Valvular Regurgitation Sheldon Litwin, M.D.

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Valvular Regurgitation Sheldon Litwin, M.D.

• Normal heart valves have minimal leakage (back
  flow, insufficiency, regurgitation) when they
  close
• Significant valvular regurgitation causes the
  heart to do excess work (like walking up a sandy
  hill)
• Over time, significant regurgitation usually
  leads to cardiac enlargement and contractile
  dysfunction

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Water flows down hill!
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Clinical goals in Valvular Disease

• Make the diagnosis
• Slow the disease progression
• Prevent complications
• Intervene at just the right time
• Not too soon, not too late

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Pathophysiology of Regurgitant Valve Lesions

• Volume load on ejecting and receiving chambers
• Chamber dilatation
• ? compliance (compensatory)
• ? wall stress (maladaptive)
• (pressure x radius)/wall thickness
• Eventual contractile failure
• Arrhythmias

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Key Concept in Valve Regurgitation

• Timing of intervention is tricky!!
• Chamber enlargement and contractile dysfunction
  develop very gradually
• Dont subject your patient to risks before it it
  necessary
• Fix the problem before damage becomes
  irreversible (may need to intervene before
  symptoms develop)

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Mitral Valve Disease

• Annulus
• Leaflets
• Chordae
• Papillary muscles
• LV

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Acute MR Etiology

• Ischemia/MI
• Posterolateral hypokinesis
• Papillary muscle rupture
• Ruptured chordae
• Endocarditis
• Systolic Anterior Motion (SAM) of mitral
  leaflet(s)

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Ischemia or MI
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Ruptured Papillary Muscle
Always causes acute, severe MR - a surgical
emergency.
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Endocarditis Valve destruction by micro organisms
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Acute MR Pathophysiology

• Flow from LV (high pressure) to LA (low pressure)
  ? ?LA pressure ? ?PCWP ? pulmonary edema
• Low compliance atria transmits LV pressure more
  directly to pulmonary capillaries
• ? forward stroke volume (low cardiac output)

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Acute MR V waves

• V wave twice the amplitude of mean PCWP
  suggests severe MR

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Acute MR Management

• Vasodilators (if BP adequate)
• Reduce afterload ? ? regurgitant volume ? ?
  forward volume
• Inotropic agents if LV function ?
• Antibiotics for SBE
• Surgery (MVR)!!!!!

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Chronic MREtiology

• Degenerative
• mitral annular calcification (MAC)
• Myxomatous degeneration/MVP
• LV dilatation
• Anorexigenic drugs (phen-fen)
• Healed endocarditis (IE or noninfectious)
• Hypertrophic cardiomyopathy
• Rheumatic

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Mitral Annulus Calcification(MAC)
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Mitral Valve Prolapse

• Syndrome vs. disease
• overdiagnosis
• Myxomatous degeneration of leaflets chordae
  (increased MMP activity)
• SBE prophylaxis if significant MR present (gt
  mild)
• Early valve repair for severe MR

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Ruptured chords/flail leaflet
LA
LV
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Congenital Heart Disease
Residual MR after repair of cleft MV (assoc. c
primum ASD)
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Nonvalvular causes of MR

• May occur without structural abnormalities o f
  valve
• Usually LV dilatation and remodeling with
  increased sphericity
• Stretch of annulus and lateral displacement of
  papillary muscles may cause malcoaptation of the
  leaflets

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LV dilatationLateral displacement Paps
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Quantification of MRsize of jet on echo
Mild-Moderate
Mod-Severe
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Quantitation of MR Regurgitant Volume

• lt 20 ml trace
• 20-30 ml mild
• 30-50 ml mod
• gt 50 ml severe

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Quantification of MR PISA
Proximal Isovelocity Surface Area Method for
calculating effective regurgitant orifice area
(ERO)
Flow through the hole must be the same as the
flow proximal to the hole (similar to
continuity equation for aortic valve area).
LV
lt 0.2 cm2 mild 0.2-0.4 cm2 mod gt0.4 cm2
severe
MV
LA
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PISA
TEE Severe MR
The bigger the PISA, the bigger the hole
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Mitral Regurgitation Grade
Grade 1 2 3 4
Jet size (color) Small, lt 4 cm2, lt10 Mod, central, 4-6 cm2, 10-30 Large central, 6-8 cm2, 30-40 Lg central, ecc, gt8cm2, gt 40, pulm vein
PVF S gt D S lt D Diastolic SFR
VC width lt 0.3 cm 0.3-0.49 0.5-0.69 gt0.7 cm
EROA (cm2) lt 0.2 0.2-0.29 0.3-0.39 gt 0.4
RV (ml) lt 30 30-44 45-59 gt60
RF () lt30 30-39 40-49 gt50
Pulm vein flow pattern, vena contracta width,
effective regurgitant orifice area, regurgitant
volume, regurgitant fraction
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Compensation in chronic mitral regurgitation

• Left atrial dilatation (? compliance)
• Smaller change in pressure with same regurgitant
  volume
• LA PCWP may stay normal for many years
• LV enlargement (to allow for maintained stroke
  volume)
• ?s wall stress

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Afterload in MR

• LV afterload (resistance to LV ejection) is
  reduced because the LA is a low pressure
  alternate pathway for ejection
• LV chamber function (EF) should theoretically be
  greater than normal if myocardial contractility
  is preserved
• Once EF is below normal, significant LV
  dysfunction exists and it is likely to get worse
  once the mitral valve is replaced

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Complications of chronic MR

• Atrial fibrillation
• LV dilatation and systolic dysfunction
• Passive pulmonary hypertension with RV dysfunction

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Chronic Compensated MR
Normal
Acute MR
70 ml
95 ml
100 ml
EDV 170 ml
LA 15 mmHg
LA 25 mmHg
LA 10 mmHg
EDV 150 ml
EDV 240 ml
70 ml
ESV 30 ml
ESV 50 ml
95 ml
ESV 50 ml
Chronic Decompensated MR
Chronic Compensated MR
Acute MR
65 ml
70 ml
95 ml
LA 25 mmHg
LA 15 mmHg
LA 25mmHg
EDV 260 ml
EDV 240 ml
EDV 170 ml
85 ml
ESV 110 ml
70 ml
95 ml
ESV 30 ml
ESV 50 ml
EF RF SV
Nl 67 0 100
AMR 82 50 70
EF RF SV
AMR 82 50 70
CCMR 79 50 95
EF RF SV
CCMR 79 50 95
CDMR 58 57 65
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Medical management of MR

• Afterload reduction, Rx of arterial HTN
• Rx heart failure (if not surgical candidate)
• SBE prophylaxis
• Rheumatic fever prophylaxis
• Rx of atrial fibrillation
• Rx of ischemia

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Surgical Rx of chronic MR

• Valve replacement replaces one disease with
  another
• Thrombosis, infection, pannus, degeneration
• Valve repair is far preferable when technically
  feasible
• Excision of prolapsing/flail segments (posterior
  leaflet) with placement of annuloplasty ring

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Timing of surgery for MR

• Old approach was to wait for symptoms, LV
  enlargement or systolic dysfunction (typically
  serial echoes were performed)
• Problem wait too long?
• With low morbidity/mortality of repair and low
  need for reoperation, trend is to recommend early
  repair for severe MR, even in asymptomatic
  patients with normal LV function

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Indications for surgery in chronic, nonischemic MR

• Class I
• Acute symptomatic MR in which repair is likely
• NYHA Class II-IV symptoms with normal LV function
  (EF gt 60) and LVESD lt 45 mm
• Symptomatic or asymptomatic with mild LV
  dysfunction (EF 50-60) and/or LVESD 50-55 mm
• Symptomatic or asymptomatic with moderate LV
  dysfunction (EF 30-50) and/or LVESD 50-55 mm

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Prosthetic Mitral Valves
Mechanical bileaflet tilting disc
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Tricuspid valve regurgitation etiology

• Pulmonary hypertension
• RV enlargement (infarct, dysplasia)
• Primary tricuspid disease
• Infectious endocarditis
• trauma
• Carcinoid
• Pacing wires/catheters
• Ebstein's anomaly
• Iatrogenic/bioptome

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Tricuspid Endocarditis
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Aortic Insuffiency (regurgitation)

• Valve normally open during systole, closed during
  diastole
• AI occurs during diastole as aortic pressure is
  higher than LV pressure during this part of the
  cardiac cycle

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Etiology of Aortic Valve Regurgitation

• Annulus
• Leaflets
• Root

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AI Etiology Aortic Root problems

• Aortic root enlargement
• Hypertension
• Marfans syndrome
• Syphillis
• Aneurysm
• Aortic dissection
• Leaflet involvement
• Shape of root/annulus
• Ruptured sinus of Valsalva
• Iatrogenic (septal myectomy)

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AI Etiology leaflet problems

• Calcification/fibrosis
• Degenerative
• Rheumatic
• Bicuspid
• Endocarditis
• Infectious
• Noninfectious
• Diet drugs

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Aortic Valve Endocarditis
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Aortic Dissection
LV
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Quantification of AIsize of color jet on echo
Mild-Moderate
Mod-Severe
Quantification is important because we usually
only operate on patients with severe AI and it is
necessary to track progression of disease
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Quantification of AI

• Pressure half time (Doppler)
• The larger the hole in the valve, the faster
  pressure equilibrates between the aorta and the
  LV diastole
• Short pressure half time indicates more severe AI
  (lt 250 ms severe)
• Diastolic flow reversal in the
• descending aorta
• Regurgitant volume
• (or fraction)

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Severe AI
Holodiastolic Flow Reversal in Descending Ao
Arch Descending Ao
arch
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AI Pathophysiology

• Flow from Aorta (high pressure) to LV (low
  pressure) ? ?LVEDP ? ?LA pressure ? ?PCWP ?
  pulmonary edema
• ? forward stroke volume (low cardiac output)
• If AI occurs gradually, LV enlargement
  compensates and it is tolerated
• If it happens suddenly, it typically causes
  pulmonary edema and/or shock

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AI signs

• Large forward stroke volume to maintain actual
  stroke volume
• Wide pulse pressure (e.g. 160/60)
• Bounding peripheral pulses
• Head bob
• Uvula swinging
• Quinckes pulses (finger nails)
• Etc.

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Acute AI Management

• Vasodilators (if BP adequate)
• Reduce afterload ? ? regurgitant volume ? ?
  forward volume
• Inotropic agents if LV function ?
• Antibiotics for SBE
• Avoid intra-aortic balloon pump (makes AI worse)
• Surgery (AVR)!!!!!

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Chronic aortic insufficiency

• LV enlargement to maintain forward stroke volume
  (?s wall stress)
• LA PCWP may stay normal for years
• LV chamber function (EF) should be normal or
  greater than normal if myocardial contractility
  is preserved
• Once EF is below normal, significant LV
  dysfunction exists and the outcome following
  valve replacement is worse

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Timing of surgery for AI

• Historical approach was to wait for symptoms, LV
  enlargement or systolic dysfunction (typically,
  serial echoes were performed)
• Problem wait too long?
• As surgical techniques and prosthetic valves
  improve, earlier surgery may be warranted
• However, aortic valve repair is not yet practical

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Surgical Rx of chronic AI

• Low EF increases mortality

• Dont wait too long

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Is it ever too late to operate in AI?
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Medical management of AI

• Afterload reduction (nifedipine, ACE inhibitors)
  - recent study suggests not helpful
• Control arterial HTN
• Treat heart failure (if not surgical candidate)
• SBE prophylaxis
• Rheumatic fever prophylaxis
• All palliative

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Mitral Valve Repair(new approaches)
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What is the best parameter to describe MR
severity?

• Quantify regurgitant volume, regurgitant
  fraction, and/or regurgitant orifice area
• Echo
• MRI

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Why is severe mitral regurgitation often
tolerated for many years?

• Dilatation of the left atrium increases the
  compliance of the receiving chamber so that
  pressure is not transmitted back to the pulmonary
  capillaries
• LV dilatation allows stroke volume to increase so
  that forward flow is maintained

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What clinical factor (related to the heart) would
make you reluctant to send a patient with severe
AI for valve replacement?

• Severe LV systolic dysfunction. Mortality of
  surgery increases as EF drops and the chances of
  recovery become less.

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Why is exercise tolerated poorly in a patient
with AS but not one with AI?

• In AS the pressure gradient increases as cardiac
  output increases.
• Diastole is selectively shortened as heart rate
  goes up. Thus, there is actually less time for AI
  to occur and regurgitant volume stays the same or
  decreases.

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2 patients have severe AI. One is very ill and
the other is Asymptomatic. Why?

• The most likely reason is the time course over
  which AI develops.
• Acute AI is tolerated poorly.
• Chronic AI is generally tolerated well.

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Indications for surgery in chronic nonischemic MR

• Class IIa
• Asymptomatic patients with preserved LV function
  and atrial fibrillation
• Asymptomatic patients with preserved LV function
  and pulmonary hypertension (PASP gt 50 mmHg at
  rest or gt 60 mmHg with exercise)
• Asymptomatic with LV EF 50-60 andLVESD lt 45 mm,
  or EV gt 60 and LVESD 45-55 mm
• Patients with severe LV dysfunction (EF lt 30
  and/or LVESD gt 55 mmHg) in whom chordal
  preservation is highly likely
• Asymptomatic with chronic MR with preserved LV
  function in whom valve repair is highly likely

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Indications for surgery in chronic nonischemic MR

• Class IIb
• Patients with MVP and preserved LV function who
  have recurrent ventricular arrhythmias despite
  medical therapy
• Class III
• Asymptomatic patients with preserved LV function
  in whom significant doubt about the feasibility
  of repair exists

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Semi-Quantitation of MRContrast Ventriculography

• Injection of radiopaque contrast material into LV
  (invasive, nephrotoxic, allergic rxns)
• Look for opacification of LA
• of beats to fully opacify
• Degree of clearing between beats
• Visualization of pulmonary veins

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Measuring AI Severity
mod
mild
sev
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Quantitation of AIContrast Aortography

• Injection of radiopaque contrast material into
  aortic root (invasive, nephrotoxic, allergic
  rxns)
• Look for opacification of LV
• of beats to fully opacify
• Degree of clearing between beats

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Acute MR Diagnosis

• Physical exam
• (tachycardia, hypotension, systolic murmur, S3,
  stigmata of SBE)
• CXR pulmonary edema
• ECG acute MI or ischemia
• Echo test of choice
• Cath

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Acute AI Diagnosis

• Physical exam
• Diastolic murmur (may be absent), tachycardia,
  hypotension, systolic murmur (flow), diastolic
  murmur(s), S3, stigmata of SBE)
• CXR pulmonary edema
• ECG nonspecific
• Echo test of choice (TEE or MRI if aortic
  dissection suspected)
• Cath little role in diagnosis