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Mitral Regurgitation 2008 David M. Leder, MD 8/20/08.

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Presentation on theme: "Mitral Regurgitation 2008 David M. Leder, MD 8/20/08."— Presentation transcript:

1 Mitral Regurgitation 2008 David M. Leder, MD 8/20/08

2 Outline Anatomy Etiology of mitral regurgitation
Management strategies for chronic severe MR Quantification of MR severity on echocardiography Advances in mitral valve repair

3 Anatomy Functionally includes: Left ventricular myocardium
Subvalvular apparatus (papillary muscles and chordae tendinea) Mitral annulus Mitral valve leaflets Left atrium

4 Anatomy:


6 Etiology of Mitral Regurgitation:
Primary: -Myxomatous -Endocarditis -Rheumatic -Trauma -Anorexic drugs Functional (Secondary): -LV systolic dysfunction -Ischemic heart disease -Hypertrophic CM

7 Functional (Carpentier) Classification:
Type I = normal leaflet motion but with annular dilatation or leaflet perforation Type II = leaflet prolapse (eg myxomatous disease) or papillary muscle rupture Type III = restricted leaflet motion. IIIa = rheumatic disease IIIb = ischemic or idiopathic cardiomyopathy.

8 Bonow, R. O. et al. J Am Coll Cardiol 2006;48:598-675
Management strategy for patients with chronic severe mitral regurgitation Bonow, R. O. et al. J Am Coll Cardiol 2006;48: Copyright ©2006 American College of Cardiology Foundation. Restrictions may apply.

9 Management – Symptomatic patients:

10 Management – Asymptomatic patients:

11 How to measure severity of mitral regurgitation:

12 I. Hemodynamic Determinants of MR
RgV = Regurgitant volume. ROA = Regurgitant oriface area. Cd = Discharge coefficient MPG = Mean systolic pressure gradient b/t the LV and LA T = Duration of MR during systole.

13 Regurgitant Oriface Area (ROA)
Typically fixed in rheumatic MR b/c the valve is fibrotic, calcified, and immobile. In DCM and myxomatous disease, it is often dynamic and load dependent. ROA is a fundamental determinant of MR severity and therefore its measurement/calculation is critical.

14 Discharge coefficient (Cd)
Is a constant. Accounts for contraction of the flow stream as it passes through the anatomic orifice. It is dependent upon orifice geometry, flow, and fluid viscosity. Is not affect by clinical variations in loading conditions.

15 Mean systolic pressure gradient (MPG)
Is a primary determinant of MR severity, but its effect on echo variables is mitigated by 2 factors: 1. Hemodynamic changes tend to move LV and LA pressures in the same direction, thus the net effect is blunted. 2. It is a function of its square root. eg. a 144mmHg gradient compared to a 100mmHg gradient only results in a 20% difference in the calculated MR volume. (ie. 12 v. 10)

16 Duration of MR during systole (T)
Particularly important in myxomatous degeneration, where late systolic MR may lead to overestimation of MR severity by techniques that rely on single frame measurements (eg PISA or vena contracta).

17 II. Mitral Valve Anatomy
Includes the leaflets, annulus, chordae, papillary muscles, and left ventricle. Severe MR seldom occurs when the mitral valve and left ventricle are anatomically normal. LA size and LV function provide clues to the severity and chronicity of MR.

18 III. Doppler Color Flow Mapping
Represents an image of the spatial distribution of velocities within the imaging plane. It can be profoundly affected by instrument settings and hemodynamic variables. Since spatial distribution of velocities is not a primary determinant of MR severity according to the Gorlin equation, some argue it should not be heavily relied upon to grade MR severity. That being said, it does offer several potential ways to assess MR severity.

19 Color Flow Jet Area Generally, larger jets which extend deep into the LA represent more MR than small thin jets. However, the correlation b/t jet area and MR severity is poor due to technical and hemodynamic limitations. Therefore avoid grading MR severity by “eyeballing” the color flow jet area. Exception: a small central jet w/ an area <4.0cm2 or <10% of LA area, is almost always mild MR.

20 Vena Contracta Width Represents the smallest, highest velocity region of a flow jet and is typically located at or just downstream from the regurgitant orifice. Should be measured in a plane perpendicular to mitral leaflet closure (eg PLA). If the regurgitant orifice is circular, then vena contracta width should be an excellent marker of the ROA. However, the regurgitant orifice in MR is often elongated along the coaptation line…ie, like a smiley face.

21 Vena Contracta Width Long-axis Short-axis

22 Vena Contracta Width Has been shown to be accurate in assessing the severity of MR. According to ASE: <0.3cm = mild MR >/=0.7cm = severe MR A strength of this method is that it works equally well for central and eccentric jets.

23 Proximal Isovelocity Surface Area (PISA)
Based on the hydrodynamic principle that the flow profile of blood approaching a circular orifice forms concentric, hemispheric shells of increasing velocity and decreasing surface area. In MR, color flow mapping is usually able to image one of these hemispheres that corresponds to the aliasing velocity of the instrument. The aliasing velocity should be adjusted to identify a flow convergence region with a hemispheric shape. The radius of this hemisphere is then measured and flow rate is calculated as the product of the surface area of the hemisphere and the aliasing velocity.

24 Proximal Isovelocity Surface Area (PISA)

25 Proximal Isovelocity Surface Area (PISA)
Assuming that the maximal PISA radius occurs at the time of peak regurgitant velocity, the maximal EROA can be derived as: PkVreg = the peak velocity of the regurgitant jet by continuous wave Doppler. Generally, an EROA >/=0.4cm2 is considered to be severe MR. <0.2cm2 is mild MR

26 Proximal Isovelocity Surface Area (PISA)
EROA = [6.28 x (.8)(.8) ml/s] / [480 cm/s] = 0.3cm2

27 Limitations of PISA It is more accurate for central jets.
In MR, the orifice shape is often elliptical rather circular/hemispheric. Any error is determining the location/radius of the orifice is squared. Therefore PISA is more accurate if the aliasing velocity can be adjusted to obtain a radius of >/=1cm. For determination of EROA, it is essential that the CW signal by well aligned with the regurgitant jet.

28 IV: Quantitative Doppler Volumetric Measurements:
In the absence of regurgitation, stroke volume should be equal at different sites, eg the mitral and aortic annulus. In the presence of regurgitation (assuming the absence of an intracardiac shunt), the flow through the affected valve is larger than through other competent valves.

29 Quantitative Doppler Volumetric Measurements:

30 Quantitative Doppler Volumetric Measurements:
Common errors: 1. Failure to measure the valve annulus properly. 2. Failure to trace the modal velocity of the pulsed Doppler tracing. 3. Failure to position the sample volume correctly, at the level of the annulus.

31 V. Adjunctive Findings Continuous wave Doppler Pulsed Doppler
-the density of the CW signal is a useful qualitative index of MR severity (a dense signal suggests worse MR) -an unusually low maximum velocity may indicate hemodynamic compromise (high LA and low LV systolic pressures) Pulsed Doppler -patients with severe MR usually exhibit dominant early filling (E>1.2m/s); an A-wave dominant inflow pattern virtually excludes severe MR. Pulmonary vein flow -with increasing severity of MR, systolic velocity in the pulmonary veins progressively decreases and reverses in severe MR.

32 Summary

33 Summary

34 Evolving Concepts and Technologies in Mitral Valve Repair

35 Key Concept: the fibrous skeleton of the heart is fixed and its length does not change with mitral valve disease.

36 Valvular-Ventricular Interactions
The collagenous matrix elements within the chordae tendineae and papillary muscles are histologically continuous with the collagen network of the heart at one end and the mitral valve annulus and leaflets at the other end. Removal of the papillary muscles and chordae results in ventricular dilatation, increased wall stress and afterload, and decreased contractile fxn. Late survival after MVR can be enhanced with the use of chordal-sparing techniques.

37 Annuloplasty Rings The annulus is a dynamic, saddle-shaped structure.
The original Carpentier ring was flat and rigid. Newer mitral rings have attempted to replicate this normal saddle shape and flexibility.

38 Annuloplasty Rings Despite a more “normal” valve physiology, superior long-term clinical results with flexible rings have not been demonstrated. The most recent annuloplasty rings are cause-specific, geometrically shaped to accommodate the underlying pathology and not to replicate the “normal” mitral annulus.

39 Commercially Available Rings and Band

40 Novel (Percutaneous) Approaches to Mitral Valve Repair

41 Coronary Sinus Approaches
Concept: Place a device in the coronary sinus to push against the posterior portion of the mitral annulus and ideally improve coaptation of the posterior and anterior mitral valve leaflets Anatomic limitations: Often the coronary sinus does not lie directly adjacent to the posterior mitral valve annulus. The CS is an atrial structure and not in the same plane as the mitral valve annulus The left circumflex artery may lie in between The distance between the CS and posterior mitral annulus increase with chronic ischemic MR

42 Coronary Sinus Approaches

43 Annular Approaches Include annular shrinking via magnets or heating.
The Mitralign device approaches the posterior annulus directly from the LV and positions stitches to allow annular cinching. The PS3 system approaches the posterior annulus from the atrial septum and tethers a device from the P2 vicinity toward the atrial septum.

44 Alfieri Revisted: Edge-to-edge surgical concept modified for a percutaneous approach. Feasibility study completed in the US and a randomized phase 2 trial is ongoing. Surgical experience with the technique demonstrated significant recurrent MR if it was not accompanied by an annuloplasty Reoperation at 5 years = 30% v. 8%, p=0.02

45 Subvalvular Approaches
Developed to treat complex ischemic mitral valve disease: 1. Approximate the papillary muscles (papillary muscle sling) 2. Pull the papillary muscles toward the annulus to release leaflets tethering. 3. Cut secondary chords to reduce tethering of the leaflets. All have been used with some success but the need is uncommon, as the majority of patients with MR undergoing coronary bypass are treated with simple annuloplasty rings.

46 Coapsys and i-Coapsys Evolved from the concept of moving the ventricle, rather than the annulus, to increase leaflet coaptation and eliminate functional MR. Can be placed off pump w/ echo guidance or via a minimally invasive approach w/ fluoro guidance. Employs a transventricular splint

47 Coapsys and i-Coapsys The pads are tightened gently to pull the ventricle into the region of the papillary muscles and also to move the posterior leaflet to better coapt with the anterior leaflet.

48 The End: Questions?

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