terms of the LA and pulmonary circulation.
Severe LA enlargement and elevated PASP >50 mm Hg.
18
Q
What are the pertinent hemodynamic consequences of severe MS?
A
Hemodynamic consequences are measured in terms of the LA and pulmonary circulation.
Severe LA enlargement and elevated PASP >50 mm Hg.
19
Q
What are symptoms associated with MS?
A
Decreased exercise tolerance. Exertional dyspnea.
Attempts at increase in flow across the valve or decreased filling time (ie exercise) will exacerbate symptoms. Pts may be asymptomatic at rest.
20
Q
What diagnostic study is recommended if rheumatic MS patient is being CONSIDERED for percutaneous mitral balloon commissurotomy (PMBC)?
A
TEE should be performed to assess for presence of LA thrombus and eval severity of MR.
*TTE is initially indicated for diagnosis, quantification of valve/LA/PA hemodynamics, assessment of MV morphology, and evaluation of other valve lesions. Helps determine suitability for PMBC.
21
Q
Echo findings of MS
A
TTE parasternal long-axis - diastolic doming.
TTE Short axis - commissural fusion (view allows for planimetry of mitral orifice).
3D echo - greater accuracy of MV area.
Doppler echo - mean transvalvular gradient (should be reported w/ HR - higher HR overestimates severity).
TR velocity - estimates RV systolic pressure.
Quantify MR and other valve lesions.
22
Q
MS pts who are PMBC candidates need what ruled out?
A
TEE should be done to look at LA thrombus and eval MR.
MR more than mild is contraindication to PMBC.
23
Q
What are the pathologic/hemodynamic end results of elevation of the transvalvular gradient across the MV?
A
Elevated LA and PV pressures.
PA intimal hypertrophy.
Chronic compensatory pulm vasoconstriction, pulm edema, inc RV EDV, tricuspid regurgitation.
LV will often be normal size w/ lower EDV.
24
Q
Pt w/ established dx of rheumatic MS has a change in symptoms, what should be done to dx?
A
TTE - quantify and compare gradient and area, eval other valves and function.
Disease progression can occur 2/2 repeat episodes of rheumatic fever => further valve damage, progressive narrowing of MV, leaflet fibrosis and thickening, worse pulm HTN, worse MR or TR or other valve lesions.
25
What pathologies/diagnoses can worsen symptoms of MS even if anatomic disease doesn't progress?
Increased hemodynamic load, such as in pregnancy.
Also new onset AF, fever, anemia, hyperthyroidism.
26
What does MR do to stroke volume and EF?
Decreased SV w/ preserved EF.
27
What is LV remodeling like in MR?
eccentric hypertrophy and chamber dilation w/ annular dilation
28
What does LV dilation 2/2 MR do to the mitral annulus?
AP and transverse diameters inverts from 3:4 => leaflet coaptation impairment, worse regurgitation
29
What is MR effect on LA?
LA dilation and thickening => inc risk of arrhythmia and thrombus
30
How do acute MR vs chronic MR differ in presentation?
In acute, LA and LV do not have time to remodel and compensate for increase in volume => acute pulm edema and cardiogenic shock
31
In what MS patients can cardiac cath be useful (other than ischemic symptoms)?
Older patients, concomitant diastolic dysfunction, LA noncompliance, intrinsic PA disease.
Discordant symptoms w/ echo findings.
Cath can measure absolute pressures at rest and exercise (exercise testing can also be done w/ Doppler) - useful to evaluate physio response of the mean mitral gradient and PA pressure.
32
In patients w/ rheumatic MS, when is VKA indicated?
A fib, prior embolic event, LA thrombus
33
In patients w/ MS and AF w/ RVR, what can be beneficial in terms of nonop AF management?
heart rate control
34
In pt w/ rheumatic MS in NSR w/ sinus tachycardia, what can be done if patient develops symptoms?
heart rate control; this may be effective only in pts w/o underlying chronotropic incompetence
35
Why is it difficult to achieve rhythm control in MS w/ AF patients?
rheumatic process leads to progressive fibrosis, enlargement of the atria, fibrosis of the internodal/interatrial tracts, and damage to the SA node
36
What are criteria for PMBC (percutaneous mitral balloon commissurotomy) in MS pts?
PMBC is preferred for rheumatic MS as 1st line...
Can be severe rheumatic MS (MVA < 1.5 cm) or progressive.
If progressive (MVA > 1.5), needs exertional symptoms, stress test w/ HD significant MS, and a pliable valve w/o clot or 2+ MR (2b).
If severe, (<1.5 MVA). Can be asx w/ pliable valve, no LA thrombus, < moderate MR (2+), and PASP >50 (2a) or new AF (2b).
If severe and sx, just needs pliable valve, no LA thrombus, and <2+ MR (1). Or not be a surgical candidate despite bad anatomy (2b).
The consideration for surgery is if they have severe MS w/ symptoms, not PMBC candidate (not pliable valve, LA thrombus, mod MR), but are a surgical candidate.
All need to be at a comprehensive valve center
37
In what MS pts is mitral valve surgery (repair, commissurotomy, replacement) indicated?
severely symptomatic (NYHA III or IV) +
w/ severe rheumatic MS (< 1.5 cm MVA) +
who are not candidates for PMBC or failed PMBC,
or require other cardiac procedures,
or don't have access to PMBC
38
Can pt w/ MS and PA HTN get PMBC?
Yes - 2a recommendation:
Asx w/ severe rheumatic MS w/ favorable morphology w/o MR or LA thrombus.
PA systolic >50 mmHg.
39
Can pt w/ MS and AF get PMBC?
2b rec: asx w/ severe rheumatic MS and favorable morphology w/o MR or LA w/ new AF.
Justification: AF is equivalent to "symptomatic" since it signifies progressive LA damage, increases thromboembolism, increases LV pressure (shorter diastolic filling interval), associated w/ worse outcomes and suboptimal PMBC results.
40
Can MS pts that are not severe by echo findings receive PMBC?
Yes. Get exercise test first.
2b: symptomatic (NYHA II-IV) w/ rheumatic MS (NOT severe - MVA >1.5 cm2), PAWP >25 or MV gradient >15 during exercise should be eval for PMBC (r/o LA thrombus, MR, intractable valves).
41
When choosing an interventional approach for MS, what is the thought process?
PMBC as long as either...
1) severe (MVA <1.5 cm2) w/ sx
2) severe w/ PA HTN (>50 mmHg)
3) severe w/ new AF
4) progressive w/ sx AND HD significance (stress test).
***Also needs pliable valve, no LA clot, and only mild MR.
Otherwise... Surgery: Commissurotomy preferred. MV replacement is last option in pts w/ severe limiting sx.
42
What valve morphology in MS would be more amenable to valve replacement (as opposed to commissurotomy)?
severe valvular thickening, subvalvular fibrosis w/ leaflet tethering; non-pliable valves
43
MS pt failed PMBC, what is next?
Surgery, preferably commissurotomy
44
MS pt meets criteria for PMBC but has moderate TR, what should be done?
surgical approach w/ tricuspid repair
45
In chronic MS unable to undergo PMBC, what should timing of surgery be?
Delayed until the pt has severe limiting sx (NYHA class III or IV).
Because natural hx of MS is slow progression over decades.
46
What is prognosis of MS pts w/ pulm HTN preop?
Worse.
It's a sign of progressive elevation of LA pressure, which affected the pulm circulation. The pulm disease may have become intrinsic.
A major reason for worse outcomes is the assn w/ worse RV fct and TR postop.
47
A progressive MS pt (ie not severe by hemodynamic measurements: >1.5 cm MVA, diastolic pressure half-time <150 ms) has shortness of breath w/ exertion, so gets exercise stress test w/ cath that shows increased gradient to >15 mm Hg w/ exercise. What does this mean?
they will benefit from PMBC
48
In MS patients w/ suboptimal valve anatomy, who can PMBC be offered to?
severely sx pts who are poor surgical candidates, even if suboptimal anatomy
pts who refuse surgery
49
How do you manage nonrheumatic calcific MS?
Determine if severe symptoms: NYHA III or IV pts,
w/ severe MS (<1.5 cm2 MVA, stage D),
w/ extensive mitral calcification,
after discussion of high procedural risk and individual pts preferences and values...
can be considered for valve intervention
These pts should be treated differently than rheumatic MS.
There is currently not a good answer (2/15/2020).
50
Other than calcification, what can cause nonrheumatic MS?
radiation therapy
MV repair w/ small annuloplasty ring
51
Initial eval for ALL patients w/ known or suspected valve heart disease (VHD)? What do they eval for?
HP - eval valve sx severity, comorbidities, HF
TTE - standard initial test, chamber size/function, valve morphology/severity, effect on pulm/systemic circ
ECG - rhythm, LV fct, hypertrophy
52
Why is CXR important for patients w/ suspected VHD?
Heart size, pulmonary vascular congestion, intrinsic lung disease, calcification of aorta/pericardium
53
What can TEE help to assess in suspected VHD patients?
High quality assessment of mitral (should be noted function can be affected by anesthetic) and prosthetic valves. Eval intracardiac masses and associated abnormalities.
54
What are the stages of VHD?
A - at risk. No VHD.
B - progressive - mild to mod severity, asx.
C1 - Asx severe w/ LV/RV compensation.
C2 - Asx severe w/ LV or RV decompx.
D - severe and symptomatic.
Intervention is typically indicated for C2 and D stage VHD.
*there are no follow-up guidelines for non-intervention.
55
What is the follow-up for stage B VHD (progressive; mild-mod asx)?
This applies to AS, AR, MS, and MR.
Mild - echo q3-5 yrs; yearly H&P.
Mod - echo q1-2 yrs; yearly H&P.
56
What is the recommended follow-up for stage C1 VHD (severe asx w/ compensated LV/RV)?
AS, AR, and MR: q6-12 mo w/ echo.
MS: q1-2 yrs w/ echo.
57
In VHD pt w/ TTE not suggestive of severe disease but in clinically symptomatic pt, what study can be done to eval?
Hemodynamic cardiac cath w/ measurements of transvalvular pressure gradients and CO.
Good for pts w/ difficult TTE.
58
How can exercise stress testing help in surgical decision making for VHD?
Sx can be slow onset, so pt hx that is equivocal (setting of severe CHD: stage C) can benefit from exercise stress testing that pushes them to stage D w/ surgical intervention recommended.
59
Principles of medical therapy for VHD?
Standard GDMT: HTN, DM, lipid control.
Exercise, diet, smoking cessation, nl BMI are other goals.
LV dysfx w/ severe VHD will benefit from surgery, but if surgery declined or not possible, then GDMT for LV dysfx should be done: diurese, ACI inh/ARB, beta block, aldosterone agonist, bivent pacing if needed.
60
In principle, what hemodynamically altering agents should be avoided in pts w/ stenotic VHD?
Blood pressure lowering
61
The maintenance of what remains the most important component of an overall healthcare program in preventing IE?
Oral health
62
What is the recommendation for primary and secondary prevention of rheumatic fever as it concerns rheumatic heart disease?
Primary prev of rheum fever is rapid detection and tx of strep pharyngitis (group A strep).
Secondary - in pts w/ previous episodes of rheumatic fever or in those w/ rheumatic heart disease, long-term antistreptococcal ppx is indicated. (COR Lvl 1).
Options:
Pen G 1.2mil U q4wks.
Pen V 200mg PO BID.
Sulfadiazine 1g PO daily.
Macrolide or azalide if allergic.
For at least 10 yrs or until 40 (pick longer one).
Recurrent infection is associated w/ worsening RHD. It does not have to be symptomatic. Rheum fever can also occur after infx is tx. Therefore abx ppx is recommended over recognition and tx in pts w/ RHD.
63
Is secondary rheumatic heart disease ppx required after valve replacement?
What agent?
How long?
Yes. Penicillin or sulfadiazine are first line. Macrolide or azalide if allergy.
At least 10 yrs or until 40 (pick longest).
Can be lifetime if high risk of gAS exposure.
64
What are AHA recs of IE ppx in dental procedures?
What situation and what population?
Before dental procedures if manipulates gingival tissue, periapical region of teeth, or perforation of oral mucosa in following:
Prosthetic cardiac valves.
Prosthetic material used in valve repair.
Previous IE.
Unrepaired cyanotic CHD, or if residual shunt or valve regurg at or near site of prosthetic patch or device.
COR 2a.
Ppx not needed for nondental procedures in specific regards to VHD itself.
65
Risk of IE is highest in what patient populations?
Prosthetic valve, previous IE, or CHD w/ residual flow distributions.
Transcatheter IE rates are equivalent.
66
Pt w/ mechanical heart valve w/ AF requiring long-term anticoag asks about NOAC instead of VKA. Response?
Not recommended.
RE-ALIGN randomized dabigatran vs warfarin and was stopped early d/t excess stroke AND bleeding in dabigatran.
67
What VHD pts can use NOACs if they have AF?
Admin anticoag on basis of CHA2DS2-VASc.
COR 1: Native VHD (except rheumatic MS).
COR 1: Bioprosthetic valve >3 mo old (VKA preferred before 3 mo).
COR 2a: Bioprosthetic valve <3 mo old if AF is new onset.
68
For pt w/ AF and rheumatic MS, what is the ideal anticoag?
Long-term VKA. These diseases coexist often w/ substantial thromboembolic risk and were thus excluded from NOAC trials and recommendations.
69
What is the mortality for MVR CABG?
9%
70
Most common early complication of surgical valve replacement?
atrial fibrillation - 1/3 of pts within 3 mo of surgery
71
What is the work up/approach for a pt w/ persistent sx after valve intervention?
First: eval to assess valve fct and ensure no persistent or recurrent stenosis/regurg or valve complication.
Second: eval and tx any concurrent cardiac dz and noncardiac conditions that may be causing sx.
Third: manage irreversible consequences of valve disease w/ GDMT (HF or pulm HTN).
72
What is the recommended approach for periodic imaging after valve intervention?
Asx pt w/ any valve intervention:
- baseline postprocedural TTE
- periodic TTEs depending on specific pt and surgery factors
73
What is ideal timing for postprocedural TTE after VHD surgery?
1-3 mo after procedure - ensures loading conditions have normalized.
Also, annual clinical f/u is recommended for all valve intervention at a primary or comprehensive valve center.
*IE no reason to repeat echo before 3 mo unless changes in clinical presentation. IE it takes around 3 mo for the heart to normalize loading conditions.
74
Describe the anatomy, valve hemodynamics, consequences, and symptoms of a patient "at risk for AS" or Stage A.
Anatomy: BAV, other congenital valve anatomy, aortic valve sclerosis.
Hemodynamics: Vmax <2m/s w/ normal leaflet motion.
75
What are the important measurements for AS patients in terms of the echo valve hemodynamics for definition of AS severity?
What levels would indicate severe?
Vmax (4 is severe, 6 is very severe)
Mean ΔP (40mm hg is severe, 60 is very severe)
EF (50 is significant)
Typical for severe, but not required for definition:
AVA (1 is severe)
AVAI (0.6 is severe)
Use in low flow states.
76
What is the echo valve anatomy you would find for a patient w/ severe AS?
severe leaflet calcification/fibrosis or congenital stenosis w/ severely reduced leaflet opening
77
When can the AVA be helpful in determining severity of AS?
In pt w/ severe symptoms and low-flow, low-gradient states, AVA <1 cm2 can help determine severe AS.
78
What measurement can help differentiate symptomatic severe low-gradient AS w/ normal EF?
SVI <35 ml/m2 measured when pt is normotensive w/ systolic <140
79
What are the hemodynamic consequences of severe AS?
LV diastolic dysfunction, LV hypertrophy, possibly pulm HTN.
80
If suspecting low-flow, low-gradient severe AS w/ reduced EF, what test can be done to determine if AS is severe?
Low-dose dobutamine stress test w/ echo or invasive hemodynamic measurements. It will show AVA <1 (fixed) and Vmax rising to 4 or more.
IE this differentiates severe AS with LV systolic dysfunction attributable to afterload mismatch from primary myocardial dysfunction with only moderate AS.
81
How can hypertension affect AS severity measurements?
May underestimate or, less often, overestimate stenosis severity. Systemic hypertension imposes a second pressure load on the LV, in addition to valve obstruction, which results in a lower forward stroke volume and lower transaortic pressure gradient than when the patient is normotensive. Thus, Doppler velocity data and invasive pressure measurements ideally are recorded when the patient is normotensive.
82
A hypertensive patient is diagnosed w/ moderate AS. It is noted that he was hypertensive (systolic >140) during testing. What should be done?
repeat measurements when the blood pressure is better controlled ensure that a diagnosis of severe AS is not missed
83
Most common reason for procedural intervention in patients with BAV?
AS
84
In asymptomatic patients w/ severe AS (stage C1, ie w/o dec LVEF <50), what can be done if the patient's sx are unclear?
Exercise testing - assess physiological changes and confirm absence of sx.
85
In asymptomatic AS patients, what chronic medical condition should be managed according to AHA guidelines by standard GDMT?
hypertension
86
In all patients w/ calcific AS, what medication is indicated for primary and secondary prevention of atherosclerosis?
statin therapy
although it should be noted that it will not prevent hemodynamic progression of AS
ie valve event rates were not reduced, but ischemic event rates were reduced by 20%
87
In AS pts s/p TAVI (TAVR), what med should be considered to reduce the long-term risk of all-cause mortality according to med therapy guidelines from AHA (2b)?
RAAS blocker (ACE inh or ARB).
Relative risk reduction rate 20-50%.
Absolute risk reduction rate 2.4-5%.
***also, treat HTN and start statin to reduce coronary events
88
A patient has an abnormal aortic valve w/ reduced systolic opening (ie AS) to severe degree. They have sx d/t AS.
Manage this.
AVR: TAVR vs SAVR.
Severe AS: V max >4. Delta P mean >40.
Otherwise nl severe AS doesn’t meet criteria.
89
A patient has an abnormal aortic valve w/ reduced systolic opening (ie AS). They have sx d/t AS.
Vmax <4. AVA <1.
What's next?
Determine LVEF. 50 is cut off. Need more info.
If <50 => Dob stress echo => Vmax >4 => AVR.
If >50 => if AVAi <0.6 and SVI <35 => AVR.
90
Asymptomatic severe AS w/ Vmax >4 and LVEF <50. Manage.
AVR.
Depressed LVEF can be 2/2 excessive afterload (afterload mismatch), and LVEF improves after AVR.
Even if LVEF is not caused by afterload mismatch, survival is still improved.
91
Asx severe AS w/ Vmax >4 and 3v CAD requiring surgery. Manage AS.
AVR.
Concurrent AVR w/ any cardiac surgery has shown a lower additive risk when compared to the risk of reoperation in 5 years (Asx AS likely to become Sx within that time).
92
What is the likely outcome of severe asymptomatic AS?
Disease progression w/ sx onset w/in 2-5 yrs. This is based off prospective clinical studies.
93
In AS pt, what echo measurement can predict better outcomes after AVR?
Mean pressure gradient. Better outcomes in pts w/ higher gradients.
Outcomes are worse w/ severe low-gradient AS but are still better w/ AVR than w/ medical therapy in those w/ low LVEF.
Expect EF to inc by 10, and may normalize if afterload mismatch was cause.
94
A patient w/ suspected low flow, low gradient, severe AS gets dobutamine stress test showing moderate AS. What should be done?
GDMT for HF w/o AVR.
High-risk, so AVR benefit is unclear. Same w/ TAVI.
95
What can be done w/ aortic valve in a small patient to ensure you're not diagnosing severe AS in a patient that actually has moderate AS?
Get AVAi. <0.6 is indicative of severe.
96
In questionably asx severe AS pts undergoing exercise stress testing, what would be considered a positive test?
Fall of 10mm systolic BP from baseline to peak exercise or significant dec in exercise as compared w/ age and sex normal standards.
SAVR is preferred (2a)
97
What asymptomatic AS pts benefit from AVR based solely on echo/hemodynamic measurements?
What kind of AVR is preferred?
Aortic velocity >5 m/s.
Mean pressure gradient >60 mmHg.
These patients are considered "very severe."
SAVR preferred (2a)
98
In asx severe AS pts, what lab value may indicate subclinical HF and LV decompensation?
BNP.
If >3x normal. SAVR (preferred - 2a)
99
In severe asx AS w/ rapid disease progression and low surgical risk, what is management?
What could be considered rapid progression?
SAVR (2a).
Rapid disease progression:
Inc in aortic velocity of about 0.3 m/s/yr.
Inc in mean gradient of 7-8 mmHg/yr.
Dec in AVA 0.15 cm2/yr.
Especially in older pts w/ calcified valves and significant hemodynamic change on serial studies.
100
Severe asx AS w/ dec LVEF <60 (>50) on 3 serial studies mgmt?
SAVR (2b).
As opposed to the grade 1 recommendation for outright LVEF <50 in severe asx AS.
101
Asx progressive AS (Vmax 3-3.9 m/s) undergoing other cardiac surgery. Do they need SAVR?
SAVR should be considered (2b).
102
In terms of AS pts requiring AVR, what are the COR 1 recommendations for bio vs mech?
Choice is based on shared decision-making including patient.
For pts of any age requiring AVR for whom VKA is contraindicated, can't be managed, or isn't wanted - give bio valve.
103
A pt w/ AS requiring AVR is <50 w/o other pmh, what is the reasonable valve choice assuming pt listens to your recommendation?
What about 50-65?
>65?
Mech valve (2a).
50-65 yrs can get individualized decision.
>65 yrs may benefit more from bio (10% replacement rate).
*Age is a major decision-making point for recommendations.
104
In pt <50 who prefers bio AVR w/ normal anatomy, what can be offered at a Comprehensive Valve Center?
replacement of aortic by pulmonic autograft (Ross)
105
What AS pts may benefit more from SAVR over TAVR?
Asx pts w/ severe AS w/ one of following (lvl 1 recommendation on choice of valve, but 2a recommendation for AVR at all):
- abnormal exercise BP response
- elevated serum BNP (300 or >3x normal)
- rapid hemodynamic progression
- very severe AS w/ velocity >5 m/s
Younger than 65 as well.
Final choice is always... based on shared decision-making.
106
For severe AS (sx or asx), requiring AVR, <65 yrs old, and have a life expectancy >20 yrs, what AVR approach is recommended?
SAVR (1)
107
Sx pts w/ severe AS, 65-80 yrs, who can get transfemoral TAVI, which AVR approach is recommended?
transfemoral TAVI or SAVR after shared decision-making
108
In surgically prohibitive pts w/ severe sx AS, what is the post-TAVI survival (ie prognosis) required to proceed?
12 mo prognosis w/ acceptable quality of life.
Otherwise, palliative care.
109
In critical pts w/ severe AS, what may be required as a bridge to SAVR/TAVR?
Perc balloon dilation (2b)
110
What valve anatomy favors SAVR in AS pts?
BAV
Subaortic (LVOT) calcification
Rheumatic valve disease
111
What's the best test for acute AR? What are you evaluating?
Echo. TTE or TEE.
Confirm presence, severity, and etiology of acute AR.
Determine if rapid equilibration of the aortic and LV diastolic pressures (pressure half time <300 ms).
Visualize the aortic root and evaluate the LV size and systolic fct.
112
When evaluating acute AR, what can be echo indicators of markedly elevated LV EDP?
short deceleration time on the aortic flow velocity curve and early closure of the mitral valve
113
What is the primary approach for diagnosis of acute aortic dissection?
CT angio
114
Explain role of IABP in patients w/ severe acute AR.
Contraindicated.
115
Most common causes of chronic severe AR in the US and other high-income countries?
Low-middle income countries?
BAV, primary diseases of ascending aorta and sinuses of Valsalva.
Rheumatic heart disease.
116
What valve anatomy correlates w/ Stage A or "at risk" AR patients?
BAV or other congenital valve anomaly.
Aortic valve sclerosis.
Diseases of the aortic sinuses or ascending aorta.
Hx of rheumatic fever or rheumatic heart disease.
IE.
117
What are valve hemodynamics in asx severe AR?
Jet width ≥65% of LVOT.
Vena contracta >0.6 cm.
Holodiastolic flow reversal in the proximal abdominal aorta.
Regurgitant volume ≥60 mL/beat.
Regurgitant fraction ≥50%.
ERO ≥0.3 cm2.
Angiography grade 3 to 4.
In addition, diagnosis of chronic severe AR requires evidence of LV dilation.
In stage B and C AR, regurgitant volume and ERO are better predictors of clinical outcome.
118
What are symptoms of pts w/ severe sx AR (stage C)?
Exertional dyspnea or angina or more severe HF symptoms.
119
In asx severe AR (stage C), describe the different hemodynamic consequences that contribute to the C1/C2 classification?
Why are these measurements important?
SEVERE ASX AR:
C1: Normal LVEF (>55%) and mild to moderate LV dilation (LVESD <50 mm).
C2: Abnormal LV systolic function with depressed LVEF (≤55%) or severe LV dilation (LVESD >50 mm or indexed LVESD >25 mm/m2).
LVEF and LVESD are predictive of development of HF sx or death in asx AR; also determinants of survival and fct results s/p surgery in Stage C2 and D; nl LVEF in stage D have significantly better long-term postop survival.
120
In pts w/ moderate or severe AR and suboptimal TTE or discrepancy b/w TTE and clinical findings, what are some other imaging studies that can help gain information?
TEE
CMR (cardiac magnetic resonance)
Cardiac cath
121
COR1 recommendations for medical therapy of chronic AR?
Asx chronic AR (stage B/C) - tx HTN (<140).
Severe AR w/ sx (D) or LV dysfx (C2) who can't undergo surgery - GDMT for reduced LVEF w/ ACE, ARB, and/or sacubitril/valsartan.
122
Is there evidence for vasodilating drugs to reduce severity of AR or alter disease course in absence of HTN?
None.
Just treat HTN and HF via GDMT.
123
In symptomatic pts w/ severe chronic AR (stage D), how does LV systolic function affect surgical indication?
It doesn't. Surgery is indicated.
Even sx AR pts w/ EF <35% have survival benefit.
Of note, there is NO surgical indication for severe chronic AR on its own.
Needs either symptoms, EF <55, other cardiac surgery (can be moderate), LV enlargement (LVESD 50 mm or 25 mm/m2), progressive decline in function x3 studies (2b), or progressive increase in LV dilation (LVEDD 65) (2b).
DO NOT choose TAVI over SAVR for chronic severe AR if surgical candidate (3:harm).
124
What is management of asx pt w/ chronic severe AR and LVEF <55 (stage C2)?
Ensure no other cause of diastolic dysfunction.
Aortic valve surgery is indicated.
125
Pt w/ severe AR (stage C or D) requires cardiac surgery for other indication, how should the valve be managed?
AVR.
This will prevent hemodynamic consequences of persistent AR in periop, and dec need for second cardiac operation in future.
126
Should surgery for AR be delayed until signs of dec LVEF (<55)?
No. Outcomes are optimal w/ higher EF, and in those w/ LV systolic dysfunction, outcomes are better before onset of symptoms.
127
Stage C AR (asx severe) pt w/ nl LVEF (>55) and LVESD > 50 mm. What is management?
AVR (2a).
These pts have a significant degree of LV remodeling.
LVESD should be indexed for small pts (>25mm/m2 is cutoff).
128
Moderate AR requiring other surgery management?
AVR (2a).
129
In asx severe AR (stage C), what progression in LVEF dysfx or inc in LVEDD is required (along w/ low surgical risk) to suggest need for AVR?
Progressive LVEF to <55 OR increase in LVEDD to >65 mm on 3 studies.
130
Is TAVI an option for AR patients?
Rarely feasible.
Only select pts w/ severe AR and HF w/ prohibitive surgical risk and w/ anatomy appropriate for transcatheter.
131
In pts w/ known BAV, what concurrent morphologies are looked for w/ TTE?
AS/AR, aortic coarctation.
Measure aortic sinuses and ascending aorta (repair aneurysm at 5 cm).
Helps eval for prediction of clinical outcomes and to determine intervention timing.
132
In pt w/ BAV, what other studies can be obtained when morphology/measurement of aortic sinuses, STJ, or ascending aorta cannot be assessed accurately on echo?
CMR angio or CT angio.
*still needs to be cross sectional, contrast needed for endovascular eval.
133
Is there any screening recommendation for BAV?
Surveillance?
1st degree relatives for TTE screening (2b).
Surveillance if previous AV surgery or ascending >4cm.
134
In BAV pts, what aortic diameter (sinuses or ascending) would require periodic imaging?
4cm.
TTE/CMR/CTA.
Interval determined by degree and rate of progression as well as fam hx of aortic dissection.
135
BAV w/ aortic sinus or ascending aortic aneurysm. What is cutoff for surgery (COR 1)?
*no risk factors for dissection or other indications for surgery
5.5 cm. Replace aortic sinuses and/or ascending.
5.0 if good center and pt low risk.
136
BAV w/ aortic sinus/ascending aneurysm and risk factors for dissection. How does this affect surgical indication?
Goes from 5.5 to 5cm (2a).
Even if no risk factors, a CVC can take them for surgery at 5cm if pt low risk (2b).
137
A patient w/ BAV requires AVR. At what aorta diameter should you consider aortic sinus/ascending replacement?
4.5 cm (2a)
138
If a pt w/ BAV requires surgery for the aorta (ascending or sinuses), can a valve-sparing surgery be considered?
At a CVC (2b).
139
In BAV w/ sx severe AS, can TAVI be considered?
At CVC and specific patient consideration (2b).
140
In pt w/ BAV and severe AR requiring AVR, under what conditions can an aortic valve repair be considered?
CVC (2b)
141
Are there different indications for procedural intervention for BAV (the valve itself) w/ AS or AR compared to tricuspid AS/AR?
No.
Unlike aneurysmal changes in size cutoffs.
142
A patient presents with acute severe AR from IE, what is the management?
Surgery should not be delayed.
More urgent signs: hypotension, pulmonary edema, low flow.
Medical therapy to reduce LV afterload may temporarily stabilize.
*Be careful with beta blockers in the setting of ascending dissection with AR.
143
What are some causes of acute MR?
disruption of different parts of MV apparatus; IE can cause leaflet perforation or chordal rupture; spontaneous chordal rupture may occur in myxomatous mitral valve disease; rupture of papillary muscles occurs in pts w/ acute STEMI (usually inferior infarct)
144
What are some medical therapy options for acute MR?
Vasodilation/decreased afterload: reduces impedance of aortic flow so that blood flows forward instead of from LV-to-LA.
Usually start with something easy to titrate - nitroprusside or nicardipine.
If hypotension is limiting, can try IABP or circulatory support device.
145
What is the major intervention for acute symptomatic severe MR?
Prompt mitral surgery, preferably mitral repair - lifesaving.
This is especially true for complete papillary muscle rupture causing very severe MR, which is poorly tolerated.
146
What is the difference b/w primary and secondary chronic MR in terms of the anatomic location?
Primary is a disease of the MV apparatus, secondary MR is a disease of the ventricle or atria.
147
What are the components of the mitral valve that can cause primary MR?
leaflets, chordae tendineae, papillary muscles, annulus - structures of the valve apparatus
148
Most common cause of primary MR in high-income countries?
mitral valve prolapse
younger: severe myxomatous degeneration
older: fibroelastic deficiency disease
149
What does severe MR show on echo in terms of valve anatomy?
Severe mitral valve prolapse with loss of coaptation or flail leaflet
Rheumatic valve changes with leaflet restriction and loss of central coaptation
Prior IE
Thickening of leaflets with radiation heart disease
150
What does severe MR demonstrate on echo in terms of valve hemodynamics?
Central jet MR >40% LA (AR: 65% LVOT)
Holosystolic eccentric jet MR (AR: holosystolic flow reversal in abd aorta)
Vena contracta ≥0.7 cm (ARL 0.6 cm)
Regurgitant volume ≥60 mL (AR: same)
Regurgitant fraction ≥50% (AR: NA)
ERO ≥0.40 cm2 (AR: 0.3)
Angiographic grade 3+ to 4+
151
What are the hemodynamic consequences of severe MR?
What are the LVEF and LVESD cutoffs for C1 and C2 severe disease?
Moderate or severe LA enlargement
LV enlargement (>4 cm)
+/- Pulmonary HTN at rest or with exercise
C1: LVEF >60% and LVESD <40 mm
C2: LVEF ≤60% and/or LVESD ≥40 mm
152
In pts w/ primary MR, when TTE provides insufficient or discordant info, what is indicated for eval of the severity of MR, mechanism of MR, and status of LV fct (stages B-D)?
TEE.
Especially useful for IE, as it can assess other possibly infected structures.
Useful intraop to provide better estimate of likelihood of successful surgical valve repair.
*Less accurate assessment of severity d/t anesthesia loading changes
153
In pt w/ primary MR, what is indicated to assess LV and RV volumes and function, and may help w/ assessing MR severity when there is a discrepancy b/w clinical and transthoracic/esophageal echo findings?
CMR
Good for volumes, bad for pathoanatomy.
No outcome data to compare w/ echo.
154
What study should you order in a patient w/ primary MR (stages B-D) who has a change in symptoms?
TTE. Confirm that sx are likely attributable to MR/its effects on LV, which will support surgical correction.
155
What are symptoms associated w/ severe MR?
Sequelae of loss of forward flow: dyspnea on exertion, orthopnea, declining exercise tolerance.
May indicate changes in LV or LA compliance, inc PA pressure, dec RV fct, or coexistence of TR.
156
In patients w/ symptomatic severe MR w/ preserved EF, is there a benefit from intervention?
Yes. Don't wait for EF to decline.
There's no evidence that diuretics affect prognosis once sx set in. MV surgery will improve natural hx.
157
A pt w/ MR develops a-fib confirmed by EKG. What other test should be ordered?
The new onset of AF is an indication for repeat TTE to look for changes in severity of MR and the status of the LV.
158
For asymptomatic pts w/ primary MR, what is surveillance?
TTE q6-12mo - check on LV fct (LVEF, LVEDD, LVESD) and PA pressure.
Trigger to operate (ie sx) reached at rate of 8%/yr.
*BNP can be used to help w/ eval of LV/LA if other data are conflicting.
*Global longitudinal strain may be a useful adjunct in assessing LV fct as it is less load dependent as LVEF.
159
Hemodynamic evaluation with L ventriculography may be useful to rule out cardiac cause of symptoms in what MR population? What will it show if non-cardiac?
A patient w/ lung disease in what appears to be less than severe MR.
Normal LA pressure (or PA wedge) and large transpulmonary gradient (diff b/w mean PA and LA [via PCWP]) suggest intrinsic pulm HTN.
160
In stage C2 or D MR (asx severe w/ LV dysfx or sx severe) where surgery is not possible or must be delayed, what are the recommendations for medical therapy?
GDMT for systolic dysfunction is reasonable: beta-block, ACE inh/ARB, aldosterone agonists.
Beta-block has the greatest effect.
For stage B and C1, vasodilator therapy is NOT indicated if pt is normotensive.
161
What is the role of stress echo/exercise fct test in primary asx (stages B and C) MR?
Establishes objective data for true tolerance and can at least create a baseline that can be trended.
Some pts may alter lifestyle to remain "asymptomatic."
162
In a patient w/ primary mitral regurgitation, which ones require surgery?
PRIMARY MR!
COR1: Stage C2 and Stage D.
COR2: Stage C1 w/ low surgical risk w/ likely repair OR worse LV diameter or EF x3.
*Don't touch moderate.
*Rheumatic MVr should be at CVC.
*Primary MR is a mechanical problem w/ only a mechanical solution
163
In stage D (VC >0.7, reg vol >60, RFrax <50, ERO >0.4) or C2 (LVEF <60 or ESD >40) pt w/ MR, which patients are recommended (2a) transcatheter edge-to-edge MV repair?
high or prohibitive surgical risk w/ anatomy favorable for transcatheter approach and life expectancy >1 yr
164
What is the principle/justification for operating on asx severe primary MR in terms of systolic dysfunction (CVC)?
Operate BEFORE true systolic dysfx occurs (EF <60, LVESD >40), and consider operating (2b) if worsening x3 on surveillance (LVEF or LVESD).
*This is why surveillance is important.
*Specialized centers can operate if low mortality (<1%) and likely repair (95% freedom from reop, 80% freedom from recurrence at 15-20 yrs).
165
Surgery of choice for isolated severe primary MR limited to less than one-half of posterior leaflet?
mitral repair; replacement is inappropriate unless repair is unsuccessful
Repair is associated with an operative mortality rate of <1%, long-term survival rate equivalent to that of age-matched general population, approximately 95% freedom from reoperation, and >80% freedom from recurrent moderate or severe (≥3) MR at 15 to 20 years after surgery.
As much as one-half of the posterior leaflet may be excised, plicated, or resuspended.
Execution of this procedure with a success rate ≥95% should be the expectation of every cardiac surgeon who performs mitral valve procedures.
166
Describe chronic secondary MR.
MR is associated with severe LV dysfunction caused by CAD (ischemic chronic secondary MR) or idiopathic myocardial disease (nonischemic chronic secondary MR).
Mitral valve leaflets and chords usually are normal or minimally thickened.
The best therapy for chronic secondary MR is not clear because MR is only one component of the disease, and restoration of mitral valve competence is not curative.
167
Severe secondary MR valve anatomy, hemodynamics, and associated cardiac findings?
Regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet.
Annular dilation with severe loss of central coaptation of the mitral leaflets.
Vena contracta ≥0.70 cm.
Regurgitant volume ≥60 mL.
Regurgitant fraction ≥50%.
ERO ≥0.40 cm2.
Regional wall motion abnormalities with reduced LV systolic function.
LV dilation and systolic dysfunction attributable to primary myocardial disease.
168
In pts w/ chronic secondary MR w/ severe sx (stage D) unresponsive to GDMT being considered for transcatheter intervention, what is indicated to determine suitability of the procedure?
TEE.
Should be used intraop to guide procedure.
169
What are the AHA 2020 guidelines for medical therapy for secondary MR?
Severe secondary MR and reduced EF should get GDMT for HF, including biventricular pacing as indicated (CRT). This therapy should be led by a cardiologist who is an expert in this area.
170
Intervention in secondary MR is all level 2. What are these recs according to AHA 2020?
Severe AND... SX or CABG
Sx severe secondary MR w/ persistent sx on GDMT and AF Rx.
Sx severe secondary MR w/ EF <50 w/ persistent sx on GDMT and favorable mitral anatomy w/o prohibitive hemodynamics => transcatheter edge-to-edge MV repair.
Stage D undergoing CABG.
171
RCT of mitral valve repair versus mitral valve replacement in patients with severe ischemic MR results?
NO DIFFERENCE in survival rate or LV remodeling at 2 yrs.
Rate of recurrence of moderate or severe MR over 2 years was HIGHER IN THE REPAIR GROUP, leading to a higher incidence of HF and repeat hospitalization.
*As opposed to how MVr is better for primary MR*
172
Most cases of significant TR are secondary and related to?
tricuspid annular dilation and leaflet tethering in the setting of RV remodeling because of pressure or volume overload, as seen in patients with pulmonary hypertension (primary or secondary to left-sided heart disease) or dilated cardiomyopathies.
*subgroup of patients with significant isolated TR attributable primarily to annular dilation, usually associated with AF in the absence of pulmonary hypertension or LV systolic dysfunction.
173
Describe severe TR in terms of valve hemodynamics and hemodynamic consequences.
Vena contracta width ≥0.7 cm (same as MR; severe AR is 0.6).
Central jet ≥50% RA (severe MR is 40% LA; severe AR 65% LVOT).
ERO ≥0.40 cm2 (same as MR; severe AR 0.3)
Regurgitant volume ≥45 mL (severe MR and AR is 60).
Dense continuous wave signal with triangular shape.
Hepatic vein systolic flow reversal (severe AR has abdominal aorta diastolic flow reversal).
Dilated RV and RA.
Elevated RA with “c-V” wave.
174
What clinical symptoms and presentation do pts w/ TR have?
Elevated venous pressure.
Dyspnea on exertion, fatigue, ascites, edema
175
What two diagnostic imaging methods are most useful in TR?
TTE is first line.
Invasive measurement of PA systolic pressure, especially if discordant b/w TTE and clinical psx.
176
What are the medical therapy recommendation for TR (2a)?
RHF signs and sx can be tx w/ diuretics.
Also treat the primary cause of HF.
177
What is the only level one recommendation for intervention in TR?
If severe TR, and undergoing L-side valve surgery, fix the TR.
178
What are complete recs for TR intervention?
If severe, do surgery in following situations:
- at time of L-side valve surgery
- R HF and primary TR
- R HF, secondary TR, poor GDMT response, dilation w/o inc PAP or L-side dz
- R HF, prior L-side valve, no PH or RV sys dec
- asx w/ primary TR and progressive RV dilation or systolic dysfx
If progressive TR, intervene at same time as L valve IF annular dilation 4cm OR prior R HF
179
Recommendations for timing of intervention for mixed AS and AR?
In symptomatic patients IF peak transvalvular jet velocity is 4 m/s, or if a transvalvular gradient of 40.
In asx pts w/ jet velocity of 4 m/s w/ LVEF <50. In this case, do SAVR.
*same as for pts w/ severe isolated AS.
180
Recommendations for AS/MR mixed valve disease procedures?
Overall, patients with severe AS and severe primary MR are best treated with SAVR and mitral valve surgery unless the surgical risk is high or prohibitive.
Procedures are based on primary valve needs and surgical candidacy.
If MR is secondary, mitral TEER can be considered as a staged procedure if persistent after transcatheter aortic valve.
181
Manage mixed MS and AR
Usually 2/2 rheumatic dz.
MS is usually more severe.
Aortography better visualizes AR flow as echo may underestimate severity.
If severe sx not responsive to diuretics, intervention should be done. Ideally:
- PMBC then AVR
- SAVR and mitral commissurotomy
182
Algorithm to decide mitral/aortic valve type - mechanical vs bio?
Need to know: VKA vs no VKA, valve position, patient age.
For AV: <50 will always get a mechanical (or Ross). 50-65 can be discussed. >65 gets bio.
For MV: <65 should be encouraged to get mechanical.
183
Decision making for anticoagulation in prosthetic valves?
Bioprosthetic: (2a) VKA for 3-6 mo, then ASA lifelong.
For bio-TAVI, option of DAPT instead of VKA.
Mechanical: note that other risk factors and mitral position require INR of 3 (instead of 2.5).
ASA can be added for other indication (CAD).
Bridging for noncardiac surgery is needed for mech + other risk factors or mitral mechanical.
184
How do you manage anticoag/antiplt therapy in heart valve patients w/ embolic events or valve thrombosis?
In general, whatever anticoagulation they are getting will be increased.
185
Management of excessive anticoag/serious bleeding in pts w/ prosthetic valves on VKA.
4-factor PCC is first line.
IV vit K if PCC fails and no need for anticoag x7 days.
186
Management of acute excessive anticoag/serious bleeding in pts w/ prosthetic valves on DOAC (ie how do you reverse dabigatran, rivaroxaban, apixaban)?
dabigatran (Pradaxa) - idarucizumab (Praxbind)
anti-xa agent (rivaroxaban or apixaban [Eliquis]) - andexanet alfa
187
Recommendations for intervention for prosthetic valve stenosis or regurgitation?
More aggressive with regurgitation.
188
Preconception management of women with native heart valve disease?
Reasons to go before conception:
Severe VHD AND symptoms.
Rheum MS that can get PMBC.
Severe AS.
Severe MR that can get repair.
Bio valve preferred if replacing either.
189
Recommendations for intervention during pregnancy in women with VHD?
Intervention is reasonable for pregnant women who have severe NYHA III or IV HF symptoms despite medical therapy.
190
Anticoag for prosthetic mechanical valves in women during pregnancy?
Warfarin <5 mg/day is ok for all trimesters.
If >5 mg, only unsafe in 1st trimester - use LMWH.
1 week before delivery, bridge w/ heparin.
4-6 hrs before delivery, stop heparin.
If unexpected delivery occurring, reverse anticoag and do C-section.
191
Management of CAD in pts undergoing valve intervention?
192
AF interventions in pts undergoing VHD interventions?
What about postop anticoag?
193
In pts who meet standard indications for intervention for VHD with another indication for nonurgent noncardiac surgery, which procedure is done first?
Cardiac procedure.
For asymptomatic pts w/ moderate VHD undergoing elective noncardiac surgery, it is reasonable to perform the elective noncardiac operation.
194
What is the workup for suspected prosthetic valve stenosis? What is the difference in workup between mechanical and bio?
TTE and TEE for all valve types. Fluoro or cine CT for mechanical valves. +/- 4D CT.
195
What is the major indication for intervention for prosthetic valve stenosis? What is the difference in intervention between mechanical and bioprosthetic?
Symptomatic severe prosthetic valve stenosis.
Mechanical can only undergo surgical repair. Hope they can tolerate.
If bio valve and not a surgical candidate, they can get ViV repair at CVC.
196
What is the workup for suspected prosthetic valve regurgitation?
TTE and TEE
197
What are the indications for intervention in prosthetic valve regurgitation?
Severe symptomatic or with intractable hemolysis or HF.
Severe asymptomatic with low surgical risk.
198
What are the options for intervention in prosthetic valve regurgitation? How is this decision made?
For bio, you can do surgical intervention vs ViV vs percutaneous repair.
If the patient is a surgical candidate, they should undergo surgical intervention (asx severe w/ low risk, sx [including HF and hemolysis] severe w/ non-prohibitive risk).
If the patient is symptomatic [including HF and hemolysis] w/ severe bioprosthetic regurgitation, and they are referred to a CVC, they can undergo percutaneous repair for paravalvular regurgitation. Otherwise, they can get ViV.
