AHA Guidelines - Valve 2020 Flashcards
What is the aorto-mitral curtain?
Where the anterior mitral leaflet unionizes with the L-non commissure of the aortic valve.
Where is the AV node in relation to the mitral valve?
immediately adjacent to the R fibrous trigone (near A3/posteromedial commissure/P3); beware placing sutures here
Describe papillary muscles of mitral valve
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.
What are the anatomic limits of the aorto-mitral curtain?
right (confluence of mitral, tricuspid, and noncoronary cusp of aortic + membranous septum) and left (fibrous continuity of the aortic and mitral valves) fibrous trigone
Which mitral leaflet is more prone to dilating and causing MR? Why?
Posterior - annular tissue is thinnest and not attached to the fibrous skeleton of the heart.
First line imaging to eval MV disease?
TTE.
TEE is used for further refinement and surgical planning.
What is the Wilkins echo score used for?
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).
For MR, which TTE and TEE views allow for eval of the 6 scallops?
TTE parasternal.
TEE transgastric.
Echo findings of MS
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.
When is cardiac cath used in workup for MV disease?
Pts older than 40 (up to 25% have disease w/o symptoms).
LV and RV ventriculography can also assess severity of disease.
Describe incidence/prevalence of rheumatic MS.
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.
What is mild/progressive MS in terms of objective measurement?
MV area > 1.5 cm2. Diastolic pressure half-time <150ms.
When is MS considered severe by valve hemodynamics?
MV area < 1.5 cm2. Or diastolic half-time 150 ms or >.
What is the pathophysiology of nonrheumatic calcific MS?
Calcification of the mitral annulus that extends onto the leaflets, resulting in narrowing of the annulus and rigidity of the leaflets.
What is the primary cause of MS?
Rheumatic disease.
How are the stages of MS defined?
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).
What are the pertinent hemodynamic consequences of severe MS?
Hemodynamic consequences are measured in terms of the LA and pulmonary circulation.
Severe LA enlargement and elevated PASP >50 mm Hg.
What are the pertinent hemodynamic consequences of severe MS?
Hemodynamic consequences are measured in terms of the LA and pulmonary circulation.
Severe LA enlargement and elevated PASP >50 mm Hg.
What are symptoms associated with MS?
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.
MS pts who are PMBC candidates need what ruled out?
TEE should be done to look at LA thrombus and eval MR.
MR more than mild is contraindication to PMBC.
What are the pathologic/hemodynamic end results of elevation of the transvalvular gradient across the MV?
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.
Pt w/ established dx of rheumatic MS has a change in symptoms, what should be done to dx?
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.
How can symptoms of MS worsen even if anatomic disease doesn’t progress?
Increased hemodynamic load, such as in pregnancy.
Also new onset AF, fever, anemia, hyperthyroidism.
What does MR do to stroke volume and EF?
Decreased SV w/ preserved EF.
What is LV remodeling like in MR?
eccentric hypertrophy and chamber dilation w/ annular dilation
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
What is MR effect on LA?
LA dilation and thickening => inc risk of arrhythmia and thrombus
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
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.
In patients w/ rheumatic MS, when is VKA indicated?
A fib, prior embolic event, LA thrombus
In patients w/ MS and AF w/ RVR, what can be beneficial in terms of nonop AF management?
heart rate control
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
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
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
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
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.
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 of “symptomatic” since it signifies progressive LA damage, increases thromboembolism, increases LV pressure (shorter diastolic filling interval), associated w/ worse outcomes and suboptimal PMBC results.
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).
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.
What valve morphology in MS would be more amenable to valve replacement (as opposed to commissurotomy)?
severe valvular thickening, subvalvular fibrosis w/ leaflet tethering
MS pt failed PMBC, what is next?
Surgery, preferably commissurotomy
MS pt meets criteria for PMBC but has moderate TR, what should be done?
surgical approach w/ tricuspid repair
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.
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.
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
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
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).
Other than calcification, what can cause nonrheumatic MS?
radiation therapy
MV repair w/ small annuloplasty ring
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
Why is CXR important for patients w/ suspected VHD?
Heart size, pulmonary vascular congestion, intrinsic lung disease, calcification of aorta/pericardium
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.
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.
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.
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.
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.
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.
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.
In principle, what hemodynamically altering agents should be avoided in pts w/ stenotic VHD?
Blood pressure lowering
The maintenance of what remains the most important component of an overall healthcare program in preventing IE?
Oral health
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.
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.
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.
Risk of IE is highest in what patient populations?
Prosthetic valve, previous IE, or CHD w/ residual flow distributions.
Transcatheter IE rates are equivalent.
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.
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.
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.
What is the mortality for MVR CABG?
9%
Most common early complication of surgical valve replacement?
atrial fibrillation - 1/3 of pts within 3 mo of surgery
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).
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
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.
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.
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.
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
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.
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
What are the hemodynamic consequences of severe AS?
LV diastolic dysfunction, LV hypertrophy, possibly pulm HTN.
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.
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.
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
Most common reason for procedural intervention in patients with BAV?
AS
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.
Is there any screening recommendation for BAV?
Surveillance?
1st degree relatives for TTE screening (2b).
Surveillance if previous AV surgery or ascending >4cm.
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.
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
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.
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
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.
Algorithm to decide mitral/aortic valve type - mechanical vs bio?
Need to know: VKA vs no VKA, valve position, patient age.
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.
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.
Recommendations for intervention for prosthetic valve stenosis or regurgitation?
More aggressive with regurgitation.
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.
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.
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.
Management of CAD in pts undergoing valve intervention?
AF interventions in pts undergoing VHD interventions?
What about postop anticoag?
Hemodynamics of Severe AS?
Hemodynamics of Symptomatic severe low-flow, low-gradient AS with reduced LVEF?
