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R O M P I C T U R E S T O P R A C T I C E P A R A D I G M S

he Role of Imaging in Chronic Degenerativeitral Regurgitation

atrick O’Gara, MD, FACC,* Lissa Sugeng, MD, FACC,‡ Roberto Lang, MD, FACC,‡aurice Sarano, MD, FACC,§ Judy Hung, MD, FACC,¶ Subha Raman, MD, FACC,�regory Fischer, MD,† Blasé Carabello, MD, FACC,** David Adams, MD, FACC,†ani Vannan, MBBS, FACC�

ew York, New York; Chicago, Illinois; Rochester, Minnesota; Boston, Massachusetts;olumbus, Ohio; and Houston, Texas

hronic degenerative mitral regurgitation (MR) is a complex problem, which requires an integrated assessment

f etiology, pathophysiology, and severity to enable informed clinical decision-making. A multidisciplinary

pproach is required, with input from the clinician, imager, and surgeon. This review begins with a discussion of

ssential echocardiographic and surgical mitral valve (MV) anatomy, which dictates suitability for repair when

ndicated. The echocardiographic and Doppler principles, which underlie the quantitation of MR severity, are

ummarized in the next section, followed by a critical examination of left ventricular systolic function in this

isorder. A brief discussion of the important role of imaging in the developing field of percutaneous MV repair

s included. The methodical and objective noninvasive assessment of degenerative MR herein reviewed is

ntended to help guide management decisions for patients with this challenging valve lesion. (J Am Coll

ardiol Img 2008;1:221–37) © 2008 by the American College of Cardiology Foundation

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he natural history of chronic mitralregurgitation (MR) depends intimatelyon its etiology, the severity of the leftventricular (LV) volume overload, left

nd right ventricular contractile performance,nd the superimposition of other destabilizingnfluences such as atrial fibrillation. Table 1ists the most common causes of chronic MRith reference to the valve level(s) most com-only affected by the specific disorders. These

auses are not mutually exclusive. There aremportant differences in the outcomes of pa-ients with ischemic versus nonischemic MR,

rom *Brigham And Women’s Hospital, Boston, Massachusetts; †University of Chicago Hospitals, Chicago, Illinois; §Mayo Cliospital, Boston, Massachusetts; �Ohio State University Medicedical Center, Houston, Texas.

anuscript received January 7, 2008; accepted January 28, 2008.

elated both to the effects of recurrent myocar-ial ischemia and to the significant contribu-ion of LV remodeling to survival and function.he approach to nonischemic MR, which wille the focus of this review, may lend itself to aore uniform set of principles focused more

pecifically on the valve lesion and LV function.The management of chronic nonischemicR poses a unique set of challenges, predi-

ated in part on the more diverse causes of thisalve disorder, the difficulty in assessing LVontractile performance in the setting of re-uced afterload, the subtle and oftentimes late

nt Sinai Medical Center, New York, New York;Rochester, Minnesota; ¶Massachusetts Generalenter, Columbus, Ohio; and **Veterans Affairs

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ppearance of symptoms, the misapplication ofasodilator therapy, uncertainty regarding the indi-ations for surgery in the asymptomatic patient, andhe still-evolving adoption of operative repair tech-iques. The potential role of percutaneous mitralalve (MV) repair is the subject of active investiga-ion. Recent improvements in surgical outcomesave frame-shifted the timing of operation earlier inhe natural history of appropriately selected patientsith chronic nonischemic MR and have forced

linicians to balance the upfront risks of surgerydeath, stroke, bleeding, failure of repair) versus theelayed consequences of progressive LV volume

overload (heart failure, atrial fibrillation,death) which, for some patients, may notdevelop for decades, if at all. To date,large-scale randomized controlled clinicaltrials comparing different treatment strat-egies have been lacking. Comparisonsacross available registry and single-centerstudies have been hampered by severalfactors, including varying definitions ofMR severity, heterogeneous patient pop-ulations, selection bias, lack of standard-ized medical and surgical therapies, anddissimilar surrogate and clinical endpoints. Management strategies have there-fore evolved empirically, and guidelines haverelied more on expert consensus opinionthan on objective measures of efficacy andsafety. Because the data available from sim-ple bedside assessment are inherently impre-cise and because the consequences of clinicaldecision-making are potentially so pro-found, additional information is required tomake appropriate treatment recommenda-tions. Noninvasive imaging and, in particu-lar, echocardiography, helps fill this void andplays a critical role in the initial and longi-tudinal assessment of patients with chronicMR. In this review, we will examine the

pplication of standardized, noninvasive imaging toedical and surgical decision-making in patients with

hronic, nonischemic MR. Critical components of theoninvasive evaluation include information regardingV anatomy, MR severity, LV size and systolic

unction, and associated findings such as estimatedulmonary artery (PA) pressures. In most instances,uch information can be obtained with standardizedchocardiographic protocols, although cardiac mag-etic resonance (CMR) and computed tomographyay provide supplementary information in se-

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itral Valve Anatomy

ormal MV anatomy. The MV is a complex-dimensional (3D) structure comprising 5 distinctut highly integrated levels:

EAFLETS. The MV has 2 leaflets, namely anteriorAML) and posterior (PML) leaflets (Fig. 1). TheML has a quadrangular shape and is attached topproximately three-fifths of the annular circumfer-nce. It typically has 2 well-defined indentationshat divide it into 3 individual scallops identified as1 (anterior or medial scallop), P2 (middle scallop),nd P3 (posterior or lateral scallop), according tohe Carpentier classification. The 3 opposing seg-ents of the AML are designated as A1 (anterior

egment), A2 (middle segment), and A3 (posterioregment). The segmental differentiation of the leaf-ets is an important tool to describe specific ana-omic conditions. The PML indentations are be-ieved to aid in leaflet opening during diastole. Theeight of the normal PML is less than one-half ofhe AML. However, both leaflets have similarurface areas. The AML has a semicircular shapend attaches to approximately two-fifths of thennular circumference. The fibrous continuity be-ween the AML and the aortic annulus in the areaf the left and noncoronary cusps is designated theortic-mitral curtain. The free edge of the AML issually continuous, without indentations. The mo-ion of the AML defines an important boundaryetween the inflow (during diastole) and outflowduring systole) tracts of the LV. A rough oroaptation zone exists on the atrial surface of theeripheral leaflet margins (Fig. 2). The normal MVay have a coaptation length of several millimeters

o ensure valve competency against normal end-ystolic pressure.

OMMISSURES. The commissures define a distinctrea where the AML and PML come together. Themount of commissural tissue varies greatly; com-issures may exist as distinct leaflet segments,

imilar to adjacent segments of the PML. Moreommonly, the commissures constitute several mil-imeters of leaflet tissue, which provide continuityetween the AML and PML at their annularnsertion. Commissural chordae have a distinctonfiguration, providing support to the commissures well as to adjacent leaflet segments. In Carpen-ier’s segmental anatomy, the anterior-lateral com-issure is referred to as AC and the posterior-

B B R E V I A T I O N S

N D A C R O N YM S

ML � anterior mitral leafle

MR � cardiac magnetic

esonance

S � coronary sinue

DV � end-diastolic volume

F � ejection fraction

RO � effective regurgitant

rifice area

SD � end-systolic dimensio

SV � end-systolic volume

CV � great cardiac vein

A � left atrium

V � left ventricular

R � mitral regurgitation

V � mitral valve

ISA � proximal isovelocity

urface area

ML � posterior mitral leafle

F � regurgitant fraction

Vol � regurgitant volume

V � stroke volume

EE � transesophageal

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HORDAE. The chordae tendineae make up theeaflet suspension system that ultimately determineshe position of and tension on the leaflets atnd-systole. Chordae originate from the fibrouseads of the papillary muscles and may be classifiedccording to their site of insertion on the leaflets.

arginal or “primary” chordae insert on the freeargin of the leaflets, prevent marginal prolapse,

nd align the rough zones to ensure coaptation.ntermediate or “secondary chordae” insert on theentricular surface of the body of the leaflets andrimarily prevent billowing and reduce tension on

Figure 1. Example of Mitral Valve With Type IIIb Dysfunction

The operative view is shown (left), and the corresponding “surgicalvolume rendering (right). Abbreviations: A1, A2, A3 � anterior mitr

Table 1. Chronic Mitral Regurgitation

Etiology

Chronic coronary artery disease

Ischemic MR

Myxomatous degeneration

Mitral valve prolapse

Barlow’s valve

Nonischemic dilated cardiomyopathy

Rheumatic heart disease

Healed infective endocarditis

Hypertrophic obstructive cardiomyopathy

Mitral annular calcification

Congenital

Connective tissue diseases

Rheumatoid arthritis

Systemic lupus erythematosus

Antiphospholipid antibody syndrome

Radiation

Drug

Ergotamines

Methysergide

Pergolide

(fenfluramine, dexfenfluramine)

AML � anterior mitral leaflet; LV � left ventricular; MR � mitral regurgitation.

valve scallops, PM � postero-medial. From Mount Sinai Medical Center

eaflet tissue (Fig. 3). They may also play a role inynamic ventricular shape and function, because ofheir contribution to ventricular-valve continuity.asal or “tertiary chordae” connect the base of theML and mitral annulus to the papillary muscle.

HE ANNULUS. The mitral annulus constitutes thenatomical junction between the LV and the lefttrium (LA) and serves as the insertion site for theleaflets. It is divided segmentally into anterior

nd posterior components. The anterior portionf the mitral annulus attaches to the fibrous

” obtained with real-time 3D transesophageal echocardiographylve scallops, AL � anterolateral; P1, P2, P3 � posterior mitral

Affected Valve Level(s)

LV, papillary muscles, annulus

Leaflets, chordae, annulus

LV, papillary muscles, annulus

Leaflets, chordae

Leaflets, chordae

AML, papillary muscles, LV

Annulus, leaflets

Anterior leaflet

Leaflets, annulus

Leaflets, chordae

Leaflets, chordae

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rigones. The right fibrous trigone comprisesortions of the mitral, tricuspid, and aortic annulind the membranous septum. The left fibrousrigone is an area made up of the left fibrousorders of the aortic-mitral curtain. The poste-ior mitral annulus is less well developed, and thebrous skeleton of the heart is discontinuous in

Figure 2. Systematic Interrogation of the MV With 2D TEE

(A) 4-chamber view obtained at 0° depicting A2 on the left and P2ing the transducer tip to 55° showing P3 on the left, A2 in the midthe transducer to 90° to visualize P3 on the left and the 3 scallopsobtained by further rotating the transducer to 120° to view P2 on timages (as visualized from the left atrial perspective) obtained withthe approximate cut planes from which the respective 2D TEE imagmedial aspect of MV; MV � mitral valve; TEE � transesophageal ecMedical Center and University of Chicago.

his region, explaining why the posterior portion p

f the annulus is prone to enlarge with LV or LAilation. The mitral annulus has a 3D saddlehape. During systole, the circumference de-reases as the commissural areas move apically,he aortic root bulges and the annulus contracts.

APILLARY MUSCLES AND THE LV. There are 2

the right. (B) Bicommissural view obtained by electronically rotat-and P1 on the right. (C) 2-chamber view obtained by rotatinge anterior mitral valve leaflet on the right. (D) Long-axis vieweft and A2 on the right. The left column correspond to MVuse of real-time 3D-TEE volume rendering. Red lines representere obtained. Ao � aorta; Lat � lateral aspect of MV; Med �

rdiography; other abbreviations as in Figure 1. From Mount Sinai

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pical and middle third of the left ventricular freeall. The anterolateral papillary muscle is often

omposed of one body or head, whereas the pos-eromedial papillary muscle may have 2 or moreeads. Each papillary muscle provides chordae tooth leaflets. The axial relationship of the chordaerevents abrasion and dyssynchrony. The anterolat-ral papillary muscle blood supply may originaterom one or more left coronary branches. Theosteromedial papillary muscle has a singular bloodupply (right or left circumflex depending on dom-nance) and is therefore particularly prone to injuryrom myocardial infarction. The attachment of theapillary muscles to the lateral wall of the LVeans the ventricle itself is also an important part of

he MV complex. Any change in ventricular geom-try that affects papillary muscle position canhange the axial relationship of the chordae andeaflets, resulting in poor coaptation.athophysiologic MV anatomy. Carpentier et al. (1)lso have proposed a pathophysiologic triad byhich MR can be described. The triad consists of

Figure 3. Intra-Operative 2D and 3D TEE Depiction of MV Prola

Schematic (upper row) and 2D as well as 3D echocardiographic exavalve prolapse (P1, middle panels) and a flail mitral valve (P2, rightviews (middle row) and real-time 3D TEE volume rendering from thwith real-time 3D TEE provide unique visualization and better undecommissures and leaflets. Abbreviations as in Figures 1 and 2.

he disease (the underlying etiology, such as Bar- o

ow’s disease or fibroelastic deficiency), the lesionse.g., chordal elongation or rupture, leaflet disten-ion, annular, leaflet and/or papillary muscle calci-cation, and annular dilation), and the dysfunctiondefined according to the systolic position of theeaflet margins in relation to the annular plane).ype I dysfunction implies normal leaflet motionith isolated annular dilation, leading to poor

eaflet coaptation. Type II dysfunction is defined byxcess motion of the margin of a leaflet segmentbove the annular plane and is the most commonype of dysfunction in degenerative MV disease. Re-tricted motion of the leaflet margin defines Type IIIysfunction, which can be further subdivided based onestriction of motion in both systole and diastoleType IIIa—usually due to fibrosis of the subvalvularpparatus) or only in systole (Type IIIb, which usuallyesults from ventricular remodeling with papillaryisplacement and leaflet tethering). Although mostatients with degenerative disease present withhordal elongation or rupture with Type II dysfunc-ion and associated annular dilation, any combination

and Leaflet Flail

les of a patient with a normal mitral valve (left panels), mitralels) as visualized with 2D TEE (long-axis mid esophageal TEEft atrial perspective (bottom row). The surgical views obtainednding of the anatomic relationships of the mitral valve annulus,

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The 2 main causes of degenerative MV diseasere Barlow’s disease and fibroelastic deficiency (2,3).arlow’s disease results in myxoid degeneration of

he MV, creating excess tissue in multiple valveegments, chordal thickening and elongation, an-ular dilation, and a tendency to calcification.hordal rupture is relatively uncommon. The Type

I dysfunction observed in Barlow’s patients occursn midsystole, resulting in a nonejection click and a

id- to late-systolic murmur due to chordal elon-ation and excess tissue. Barlow’s disease is usuallyiagnosed in young adulthood, and patients oftenemain asymptomatic with well-preserved LV sizend function for many years. In contrast, fibroelasticeficiency results from loss of mechanical integrityue to abnormalities of connective tissue structurend/or function, leading to chordal thinning, elon-ation, and/or rupture, with classic findings ofrolapse and MR of varying severity. The prolaps-ng segment may be distended, but the remainingegments of the valve may be entirely normal.ibroelastic deficiency is the most common form ofrganic mitral valve disease for which surgery isequired. The noninvasive assessment of these 3athophysiologic elements informs clinical decision-aking and helps direct surgical referral and planning.

ncreasing degrees of complexity should prompt pref-rential referral to a specialized center of excellence.urgical and echocardiographic MV anatomy. The

V can be displayed in 3 different ways as shown inigures 4A to 4C. The anatomically correct orien-

ation displays the valve from the base of the hearts if the imager were positioned in the left atriumooking down toward the LV. In this view, theatient’s left and right side correspond to themager’s left and right side, whereas the AML andML appear in their appropriate positions. The

Figure 4. Mitral Valve Displays

(A) Anatomical view. (B) Transesophageal view (MV view as visualizthese examples were obtained with the use of real-time 3D transesThe mitral valve is visualized from the left atrial perspective. From M
as in Figure 1.
ateral and medial aspects of the valve are to the leftnd right, respectively. The transesophageal vieworresponds to the orientation of the MV found inhe transgastric basal short axis view (Fig. 4B). Thisnatomically “incorrect display” used in all ultra-ound platforms results from rotating the anatom-cal view 180°. In this view, the operator’s left andight sides are reversed relative to the patient. Theurgeon’s view (Fig. 4C), which can be easilybtained with real-time transesophageal echocardiog-aphy (TEE), displays the valve in a manner similar tohe one encountered when examining it through anpened LA, standing to the right of the patient.

A systematic 2D TEE examination of the MVonsists of 4 standard midesophageal views (4-hamber, bicommissural, 2-chamber, and long-axisiews) and the transgastric basal short-axis viewFig. 2). It should be noted that the classification ofhe MV scallops in any given plane may varyccording to the individual anatomy. It is crucial tonsure that the imaging plane does not fore-shortenhe LV because this may lead to misidentification ofhe individual scallops. Accordingly, orientation tonternal landmarks such as the commissures isaramount to enhance diagnostic accuracy. Thisystematic approach is also useful in identifying thencompetent segment. A regurgitant jet arisingrom the left coaptation point indicates involvementf P3/A3, whereas a jet arising from the rightuggests involvement of A1/P1. With the use of 3DEE, the MV annulus and leaflets are best dis-layed when obtained in zoom mode to avoid stitchrtifacts that may occur in a wide-angled acquisi-ion. To simulate a surgeon’s view of the valve, theD TEE image is positioned with the aortic valve athe 11-o’clock position (Fig. 1). The LV view isnother orientation from which to assess the valve,

n the transgastric basal short axis view. (C) Surgeon’s view. Allageal echocardiography volume rendering using zoomed views.nt Sinai Medical Center and University of Chicago. Abbreviations

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articularly in patients with pathology involving theubmitral apparatus. If the subvalvular mitral appa-atus or LV constitutes the area of interest, aide-angled acquisition consisting of 4 smalleredges of volume obtained over 4 cardiac cycles

hould be obtained to demonstrate papillary muscleocation or quantitate LV function. Figures 5 and 6emonstrate examples of patients with mitral valveail and prolapse as visualized with 2D TEE andD TEE.The 3D TEE parameters of interest include: 1)

he major 3D axes of the annulus, anteroposteriornd anterolateral-posteromedial diameters, and an-ular height; 2) 3D curvilinear leaflet lengths of thenterior middle scallop, across its central portionrom the annulus to the central coaptation bordernd of the corresponding posterior middle scallop;) anterior and posterior leaflet surface areas, ex-luding the leaflet contact areas; 4) the angle be-ween the aortic valve annulus (assumed to belanar) and a least-squares fit plane of the mitralnnulus; and 5) the distances between the commis-ures and papillary muscles (Fig. 7). Measurementf these parameters may aid in understanding the

Figure 5. Example of a Patient With a P2 Flail Mitral Valve

Examples of patients with P1 prolapse (top left); P2 flail mitral valvP3 flail mitral valve (black arrow, bottom left); and Barlow’s syndroP3) (bottom right). All images were obtained with real-time 3D-TEE
perspective.
echanism of MR, improve surgical planning, andelineate annular and annuloplasty ring dynamicsefore and after operation. Higher-resolution 3DEE images enable improved quantitation of LV

unction.

uantitation of MR

uantitation of MR severity is essential for clinicalecision-making. Referral for surgery is not appro-riate for the asymptomatic patient without confir-ation that the MR is severe by standardized

riteria. The use of descriptive terms such as “mod-rately severe” can be highly subjective and influ-nced by any one of several treatment biases. Themportance of MR quantitation has been empha-ized by the guideline writing committees of themerican College of Cardiology/American Heartssociation and the European Society of Cardiol-gy (4). The severity of MR, in turn, should dictatehe associated degree of LV and LA enlargement,s well as PA pressure elevation, in patients withsolated valve disease. The use of 2D Dopplerchocardiographic quantitation proves sufficient for

allop (black arrow) with a ruptured chord (red arrow, top right);with floppy mitral valve with multiple leaflet prolapse (P1, P2 andume rendering. The mitral valves are visualized from the left atrial

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ost patients, though 3D TEE and CMR mayrovide more accurate information in selected cases.rinciples. A comprehensive approach to the assess-ent of MR severity is required. Specific findings

elated to MV anatomy, supportive findings, whichnclude chamber sizes, intra-cardiac flows, and PAressures, as well as quantitative findings regardingegurgitant volume (RVol) and effective regurgitantrifice area (ERO), constitute the basic features ofn integrated assessment. Reporting of MR severityhould be consistent with the ASE criteria forescriptive and semi-quantitative grading shown inable 2.ualitative echo-Doppler assessment. The entire

Figure 6. Correlative 3-D and 2-D TEE MV Anatomy

Example of a patient with a P2 flail mitral valve. (A) Four-chamber vTwo-chamber view obtained by rotating the transducer to 90° to vileaflet on the right; (C) Long-axis view obtained by further rotatingA2 on the right. The direction of the color jet in the long-axis viewumn images correspond to the mitral valve image (as visualized frorendering. The red arrows represent the approximate cut planes froscallops of the anterior mitral valve and P1, P2, P3 � scallops of th

V apparatus should be examined carefully and the c

olor scale optimized. Mild MR is characterizedualitatively as a small jet confined to early or lateystole with small/absent flow convergence and aarrow vena contracta. In the absence of intrinsicV systolic or diastolic dysfunction, the LV and theA dimensions also are normal. Qualitative assess-ent of larger or more eccentric jets is more

ifficult. Flail leaflet or ruptured papillary muscleost often is associated with severe MR, although

he regurgitant load may be only moderate byuantitative criteria in as many as 15% of patients.ystolic flow reversal in the pulmonary veins byulsed-wave Doppler is relatively easy to demon-trate and is specific for severe MR. Other signs

obtained at 0° depicting A2 on the left and P2 on the right; (B)ize P3 on the left and the 3 scallops of the anterior mitral valvetransducer to 120° to view the flail P2 segment on the left andttom left) is away from the side of the flail lesion. The left col-he left atrial perspective) obtained using real-time 3D-TEE volumehich the respective 2D TEE images were obtained. A1, A2, A3 �

sterior mitral valve.

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f a large flow convergence, a jet with a wide venaontracta, and a large, wall-impinging or swirlinget pattern. Interpretation of these signs is subject toide interobserver variability. High jet density by

ontinuous-wave Doppler, a dominant mitral E,nd dilated LA and LV chambers, support theiagnosis of severe MR. There are several addi-ional limitations to the qualitative assessment of

R. First, there are no specific criteria for theesignation of moderate MR, other than the ab-ence of findings consistent with either mild orevere MR (4). Second, interpretation of color flowatterns of MR can be highly subjective, thuslurring the distinction between moderate and se-ere. It is widely appreciated that eccentric jets tendo underestimate and central jets to overestimateVol (5). Third, although specific signs have highositive predictive value, they lack sensitivity for theetection of severe MR. These limitations have ledo the development of quantitative methods forssessment of MR (4).uantitative Doppler echocardiographic assessment.uantitation is based on hydrodynamic principleshich rely on the noncompressibility of blood and

he continuity or conservation of mass. Flow can be

Figure 7. Examples of 3D Renderings of the Mitral Valve ObtainQuantitative Analysis of the Mitral Apparatus

Examples of 3D renderings of the mitral valve obtained from 3D-TEmitral apparatus. (Top, Left) Antero-posterior diameter is shown inlet surface area (hatched) with posterior middle scallop leaflet prola� anterior, P � posterior, AL � anterolateral, PM � posteromedial,

alculated as: flow � (vessel area) · (mean velocity of c

lood). These concepts are used to measure the 3arameters indicative of MR severity: 1) RVol (theolume in ml/beat regurgitated each systole), a mea-ure of absolute volume overload; 2) regurgitantraction (RF, the percentage of the total LV strokeolume represented by the RVol), a measure ofelative volume overload; and 3) ERO (the meanrea of the systolic regurgitant orifice), a measure ofesion severity.

These parameters of MR severity are measuredith the use of 3 validated methods: 1) quantitativeoppler (4) is based on measurement by pulsed-ave Doppler of mitral and aortic stroke volumessing the product of mitral and aortic annular areasimes their integral of forward blood velocity (tissueelocity integral [TVI]). Regurgitant volume isalculated as the difference between mitral andortic stroke volume, RF as the ratio of RVol toitral (total) stroke volume, and ERO as the ratioVol to the regurgitant jet TVI; 2) quantitative 2D

chocardiography (4) is based on the same princi-les, but mitral stroke volume is replaced by that ofV stroke volume by tracing end-diastolic andnd-systolic LV volumes; and 3) proximal isoveloc-ty surface area (PISA), which focuses on the flow

From 3D-TEE Data Set With Software Designed for

taset using software designed for quantitative analysis of then. (Top, Right) Annular height. (Bottom Left) Anterior mitral leaf-. (Bottom, Right) Angle between the mitral and aortic annuli. A� aorta, TEE � transesophageal echocardiography.

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Fig. 8), as observed with color-flow imaging (6).he color scale baseline is shifted downward to

nsure measurability of the flow convergence radiusnd velocity. Flow through the convergence zone (andence through the regurgitant orifice) is calculated ashe product (area of flow-convergence hemisphere) ·aliasing velocity). This velocity term is indicated byhe machine (junction blue-yellow). Effective regurgi-ant orifice area is calculated as the ratio of flow toeak regurgitant velocity and RVol as the product ofERO) · (regurgitant TVI) (7). Thus, it is possibleuring a single examination to measure RVol andRO by the use of multiple methods.

Figure 8. Principles of the PISA Method of MR Quantitation

The flow convergence is indicated by the large open hemi-sphere observed in perspective and the jet of MR by the largearrow at the bottom. V1 is the velocity on the flow conver-gence hemisphere (white arrows) whereas the jet velocity isV2. The right side indicates the calculation of regurgitant flow(Flow 2) and effective regurgitant orifice area (ERO). R is theradius of the hemisphere of flow convergence. MR � mitral

Table 2. Grading MR by Doppler Echocardiography

Additional Wording Mild

Angiographic grading 1�

Specific signs ● Small central jet area �4 cm2

or �20% of LA● Vena contracta width �0.3cm

● No or minimal flowconvergence

Supportive signs ● Systolic dominant flow inpulmonary veins

● A-wave dominant mitralinflow

● Low density CW-Doppler MRsignal

● Normal LV size● Normal LA size

Quantitative parameters

RVol, ml/beat �30

RF, % �30

ERO, cm2 �0.20

Modified from Zoghbi et al. (4).ERO � effective regurgitant orifice area; LA � left atrium; LV � left ventricle;

gregurgitation; PISA � proximal isovelocity surface area.

ccuracy and reproducibility. Quantitation requiresttention to detail, repetition, and quality control.he PISA method requires close zooming andownshift of the color baseline tailored to obtain annconstrained flow convergence of almost circularhape (Fig. 9). The flow convergence radius shoulde measured at peak regurgitant velocity, whichsually occurs near the T-wave on the electrocar-iogram. Regurgitant flow, and therefore ERO,ay vary throughout systole as a function of the

ause of the MR. Continuous-wave Doppler shoulde recorded with a single-crystal transducer, andttention paid to avoid incorporation of partialystolic signals (early and late). Simplified estimatesf RVol may be derived from the ratio of flow/3.25.ultiple measurements of these parameters should

e made and the values for RVol and ERO averaged.Emerging technologies for the assessment of MR

everity may prove useful. Real-time 3D TEE holdsromise for volume measurement, jet characteriza-ion, and definition of proximal flow convergence.ardiac magnetic resonance is of limited value for

ssessment of MV structure and motion, but it cane use to provide highly accurate quantitation of LVnd regurgitant volumes. The ERO measurementsannot be reliably obtained with this technique.nterpretation and integration. The qualitative anduantitative characterization of MR must be inte-

Moderate

Severeild to

oderateModerate to

Severe

3� 4�

R more than mild, but nocriteria for severe MR

● Vena contracta width �0.7cmwith large central MR jet (area�40% of LA) or with a wall-impinging jet of any size.

● Large flow convergence● Systolic flow reversal inpulmonary veins

● Prominent flail leaflet orruptured papillary muscle

R more than mild, but nocriteria for severe MR

● Dense, triangular continuous-wave Doppler signal

● E-wave dominant mitralinflow (E �1.2 m/s)

● Enlarged LV and LA size,(particularly with normal LVfunction)

30–44 45–59 �60

30–39 40–49 �50

20–0.29 0.30–0.39 �0.40

� mitral regurgitation; RF � regurgitant fraction; RVol � regurgitant volume.

MM

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al treatment and long-term follow-up. For pa-ients with isolated mild or moderate nonischemic

R with preserved LV size and function, expectantanagement with periodic surveillance is appropri-

te. It is for patients with isolated, severe MR thatiming of surgery becomes critical. Many suchatients are asymptomatic and thus reliance onbjective and standardized noninvasive data is nec-ssary for clinical decision-making. Designation of

R as severe must be verifiable across the spectrumf parameters reviewed above and summarized inable 2.

he LV in Chronic MR

igure 10 depicts the stages that an untreatedatient with severe MR might experience (8). Incute, severe MR (Fig. 10B), there is suddenistension of the LA, producing LA hypertensionnd pulmonary congestion. Increased LV preload isanifested by slightly increased end diastolic vol-

me (EDV) whereas the regurgitant pathway forjection into the LA decreases LV afterload andnd systolic volume (ESV). These changes act inoncert to increase total stroke volume (SV) but notnough to normalize forward SV. Thus, the patientas decreased forward output and pulmonary con-estion and is in heart failure despite normal LVontractile function. If the patient survives the acutensult and is left untreated, or if the MR develops

00..2222 AAlliiaassiinngg vveelloocciittyy

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Figure 9. Calculation of PISA Derived ERO

The left image is a zoomed view of the flow convergence zone witan aliasing velocity of 22 cm/s. The radius (R) of the flow convergenat 336 ml/s. The right image shows continuous-wave Doppler meais calculated at 67 mm2 or 0.67 cm2, as the ratio of flow to velocity

ore gradually over time, he or she may enter a e

hronic compensated phase (Fig. 10C). In thishase, eccentric hypertrophy has developed, in-reasing EDV. The radius term in the Laplacequation is increased, but systolic wall stress doesot increase. The increase in EDV more thanffsets the increase in ESV, so that total SV isncreased, in turn increasing forward SV. An en-arged, compliant LA can accommodate the RVolt lower pressure, relieving pulmonary congestion.n this phase, the patient may be completely asymp-omatic. How long the patient remains in this phases quite variable, depending on whether the MRorsens and probably on genetic variations in tol-

rance of the volume overload. Eventually, severeR leads to muscle dysfunction and decompensa-

ion (Fig. 10D). In this phase, a weakened LV cano longer shorten adequately and ESV increases,ecreasing total and forward SV while increasingA and LV filling pressures. Symptoms of heart

ailure may develop, but some patients remainsymptomatic or fail to recognize deterioration inunctional status. Importantly, ejection fractionEF) may remain in the “normal” range, belying theresence of LV dysfunction (9).jection fraction. Ejection fraction has, during theast 4 decades, become the most widely used de-criptor of LV function. All imaging techniques cane used to determine LVEF. However, the issue atand for the clinician is to determine whether orot the patient with MR is entering the phase of

city = 67 mm2city = 67 mm2

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lor-flow imaging and down-shifting of the baseline resulting inis measured using the 2 crosses shown and the flow is calculatedment of the peak regurgitant velocity (MR velocity). The ERO area� left ventricle; other abbreviations as in Figure 8.

eloelo

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arly LV muscle dysfunction, a phase when correc-

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ion of MR must be undertaken to prevent perma-ent myocardial damage. The major function of anyuscle including the myocardium is to develop

orce. Obviously, EF has no force term in itsxpression. What the clinician would like to knows whether contractility, the innate ability of the

yocardium to generate force, has begun to decline.he ideal measure of contractility would be aeasure independent of afterload and preload, sen-

Figure 10. The Pathophysiologic Stages of MR

(A and B) Normal physiology (N) is contrasted with that of acuteMR increases sarcomere length (SL), augmenting preload. IncreasThe new pathologic pathway for ejection into the left atrium (LAallowing the left ventricle to eject more completely. Enhanced eresult, the total stroke volume increases to 140 ml, but becauseward stroke volume (FSV) decreases. Ejection fraction (EF) increa(C) Chronic compensated mitral regurgitation. In this phase of MEDV, which allows for a large increase in total stroke volume (19pliant LA can accommodate the regurgitant volume at a lower pand EF remains increased. (D) Chronic decompensated mitral regage caused by prolonged severe volume overload. Impaired CF rincreases. There is a further increase in diastolic volume, which iin total and forward stroke volumes. Concomitantly, increased EDalignment and regurgitant fraction increases. Ejection fraction isnormal range.

itive to changes in inotropic state, insensitive to e

V size, and easy to apply (10). Unfortunately, nouch measure exists but EF, which is easy to apply,as become the cornerstone of LV functionssessment.

Unfortunately, EF is especially suspect in pa-ients with MR because it is load sensitive and bothfterload and preload are altered in patients with

R (11). Increased pre-load and reduced afterloadct in concert to increase EF beyond what would be

tral regurgitation (MR). In acute MR, the volume overload ofSL is reflected by an increase in end-diastolic volume (EDV).duces afterload as quantified by end-systolic stress (ESS),on is reflected by a fall in end-systolic volume (ESV). As ais regurgitated into the LA (regurgitant fraction [RF] 0.50), for-although contractile function (CF) is normal but not increased.ccentric cardiac hypertrophy produces a further increase inl) so that FSV returns to nearly normal. The enlarged and com-ure, so that left atrial pressure declines. CF remains normal,itation. In this phase, CF has been reduced from muscle dam-ces the effectiveness of left ventricular ejection and ESVt compensatory for the increase in ESV, resulting in a decreaseorsens the MR by annular dilation and papillary muscle mal-

uced from the compensated state but often remains within the

mied) rejecti50%ses,R, e0 mressurgedus noV wred

xpected from inotropic state. Thus, patients with

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ubstantial LV dysfunction may still have a normalF (9,12) To overcome this deficiency the clinicalse of EF in MR patients, a greater limit for normalas been set. Although in most subjects the lower

imit of normal for EF is 0.55, MR patients withF �0.60 have been noted to have an impairedrognosis (9,13). The EF is further compromisedecause it is often estimated rather than measuredrecisely, making it unclear whether the distinctionetween an EF of 0.60 and 0.55 is accurate. Becausef the imprecision of EF in assessing LV function,specially in MR, other measures have been ex-lored.nd-systolic dimension (ESD) and volume. A numberf studies have examined whether ESV or ESD isredictive of outcome in chronic MR (14–16). Theolume to which the LV contracts at the end ofystole is determined by contractility, afterload, andccentric remodeling, but not by pre-load. Thus,SV and ESD are independent of one of the factors

onfounding the use of EF in assessing LV functionn MR. Additionally, afterload tends to increase inhe late stages of MR whereas, at the same time,ontractility tends to decrease. An increased LV-SD (�40 mm) and an LVEF �0.60 are indica-

ors of LV systolic dysfunction, portend poor long-erm prognosis, and generally are accepted asndications for surgery even in the absence ofymptoms (17). Thus, the determination of ESV orSD is an important component of the noninvasive

ssessment of patients with MR. Left ventricularimensions can be accurately obtained with 2Dechniques. Volume determinations are more pre-ise with 3D TEE and CMR.ontractile reserve. The response to exercise stressssessed with echocardiography has also been usedo identify subclinical LV systolic dysfunction inatients with asymptomatic MR. Impaired con-ractile reserve with exercise (defined as an in-rease in EF �0.04) has been shown to predictorsening LV function in medically treated pa-

ients. Reduced reserve also helps to predictmmediate post-operative LV systolic dysfunc-ion and early cardiac events in patients under-oing surgery (18).yocardial function. Doppler imaging of LV myo-

ardial segments has been used as a surrogatearker of LV function (19). Systolic tissue Doppler

elocities have been shown to correlate with LVunction, to identify subclinical LV dysfunction,nd to predict post-operative LV function in pa-
ients with asymptomatic MR (20,21). p
Myocardial strain is defined as a change in lengthompared with a reference initial length. In contrasto velocity of contraction, strain imaging is notnfluenced by global cardiac motion but may benfluenced by large variations in loading conditions22). Strain rate is the change of strain over time23). Both strain and strain rate have been demon-trated to correlate well with LV function, whereintrain appears to correlate with the stroke volumend strain rate with LV contractility assessed bynvasively derived dP/dt (24). Strain and strain rateelp identify subclinical LV dysfunction in patientsith asymptomatic severe MR and correlate with

ontractile reserve with exercise; strain and strainate are significantly greater in patients with ade-uate contractile reserve (25). Moreover, strain andtrain rates have been shown to decrease even beforehanges in LV chamber dimensions occur, i.e., beforeV systolic dimension exceeds 4.5 cm (26). Limita-

ions of strain imaging include its dependence onre-load, afterload, and imaging angle. To correct forhe influence of preload on strain/strain rate andbtain a more pure measure of contractility, Marciniakt al. (26) devised geometry-compensated deforma-ion indices, which are calculated by dividing strainnd strain rate by EDV. The geometry compensatedeformation indices are decreased in patients with LVystolic dimension �4.5 cm (22). However, the incre-ental value of accurately identifying preclinical LV

ysfunction remains to be determined.

ole of Imaging in Ongoing Investigationsf Percutaneous MV Repair

ecently, there has been considerable interest inercutaneous MV repair. One approach, whichdopts the principles of the Alfieri surgical tech-ique, involves the deployment of a clip or stitch toring the leaflet edges together (Fig. 11). In therocess, a double orifice valve is created. A secondpproach aims to reduce mitral annular circumfer-nce via placement of a device in the coronary sinusFig. 11). These coronary sinus devices reshape theosterior mitral annulus.Pre-, intra-, and post-procedural imaging is crit-

cal to the successful use of these devices. There arebasic imaging objectives: 1) evaluate the mecha-

ism and severity of MR; 2) determine anatomicuitability for device repair; 3) guide deployment ofhe device; and 4) assess stability and outcome ofepair. Table 3 lists key imaging factors for each ofhe percutaneous techniques. For edge-to-edge re-
air, TEE is the most widely used approach to

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dentify the location of abnormal anatomy, anduide the procedure. Mid-esophageal long-axis andommissural TEE views are particularly helpful toenter the clips over the MV orifice, and theransgastric short-axis view is used to grasp theeaflet edges. A successful and smooth procedure isighly dependent on communication between thechocardiographer and interventionalist. Guidance

Percutaneous MV Repair Approaches

of edge-to-edge MV repair (Alfieri procedure; (top) and percuta-al annuloplasty (bottom), capitalizing on the relationshiphe coronary sinus and the annulus.

Table 3. Noninvasive Assessment for Percutaneous Mitral Valve

Edge-to-edge repair

● Identify mechanism of MR: degenerative flail segment with flail w

● Ensure origin of regurgitant jet is within central two-thirds of coap

● Quantitate MR

● Guide clip deployment

● Assess reduction of MR post-clip and stability of clip placement

Coronary sinus

● Pre-procedural CCT for coronary sinus anatomy

Œ Assess location of coronary sinus relative to mitral annulus: su

Œ Assess location of coronary sinus, left circumflex artery and ca

Œ Assess maximal distances between coronary sinus and mitral a

● During and post-procedure

Œ TEE to assess reduction in MR

● Post-procedure

Œ CCT to assess device position and extent of mitral annular rem

CCT � cardiac computed tomography; MR � mitral regurgitation; TEE � transesop

ith TEE may be significantly improved with these of 3D imaging, allowing for more preciseelivery of the catheter towards the leaflet edges.oronary sinus (CS) technique. These devices mimicurgical annuloplasty, which reduces mitral annularrea by moving the posterior annulus anteriorly ory decreasing the circumference of the posteriornnulus. In developing nonsurgical approaches to

V repair, it has been appreciated that the cardiaceins typically encircle the mitral annulus. Theseeins could serve as the anatomic target for percu-aneously deployed devices that effectively reducehe ERO by exerting inward pressure on the mitralnnulus. The typical configuration of the majorardiac veins is shown in Figure 12. The CS andreat cardiac vein (GCV) form a continuous cardiacenous landing zone for a MV repair device deliv-red transvenously. However, cardiac veins exhibitreat variability in extent, distribution, and ana-omic location. The first variable to consider foruccessful device deployment is the anatomy of theS-GCV. Distance of the CS-GCV from theitral annulus in the superior-inferior dimension asell as in the radial direction from the center of theitral valve may be important (27). This varianceay be an important factor determining the likeli-

ood of procedural success. A device that encirclesrimarily the LA free wall may simulate cor tria-riatum without affecting a decrease in the MVRO. Other relevant variables include the length of

he CS-GCV and the extent to which these veinsverlie the mitral annulus. Another important an-tomic variable is the course of the left circumflexrtery and its branches (28).

air

�1.5 cm vs. ischemic or functional etiology

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Coronary venous imaging may be preferred byhe interventionalist for immediate recognition ofnatomic landmarks, but does not provide concom-tant information regarding cardiac and mitral ap-aratus anatomy that may ultimately determinerocedural success. Simultaneous transesophagealr intracardiac echocardiography help overcomehese deficiencies. The use of cardiac computedomography allows the simultaneous visualizationf venous, coronary artery, and cardiac anatomy. Itemains to be determined what geometries pose thereatest risk for myocardial ischemia from extrinsicoronary compression. Simultaneous rendering ofenous and coronary artery anatomy with cardiacomputed tomography affords such definition. These of CMR has a limited role at the present time,lthough recent developments in technology maymprove the utility of this technique (29). A mul-imodality imaging approach holds promise fornatomic definition of the coronary sinus and LVuring the procedure. Left ventricular volumesbtained by 3D echocardiography can be superim-osed on reconstructed images of the coronary sinussing high speed rotational coronary venous angiog-aphy (29). This strategy of integrating echocardio-raphic and angiographic data to reconstruct coronaryinus and LV anatomy holds great potential.

ntegrated Decision-Making

ow should the clinician use the information gath-red from the history, examination, and noninvasivemaging to construct the most appropriate manage-

Figure 12. Cardiac Computed Tomography of Coronary Sinus

(Left) Typical configuration of major cardiac veins. The volume-rendular vein (AIV) draining into the great cardiac vein (GCV), which in tvein branches. The posterior interventricular vein (PIV) is also notedmode of rendering isotropic CT data allows for segmentation of thecates the anterior interventricular vein. (Right) Coronary artery andand left circumflex coronary artery (arrowhead) lie in the atrioventrnary sinus in this patient. The potential for myocardial ischemia indAo � aortic valve, LV � left ventricle.

ent plan for any individual patient with chronic,

onischemic MR? After verification of the diagno-is, one approach begins with designation of symp-om status (10). The onset of symptoms is a Class Indication for surgical referral, preferably with re-air, provided: 1) the MR is severe by quantitativeeasures and the likely cause of the symptoms

eported and 2) and LV systolic function is normalr only moderately impaired (EF �0.30, ESD5.5 cm). For patients with more severe degrees ofV dysfunction (EF �0.30, ESD �5.5 cm), sur-ery is appropriate when chordal preservation (withither repair or replacement) is likely (Class IIa).

There is a relatively greater reliance on noninva-ive imaging for the management of asymptomaticatients with nonischemic MR, particularly whenonsidering the indications for surgical repair. Un-er these circumstances, the risk-benefit analysisust be extremely favorable and driven in largeeasure by the availability of an expert surgeonith a proven track record of outstanding results.alve replacement is an unacceptable outcome for

he asymptomatic patient. The following questionsust be answered from the noninvasive data:

. Is the MR severe?a. No. Establish schedule for clinical and TTE

surveillance.b. Yes. Establish schedule for clinical and TTE

surveillance and consider whether early sur-gery might be warranted depending on theanswers to the questions which follow.

. Is LV function preserved?a. No. If MR is severe and EF �0.60 or ESD

computed tomography (CT) data show the anterior interventric-becomes the coronary sinus (CS) upon receiving additional lateraliddle) Coronary sinus in a curved multiplanar CT format. Thisronary sinus along its entire length (arrows). The arrowhead indi-nary sinus anatomic relationship. Both the coronary sinus (arrow)ar groove, with the circumflex artery lying underneath the coro-d by extrinsic compression from an overlying venous device exists.

eredurn. (Mcocoroiculuce

�4.0 cm, refer to surgery (Class I).

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b. Yes. If MR is severe, and EF �0.60 withESD �4.0 cm, consider early surgical referraldepending on likelihood of repair and avail-ability of surgical expertise (Class IIa).

. Is PA hypertension present?a. No. If PA systolic pressure �50 mm Hg at rest

and/or �60 mm Hg with exercise, establishschedule for clinical and TTE surveillance.

b. Yes. If MR is severe and PA systolic pressure�50 mm Hg at rest or �60 mm Hg withexercise, consider early surgical referral (Class IIa).

. What is the mechanism of the MR and there-fore the feasibility of primary repair?a. Myxomatous degeneration/fibroelastic deficiencyb. Other: Barlow’s, congenital, and so on

. Is there a very high (>95%) likelihood ofsuccessful repair?a. Yes. Consider early referral to an experienced

surgeon at a high volume center of excellence

al. Application of color Doppler flowsus chronic mitral rColl Cardiol 1984;

b. No. Establish clinical and TTE surveillance.

Decision-making of this nature requires the col-aborative input of the clinician, echocardiographer/mager, and the surgeon. With appropriate training,ttention to detail, informed understanding of nat-ral history, more widespread adoption of standard-zed evaluation and treatment protocols, and furtherdvances in surgical and intraoperative manage-ent, outcomes for patients with nonischemic MRill continue to improve. The potential role ofercutaneous repair has not yet been established.

cknowledgmentshe authors acknowledge the contributions Francescorigioni, MD, of Mayo Clinic, Rochester, Minne-

ota; and Kumudha Ramasubbu, MD, of Baylorollege of Medicine, Houston, Texas, for their valu-

ble contributions to the manuscript.

eprint requests and correspondence: Dr. Mani A. Van-an, The Ohio State University, 473 West 12th Avenue,HLRI, Suite 200, Columbus, Ohio 43210. E-mail:

(Class IIa). [email protected].

1

1

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