Mitral Valve Diseases

Searchable, collapsible flashcards covering normal mitral apparatus, mitral stenosis, mitral regurgitation, echocardiographic assessment, balloon valvuloplasty, PISA, and advanced quantitative parameters.

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Q1 Describe the normal mitral valve apparatus, including its components, chordae, leaflets/scallops/segments, echocardiographic views, and papillary muscle blood supply.
  • Six components of the mitral apparatus: leaflets, annulus, chordae tendineae, papillary muscles, left atrial wall, and left ventricular wall.
  • Chordae tendineae: connect mitral leaflets to the papillary muscles and LV wall.
    • Primary chords: attach to the leaflets’ edge.
    • Secondary chords: attach to the leaflets’ body.
    • Tertiary chords: found only in the posterior mitral leaflet; attach to the basal leaflet area and annulus.
  • Mitral leaflets:
    • Two leaflets: a larger anterior leaflet and a crescent-shaped posterior leaflet.
    • The posterior leaflet is divided into three scallops: by indentations; lateral to medial: P1, P2, P3.
    • Corresponding anterior leaflet coapting segments: A1, A2, A3.
    • Two commissures: separate the leaflets at the edges: lateral commissure and medial commissure.
  • Echocardiographic views:
    • 3D surgeon’s view: mitral valve viewed from the LA perspective, with the aorta placed at 12 o’clock to match the operative orientation.
    • 2D echocardiography: mitral valve is viewed from the LV perspective.
  • Papillary muscles:
    • Two major papillary muscles: posteromedial and anterolateral; each may have multiple heads and provide chordae to the corresponding half of both leaflets.
    • A third accessory papillary muscle: may occasionally be present.
    • Blood supply:
      • Anteromedial/anterolateral papillary muscle: dual blood supply from the left anterior descending coronary artery and a diagonal or marginal branch of the left circumflex artery.
      • Posteromedial papillary muscle: single blood supply from the posterior descending branch; therefore it is more susceptible to ischemic injury.
Q2 List the causes of mitral stenosis and describe the distinguishing features of rheumatic MS, degenerative MS/MAC, inflammatory MS, and congenital MS.
  • Etiology of MS
    • Acquired: rheumatic MS; degenerative; inflammatory (systemic lupus, carcinoid heart disease, drug-induced valvulopathy).
    • Congenital: parachute MV, supravalvular stenosis, double orifice mitral valve.
    • Rheumatic fever is the most common cause of MS worldwide.
  • Rheumatic MS
    • Morphological hallmark: commissural fusion, best seen in PSAX view.
    • 3D echo demonstrates fusion best from the LV perspective.
    • Commissural fusion prevents full anterior leaflet opening, causing diastolic restriction, anterior leaflet doming, and the “hockey stick” appearance.
    • Thickening and calcification start at leaflet tips and commissures, then extend to the rest of the leaflets and chordae.
    • M-mode hallmarks: increased leaflet echogenicity, decreased excursion, reduced anterior-posterior leaflet separation, decreased E-F slope (inversely correlates with stenosis severity), and paradoxical anterior diastolic motion of the posterior mitral leaflet due to tip tethering.
  • Degenerative MS and mitral annular calcification (MAC)
    • Age-related degenerative MS: characterized by mitral annular calcification without commissural fusion; leaflets may be thickened/calcified with restricted motion.
    • MAC grading based on posterior mitral annulus calcification:
      • Mild: ≤ one third of posterior annulus calcified.
      • Moderate: one third to two thirds of posterior annulus calcified.
      • Severe: ≥ two thirds of posterior annulus calcified.
    • Severe MAC can occur with normal mitral leaflets.
    • MAC may have a mobile component with increased risk of embolization.
    • Caseous MAC: rare; central liquefaction necrosis appears as an echolucent core within annular calcification; texture is toothpaste-like and composed of calcium, fatty acids, cholesterol, and macrophages; linked to stroke from embolization; differentials include tumor and abscess.
  • Inflammatory MS
    • Classically SLE causes Libman-Sacks endocarditis/verrucous endocarditis: sterile valvular vegetation composed of immune complexes, hematoxyline bodies, and platelet thrombi.
    • Lesions may heal with fibrosis/calcification and rarely cause valvular dysfunction.
    • Echo appearance: rounded mass affecting the free edge of mitral leaflets; in short-axis view, diffuse thickening at the mitral free edge without commissural fusion.
  • Congenital MS
    • Supravalvular stenosis ring: fibrous membrane just superior to the MV and inferior to the LA appendage; not to be mistaken for cor triatriatum sinister.
    • Cor triatriatum sinister: fibrous/fibromuscular perforated membrane divides the LA into a posterior-superior chamber receiving pulmonary venous flow and an anterior-inferior chamber containing the LA appendage; perforation size dictates clinical presentation from early infancy to asymptomatic.
    • Parachute MV: single papillary muscle onto which all chordae attach, or two papillary muscles very close together; limits mobility of otherwise normal leaflets and causes obstruction. Hallmark is demonstration of a single papillary muscle; associated with cleft MV, ostium primum ASD, or Shone’s complex.
    • Double orifice MV: rare congenital anomaly with two mitral orifices that may cause obstruction.
Q3 How is mitral stenosis severity classified, and how is mitral valve area measured by planimetry, pressure half-time, continuity equation, and PISA?
  • MS severity classification (since 2014): based on valve area alone.
    • Normal MV area: 4–6 cm².
    • Progressive MS: MV area >1.5 cm².
    • Severe MS: MV area ≤1.5 cm².
    • Other severity indices are important supportive elements.
  • Planimetry
    • Best correlation with anatomic valve area in rheumatic MS.
    • In rheumatic MS, the mitral apparatus is funnel-shaped with the smallest orifice at the leaflet tips, so planimetry must be performed at the leaflet tips.
    • 2D planimetry: obtain mitral short-axis view with a careful, slow sweep to visualize the smallest orifice.
    • Biplane-assisted 2D planimetry: more accurate; align the orthogonal plane cursor in long-axis view at the mitral leaflet tips.
    • 3D planimetry: most accurate and superior when image quality is good; view the MV from the LV perspective.
    • Advantage: planimetry is not affected by loading conditions or beat-to-beat variation seen with PHT and continuity methods.
  • Pressure half-time (PHT)
    • As MS worsens, pressure decline and LV filling take longer, so PHT becomes prolonged.
    • Formula: \( \text{MVA (cm}^2\text{)} = \frac{220}{\text{PHT}} \)
    • PHT is measured on CW mitral inflow signal.
    • If mitral inflow is bimodal: measure PHT from the mid-diastolic slope.
    • In atrial fibrillation: do not measure PHT from short-diastole cycles; average multiple appropriate diastolic-duration cycles.
    • PHT depends on LV and LA compliance and is inaccurate in severe LV diastolic dysfunction or significant aortic regurgitation.
  • Continuity equation
    • Well validated, but:
      • Do not use LVOT SV in significant aortic regurgitation.
      • Avoid in atrial fibrillation or significant beat-to-beat variation.
  • PISA method
    • Rarely used for MVA but applicable.
    • Because mitral leaflets affect the hemisphere area, use angle correction:
      • \( \text{MVA} = 2\pi r^2 \times \frac{V_1}{V_2} \times \frac{\Theta}{180} \)
      • r = flow convergence radius; V₁ = Nyquist limit; V₂ = peak velocity of mitral inflow; Θ = angle of the mitral leaflets.
    • Peak mitral velocity and isovelocity hemisphere radius should be measured at a matched cardiac cycle frame.
Q4 Discuss the mean pressure gradient in mitral stenosis, the inter-atrial shunt association, and supportive echocardiographic findings.
  • Mean pressure gradient
    • Derived from CW tracing of mitral inflow.
    • Optimize ultrasound beam angle to be as parallel as possible to flow; use color flow Doppler to direct the CW cursor.
    • In MS, LV filling occurs during entire diastole, so gradient depends on diastole duration:
      • Short diastole/fast heart rate: less LV filling → higher LA pressure and higher mean gradient.
      • Longer diastole/slow heart rate: more LV filling → lower LA pressure and lower mean gradient.
    • Therefore the mean gradient is dynamic and should be reported with heart rate.
    • Associated MR also influences mean gradient.
    • In atrial fibrillation, average the mean gradient from 5–8 consecutive beats.
    • Mean gradient <5 mmHg is unlikely in severe MS.
    • Mean gradient does not determine intervention, which is based primarily on MVA and symptoms, except in symptomatic patients with MVA >1.5 cm² undergoing stress testing for hemodynamic assessment, where mean gradient is a key player.
  • Inter-atrial shunt association
    • Lutembacher syndrome: rheumatic MS + congenital ASD; the LA vents high pressure to the RA.
    • In this setting, MV pressure gradient, PHT, and LA size are no longer accurate indices of MS severity.
    • Similar pathophysiology occurs with iatrogenic ASD and stretched PFO.
    • MVA by planimetry remains accurate.
  • Supportive findings
    • LA size: severe MS → LA likely severely enlarged; less severe MS → LA usually mild to moderately enlarged.
    • PASP: severe MS → PASP usually elevated >30 mmHg secondary to elevated LA pressure and pulmonary venous congestion; less severe MS → PASP usually normal at rest.
Q5 How is suitability for balloon valvuloplasty assessed? Include the Wilkins score and additional predictors.
  • Wilkins score: most widely adopted echocardiography-based scoring system for balloon valvuloplasty suitability.
    • Assesses four variables: leaflet thickening, leaflet mobility, calcification, and degree of subvalvular thickening.
    • Each variable is assigned 1–4 according to table 10-1.
    • Score 4–8: predicts favorable balloon valvuloplasty outcome.
    • Higher score: predicts increased risk of adverse outcome; consider alternative therapy.
Table 10-1: Wilkins Score for Balloon Valvuloplasty Suitability
Grade Mobility Thickening Calcification Subvalvular Thickening
1 Highly mobile valve with only leaflet tips restricted Leaflets near normal thickness (4–5 mm) Single area of increased echo brightness Minimal thickening just below mitral leaflet
2 Leaflet mid and base have normal mobility Mid leaflets normal, considerable thickening at margins (5–8 mm) Scattered areas of brightness confined to leaflet margins Thickening of chordal structure extending to 1/3 of chordal length
3 Valve continues to move forward in diastole Thickening extending through entire leaflet (5–8 mm) Brightness extending into leaflet mid-portion Thickening extending to distal third of chords
4 No or minimal forward leaflet movement in diastole Considerable thickening of all leaflet tissue >8–10 mm Extensive brightness throughout leaflets Extensive thickening and shortening extending down to papillary muscle
  • Additional predictors
    • Wilkins score should not be used alone.
    • Degree of MR must be considered: moderate to severe MR is a contraindication because MR is expected to worsen after balloon dilatation.
    • Commissural fusion pattern predicts outcome:
      • Unilateral commissural fusion and calcification: may cause the balloon to tear the unfused commissure without altering the fused commissure, resulting in significant MR.
      • Bilateral commissural fusion is more favorable.
Q6 Classify MR mechanisms and describe myxomatous degeneration, MVP, flail/partial flail, scallop localization, and mitral annular disjunction.
  • MR mechanism classification
    • Primary MR: pathological mitral leaflets.
    • Secondary MR: distortion of the mitral apparatus secondary to LV or LA remodeling.
    • This classification greatly impacts therapeutic approach and outcome.
  • Carpentier classification (based on leaflet motion)
    • Type I: normal leaflet motion; MR caused by annular dilatation or leaflet perforation.
    • Type II: excessive leaflet motion (prolapse/flail leaflets).
    • Type III: restricted leaflet motion.
      • IIIa: restricted in systole and diastole, e.g., rheumatic MR.
      • IIIb: restricted in systole, seen in LV dilatation.
  • Myxomatous degeneration
    • Most common cause of primary MR; mitral valve prolapse (MVP) is the most common presentation.
    • MVP is a spectrum: fibroelastic deficiency at the mild end and Barlow’s disease at the severe end, with overlap.
    • Fibroelastic deficiency: focal loss of mitral integrity/connective tissue while leaflets remain thin; typically affects one leaflet; valve is redundant with excessive motion.
    • Barlow’s disease: diffuse leaflet thickening and redundancy due to mucopolysaccharide infiltration; typically involves both leaflets and chords.
    • Both can present as MVP or flail leaflet/segment.
  • MVP definition
    • Echo definition: displacement of the mitral leaflet into the LA ≥2 mm from the mitral annular plane, seen in PLAX or apical long-axis views.
    • Do not use apical 4-chamber or 2-chamber views to diagnose MVP because the saddle-shaped annulus is displayed at its lower point, producing false prolapse.
    • Mitral annular plane is defined from leaflet insertion to leaflet insertion.
    • M-mode can demonstrate prolapse and involved leaflet when the cursor is aligned through the MV in PLAX or PSAX views.
    • Billowing: excessive systolic leaflet motion toward the LA below the annular plane but <2 mm; not prolapse.
  • Flail and partial flail
    • Flail leaflet: extreme prolapse; edge and body of leaflet are located in the LA. Diagnosed by leaflet tip pointing toward the LA.
    • Caused by ruptured chords or, more extremely, ruptured papillary muscle.
    • Partial flail: leaflet tip points toward LA without involvement of the leaflet body; commonly caused by a ruptured primary chord, seen more often in rheumatic valves with stiff, non-redundant leaflets.
  • Scallop/segment localization
    • At the coaptation point, two corresponding leaflets are viewed; e.g., P2 at one edge implies A2 at the other edge.
    • A2 and P2 are usually seen when the aortic valve is in view.
    • Apical 2-chamber view: when the cutting plane is at the right angle, the two commissures are viewed; called the “commissural view”; sometimes two MR jets may be seen.
    • Most accurate localization is by 3D echo enface view from the LA perspective:
      • Prolapse: bulge without crossing over to the opposite leaflet.
      • Flail: bulges toward the atrium and crosses over to the opposite leaflet.
    • Automated 3D mitral quantification can produce a color-coded parametric map showing billowing height and location.
  • MR direction in prolapse/flail
    • MR in flail leaflet is usually severe.
    • Jet is eccentric and opposite to the diseased leaflet, except bileaflet prolapse, where the jet may be central.
  • Mitral annular disjunction (MAD)
    • Detachment of ventricular myocardium from the mitral annulus.
    • Typically associated with MVP, but independent MAD can occur.
    • Associated with increased lateral wall longitudinal strain (supranormal).
    • MAD degree correlates with papillary muscle fibrosis and ventricular arrhythmia.
Q7 Describe other primary MR etiologies, secondary/functional MR, ischemic MR, tenting, SAM, and the causes of anteriorly vs posteriorly directed eccentric MR jets.
  • Other primary MR etiologies
    • Rheumatic MR: rheumatic MV usually presents as MS, but severe calcification can fix leaflets and prevent full coaptation, causing MR with MS. Rheumatic MR can also occur without commissural fusion and MS. Chordal rupture may cause flail or partial flail.
    • Endocarditis:
      • Libman-Sacks endocarditis may cause valvular dysfunction including regurgitation.
      • Bacterial endocarditis can destroy the valve and cause significant MR; it can also cause leaflet perforation with significant MR.
    • Cleft mitral valve: congenital; may be isolated or associated with parachute MV and ostium primum ASD. Commonly affects the anterior leaflet, much less often the posterior leaflet. Echo shows an echo-free space in the involved leaflet on short-axis view, with color Doppler regurgitation within the defect. Clinical course ranges from asymptomatic with mild MR to severe MR with early presentation.
  • Secondary (functional) MR
    • Leaflets are normal or minimally affected but typically tethered.
    • Includes:
      • LV remodeling.
      • Mitral annular dilatation secondary to LV or LA dilatation.
      • Ischemic MR.
    • LV adverse remodeling/dilatation from cardiomyopathy symmetrically pulls both leaflets apically and causes central MR.
    • Ischemic MR: MR with normal mitral leaflet structure resulting from coronary artery disease—myocardial ischemia, infarction, or ischemic LV remodeling.
      • Regurgitation is usually posteriorly directed, but can be central depending on leaflet involvement and LV remodeling.
      • Ischemic LV remodeling commonly affects the posterior leaflet more, producing a posteriorly directed jet.
    • In secondary MR, the anterior leaflet body is often tethered apically, creating a “seagull” or “hockey stick” appearance; this should not be confused with rheumatic MV, which has thickening and commissural fusion.
    • Papillary muscle dysfunction:
      • Usually affects the posteromedial papillary muscle because of its single blood supply.
      • Causes restricted systolic motion of the posterior mitral leaflet.
      • Diagnosed by a fixed or minimally mobile posterior leaflet in the setting of ischemia or regional wall motion abnormality involving the inferior/inferolateral LV wall, with a posteriorly directed MR jet.
    • Systolic tenting: hallmark of secondary MR due to LV remodeling.
      • Produced by apical leaflet tethering.
      • Tenting height, area, and volume correlate with severity but are not accurate for severity grading.
      • Tenting height/area are measured in PLAX, apical 3-chamber, or apical 4-chamber views by identifying the annular line and measuring height to the coaptation line and the area below.
      • 3D mitral quantification can measure tenting volume.
  • MR and systolic anterior motion (SAM)
    • SAM of the anterior mitral leaflet: part of the leaflet is pushed/pulled anteriorly into the LVOT.
    • Can cause significant LVOT obstruction and significant MR.
    • The posterior leaflet remains at the coaptation point while the anterior leaflet moves into the LVOT, creating a posteriorly oriented gap and a posteriorly directed MR jet.
    • SAM can be demonstrated by M-mode.
    • Typically seen in hypertrophic obstructive cardiomyopathy, but significant SAM can occur without hypertrophic cardiomyopathy.
    • Mechanism is not solely Venturi effect; the anterior mitral leaflet is involved and is usually elongated (>3 cm) in SAM, along with other factors.
  • Etiology by eccentric MR direction
    • Anteriorly directed jet: caused by prolapse/flail posterior leaflet.
    • Posteriorly directed jet: caused by:
      • Prolapse/flail anterior leaflet.
      • Ischemic MR.
      • SAM.
Q8 How is MR severity assessed with color Doppler, vena contracta, CW Doppler, PW Doppler, and chamber volumes?
  • Color Doppler
    • Regurgitant jet area is excellent for ruling out MR but not reliable for grading.
    • Severe MR with low blood pressure/sedation may show a small jet; hypertensive mild MR may show a large jet.
    • Momentum = Orifice area × Velocity²: \( \text{Momentum} = \text{Orifice area} \times \text{Velocity}^2 \)
    • Coanda effect: an eccentric wall-hugging jet attaches to a nearby surface; jet area appears small and MR is underestimated.
    • Lower Nyquist limit recruits lower-velocity flow into the jet area, making the jet appear larger.
    • Findings suggestive of severe MR:
      • Central jet area >50% of LA area.
      • Eccentric jet wraps around the LA and enters pulmonary veins.
  • Vena contracta (VC)
    • Narrowest area of the jet as it passes through the valve.
    • Ideally measured in PLAX using axial resolution.
    • Independent of flow and driving pressure gradient.
    • Cutoffs:
      • <0.3 cm: mild MR.
      • 0.3–0.7 cm: moderate MR.
      • >0.7 cm: severe MR.
    • AR and MR VC cutoffs differ because AR occurs in diastole, which is longer than systole; AR leaks more volume than MR at the same VC.
    • VC is equally accurate for central and eccentric jets, but in multiple jets, VC width is inaccurate and cannot be cumulatively added.
    • 3D VC area (VCA) can be measured by multiplanar reconstruction; VCA correlates well with EROA and may be used as EROA. In multiple jets, VCA can be cumulatively added with reasonable accuracy.
  • CW Doppler
    • Triangular, early-peaking jet: indicates quick LV-LA systolic equilibrium from severe MR.
    • Dense MR jet compared with forward flow density suggests severe MR.
    • Faint rounded jet indicates trace to mild MR.
  • PW Doppler
    • Mitral inflow PW at leaflet tips:
      • Severe MR raises LA pressure and produces a high early filling wave.
      • E ≥1.2 m/s suggests severe MR in a native valve.
      • High LA pressure due to diastolic dysfunction should be considered, especially in secondary MR.
      • Low E velocity with A-wave dominance excludes severe MR.
    • Pulmonary vein PW Doppler:
      • Very useful for grading, especially on TEE.
      • TTE usually detects only the right upper pulmonary vein, which is subject to aliasing and contamination; TEE can sample all four pulmonary veins.
      • Pattern depends on LA pressure:
        • Systolic dominance: normal LA pressure; excludes severe MR.
        • Systolic blunting with diastolic dominance: occurs as LA pressure increases.
        • Systolic reversal: occurs in severe MR when the jet enters the pulmonary veins.
      • In eccentric MR, the jet may selectively enter one pulmonary vein and cause systolic reversal in only that vein, even with moderate MR.
      • Systolic reversal in more than one pulmonary vein is specific for severe MR.
      • Differentials for systolic blunting: grade 2 LV diastolic dysfunction and atrial fibrillation.
  • LV and LA volumes
    • Chronic severe MR imposes volume overload on the LV and LA.
    • In chronic severe MR, LV and LA dilatation are expected.
    • Normal LA size excludes chronic severe MR.
Q9 How is MR quantified, and what are the overall grading criteria for chronic MR?
  • Quantification principles
    • Quantification is superior to visual assessment and should be applied whenever MR is more than mild.
    • Elements: regurgitant volume (RVol), regurgitant fraction (RF), and effective regurgitant orifice area (EROA).
  • PISA method
    • Accurate for MR quantification, but less accurate and more difficult in eccentric jets.
    • PISA gives EROA at a single point in systole, but EROA may be dynamic.
    • In MVP with late systolic MR, EROA by PISA is at peak regurgitation velocity; regurgitant volume is smaller than EROA.
    • Because clinical consequences depend on regurgitant volume, grade by RVol, not EROA, in MVP and late systolic MR.
    • In secondary MR, the regurgitant orifice is often crescent/elliptical, so PISA underestimates EROA.
    • An elliptical orifice is suggested by 3D VCA or different VC widths in apical 4-chamber and apical 2-chamber views.
  • Volumetric method
    • When accurate, eliminates PISA limitations.
    • EROA derived from regurgitant volume represents the averaged EROA over the MR duration.
  • Overall grading
    • MR should be graded comprehensively using all variables.
    • Quantification is more accurate.
    • ASE 2017 valvular regurgitation guidelines: if ≥4 specific criteria for mild or severe MR are present, MR may be graded accordingly without quantification.
ASE 2017 Valvular Regurgitation Guidelines — Chronic MR Grading Criteria
Feature Mild Moderate Severe
MV morphology No or mild leaflet abnormality Moderate leaflet abnormality/tenting Severe valve lesion: flail, ruptured papillary muscle, large perforation, severe tenting, or malcoaptation
LA and LV size Usually normal Normal/mildly dilated Dilated
Color flow jet area (Nyquist 50–70 cm/s) Small, central, often brief Variable Large central jet (>50% of LA) or eccentric wall-impinging
Flow convergence (Nyquist 30–40 cm/s) Not visible, transient or small (<0.3 cm) Intermediate Holosystolic, large (>1 cm)
CW Doppler jet Faint/partial/parabolic Dense but partial or parabolic Holosystolic/dense/triangular
VC width (cm) <0.3 0.3–0.6 ≥0.7 (>0.8 for averaged biplane)
Pulmonary vein flow Systolic dominance Normal or systolic blunting Systolic blunting or reversal
Mitral inflow A-wave dominant Variable E-wave dominant (>1.2 m/s)
EROA (cm²) <0.2 0.2–0.29 0.3–0.39
RVol (mL) <30 30–44 45–59
RF (%) <30 30–39 40–49
Q10 Describe the inter-atrial shunt association with severe MR, acute MR, and diastolic MR. Include the source references.
  • Inter-atrial shunt association with MR
    • Recently described: severe MR secondary to a flail leaflet with normal LA and LV size can occur with an associated ASD.
    • Pathophysiology is similar to Lutembacher syndrome: the MR volume overload is transferred to the right side.
    • Patients may present with normal LV and LA size but dilated RV and RA.
  • Acute MR
    • Rare but causes significant hemodynamic compromise.
    • Etiology: usually ruptured chord with flail leaflet, ruptured papillary muscle, or leaflet destruction by endocarditis.
    • Jet is usually eccentric.
    • Presentation: pulmonary edema and hypotension.
    • Eccentric acute jet may selectively enter one pulmonary vein, causing unilateral pulmonary edema.
    • Because of eccentric jet, hypotension, and rapidly elevated LA pressure, the MR jet velocity is low and brief, so MR severity is underestimated or not appreciated.
    • Pulmonary vein systolic reversal is common.
    • Significant MR lowers LV afterload, producing a hyperdynamic LV; clinical findings plus hyperdynamic LV and low stroke volume suggest acute MR.
    • TTE is not sensitive for determining the mechanism of acute MR and may miss the diagnosis; TEE is superior and should always be considered when acute MR is suspected.
  • Diastolic MR
    • See chapter 6.
  • Source references
    1. Rick A. Nishimura et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2014;63(22):e57-e185.
    2. Hanan Alrammah, Sami Ghazal. Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy. J Saudi Heart Assoc. 2018;30(4):336-339.
    3. Zoghbi, William A. et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation. J Am Soc Echocardiogr. 2017 Apr;30(4):303-371.
    4. Ghazal SN. Chronic Severe Mitral Regurgitation with Normal Left Ventricular Size - A Case with Coexisting Atrial Septal Defect. J Cardiovasc Echogr. 2018 Apr-Jun;28(2):133-137.