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

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

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

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

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

4 Harvard Medical School Anatomy:

5 Harvard Medical School

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

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

9 Harvard Medical School Management – Symptomatic patients:

10 Harvard Medical School Management – Asymptomatic patients: >90%

11 Harvard Medical School How to measure severity of mitral regurgitation:

12 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School Vena Contracta Width Long-axis Short-axis

22 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School Proximal Isovelocity Surface Area (PISA)

25 Harvard Medical School 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 Proximal Isovelocity Surface Area (PISA)

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

27 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School Quantitative Doppler Volumetric Measurements:

30 Harvard Medical School 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 Harvard Medical School V. Adjunctive Findings Continuous wave 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 Harvard Medical School Summary

33 Harvard Medical School Summary

34 Harvard Medical School Evolving Concepts and Technologies in Mitral Valve Repair

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

36 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School Commercially Available Rings and Band

40 Harvard Medical School Novel (Percutaneous) Approaches to Mitral Valve Repair

41 Harvard Medical School 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 Harvard Medical School Coronary Sinus Approaches

43 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School 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 Harvard Medical School The End: Questions?


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