El pesaje del trabajo es muy alto y la Eur J Echo no esta disponible en HINARI por lo que se brinda información en WORD e imágenes en otro file adicional.Se puede reacondicionar con programa convertidor

GUIDELINES

Recommendations for chamber quantification*Roberto M. Lang, Michelle Bierig, Richard B. Devereux,Frank A. Flachskampf*, Elyse Foster, Patricia A. Pellikka,Michael H. Picard, Mary J. Roman, James Seward,Jack Shanewise, Scott Solomon, Kirk T. Spencer,Martin St. John Sutton, William StewartMed. Klinik 2, Erlangen University, Ulmenweg 18, 91054 Erlangen, GermanyReceived 7 November 2005; accepted 23 December 2005Available online 2 February 2006KEYWORDSStandards;Measurements;Volumes;Linear dimensions;QuantificationAbstract Quantification of cardiac chamber size, ventricular mass and functionranks among the most clinically important and most frequently requested tasks ofechocardiography. Over the last decades, echocardiographicmethods and techniqueshaveimproved and expandeddramatically, due to the introduction of higher frequencytransducers, harmonic imaging, fully digital machines, left-sided contrast agents, andother technological advancements. Furthermore, echocardiography due to its portabilityand versatility is now used in emergency rooms, operating rooms, and intensivecare units. Standardization of measurements in echocardiography has been inconsistentand less successful, compared to other imaging techniques and consequently,echocardiographic measurements are sometimes perceived as less reliable. Therefore,the American Society of Echocardiography, working together with the EuropeanAssociation of Echocardiography, a branch of the European Society of Cardiology, hascritically reviewed the literature and updated the recommendations for quantifyingcardiac chambers using echocardiography. This document reviews the technicalaspects on how to perform quantitative chamber measurements of morphology andfunction, which is a component of every complete echocardiographic examination.ª 2006 The European Society of Cardiology. Published by Elsevier Ltd. All rightsreserved.Abbreviations: LV, left ventricle; LA, left atrium; RA, right atrium; RV, right ventricle; LVID, left ventricular internal dimension;LVIDd, left ventricular internal dimension at end diastole; LVIDs, left ventricular internal dimension at end systole; SWTd, septal wallthickness at end-diastole; PWTd, posterior wall thickness at end-diastole; EBD, endocardial border delineation; TEE, transesophagealechocardiography; MI, myocardial infarction.* A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and the Task Force on ChamberQuantification, developed in conjunction with the American College of Cardiology Echocardiography Committee, the AmericanHeart Association, and the European Association of Echocardiography, a branch of the European Society of Cardiology.* Corresponding author. Tel.: þ49 9131 853 5301; fax: þ49 9131 853 5303.E-mail address: frank.flachskampf@rzmail.uni-erlangen.de (F.A. Flachskampf).1525-2167/$32 ª 2006 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.doi:10.1016/j.euje.2005.12.014

Introduction

Quantification of cardiac chamber size, ventricularmass and function ranks among the most clinicallyimportant and most frequently requested tasks ofechocardiography. Standardization of chamberquantification has been an early concern in echocardiographyand recommendations on how tomeasure such fundamental parameters are amongthe most often cited papers in the field.1,2 Overthe last decades, echocardiographic methods andtechniques have improved and expanded dramatically.Improvements in image quality have beensignificant, due to the introduction of higher frequencytransducers, harmonic imaging, fully digitalmachines, left-sided contrast agents, andother technological advancements.Furthermore, echocardiography has become thedominant cardiac imaging technique, which due toits portability and versatility is now used inemergency rooms, operating rooms, and intensivecare units. Standardization of measurements inechocardiography has been inconsistent and lesssuccessful, compared to other imaging techniquesand consequently, echocardiographic measurementsare sometimes perceived as less reliable.Therefore, the American Society of Echocardiography,working together with the European Associationof Echocardiography, a branch of theEuropean Society of Cardiology, has criticallyreviewed the literature and updated the recommendationsfor quantifying cardiac chambers usingechocardiography. Not all the measurements describedin this document can be performed in allpatients due to technical limitations. In addition,specific measurements may be clinically pertinentor conversely irrelevant in different clinic scenarios.This document reviews the technical aspectson how to perform quantitative chamber measurementsand is not intended to describe the standardof care of which measurements should be performedin individual clinical studies. However,evaluation of chamber size and function is a componentof every complete echocardiographicexamination and these measurements may havean impact on clinical management.General overviewEnhancements in imaging have followed technologicalimprovements such as broadband transducers,harmonic imaging and left-sided contrastagents. Nonetheless, image optimization stillrequires considerable expertise and attention tocertain details that are specific to each view(Table 1). In general, images optimized for quantitationof one chamber may not necessarily be optimalfor visualization or measurement of othercardiac structures. The position of the patient duringimage acquisition is important. Optimal viewsare usually obtained with the patient in the steepleft-lateral decubitus position using a cut-out mattressto permit visualization of the true apex while

avoiding LV foreshortening. The patient’s left armshould be raised to spread the ribs. Excessivetranslational motion can be avoided by acquiringimages during quiet respiration. If images areobtained during held end-expiration, care mustbe taken to avoid a Valsalva maneuver, whichcan degrade image quality.Digital capture and display of images on theechocardiographic system or on a workstationshould optimally display images at a rate of atleast _30 frames/second. In routine clinical practicea representative cardiac cycle can be used formeasurement as long as the patient is in sinusrhythm. In atrial fibrillation, particularly whenthere is marked RR variation, multiple beatsshould be used for measurements. Averaging measurementsfrom additional cycles may be particularlyuseful when R-R intervals are highly irregular.When premature atrial or ventricular contractionsare present, measurements should be avoided inthe post-ectopic beat since the length of the preceding cardiac cycle can influence ventricularvolume and fiber shortening.Harmonic imaging is now widely employed inclinical laboratories to enhance the images especiallyin patients with poor acoustic windows.While this technology reduces the ‘‘drop-out’’ ofendocardial borders, the literature suggests thatthere is a systemic tendency for higher measurementsof LV wall thickness and mass and smallermeasurements of internal dimensions and volumes.3,4 When analyzing serial studies on a givenpatient, differences in chamber dimension potentiallyattributable to imaging changes from thefundamental to the harmonic modality are probablysmaller than the inter and intra-observer variabilityof these measurements. The best techniquefor comparing serial changes in quantitation is todisplay similar serial images side-by-side andmake the same measurement on both images bythe same person, at the same time.5 It is importantto note that most measurements presented in thismanuscript are derived from fundamental imagingas normative values have not been establishedusing harmonic imaging.Left-sided contrast agents used for endocardialborder delineation (EBD) are helpful and improvemeasurement reproducibility for suboptimal studiesand correlation with other imaging techniques.While the use of contrast agents has beenreviewed elsewhere in detail,6 a few caveats regardingtheir use deserve mention. The mechanicalindex should be lowered to decrease the acousticpower of the ultrasound beam, which reduces bubbledestruction. The image should be ‘‘focused’’on the structure of interest. Excessive shadowingmay be present during the initial phase of bubbletransit and often the best image can be recordedseveral cardiac cycles following the appearanceof contrast in the left ventricle. When less than

80% of the endocardial border is adequately visualized,the use of contrast agents for EBD is stronglyrecommended.7 By improving visualization of theLV apex, the problem of ventricular foreshorteningis reduced and correlation with other techniquesimproved. Contrast enhanced images should belabeled to facilitate the reader identification ofthe imaging planes.Quantitation using transesophageal echocardiography(TEE) has advantages and disadvantagescompared to transthoracic echocardiography(TTE). Although visualization of many cardiacstructures is improved with TEE some differencesin measurements have been found between TEEand TTE. These differences are primarily attributableto the inability to obtain from the transesophagealapproach the standardized imagingplanes/views used when quantifying chamber dimensionstransthoracically.8,9 It is the recommendationof this writing group that the same rangeof normal values for chamber dimensions and volumesapply for both TEE and TTE. In this manuscript,recommendations for quantification usingTEE will primarily focus on acquisition of imagesthat allow measurement of cardiac structuresalong imaging planes that are analogous to TTE.In addition to describing a parameter as normalor abnormal (reference values), clinical echocardiographersmost often qualify the degree ofabnormality with terms such as ‘‘mildly’’, ‘‘moderately’’or ‘‘severely’’ abnormal. Such a descriptionallows the clinician to not only understandthat the parameter is abnormal but also thedegree to which their patient’s measurementsdeviate from normal. In addition to providingnormative data it would be beneficial to standardizecutoffs for severity of abnormality acrossechocardiographic laboratories, such that moderatelyabnormal had the same implication in alllaboratories. However, multiple statistical techniquesexist for determining thresholds values, allof which have significant limitations.10

The first approach would be to define cutoffsempirically for mild, moderate and severe abnormalitiesbased on standard deviations above/below the reference limit derived from a groupof normal subjects. The advantage of this methodis that this data readily exists for most echocardiographicparameters. However, this approachhas several disadvantages. Firstly, not all echocardiographicparameters are normally distributed, orGaussian in nature, making the use of standarddeviation questionable. Secondly, even if a particularparameter is normally distributed in controlsubjects, most echocardiographic parameterswhen measured in the general population havea significant asymmetric distribution in one direction(abnormally large for size or abnormallylow for function parameters). Using the standarddeviation derived from normal subjects leads to

abnormally low cutoff values which are inconsistentwith clinical experience, as the standarddeviation inadequately represents the magnitudeof asymmetry (or range of values) towards abnormality.This is the case with LV ejection fraction(EF) where 4 standard deviations below the mean(64 G 6.5) results in a cutoff for severely abnormalof 38%.An alternative method would be to defineabnormalities based on percentile values (95th,99th, etc.) of measurements derived from a populationthat includes both normal subjects andthose with disease states.11 Although this data may still not be Gaussian, it accounts for the asymmetricdistribution and range of abnormality presentwithin the general population. The major limitationof this approach is that large enough populationdata sets simply do not exist for mostechocardiographic variables.Ideally, an approach that would predict outcomesor prognosis would be preferred. That isdefining a variable as moderately deviated fromnormal would imply that there is a moderate riskof a particular adverse outcome for that patient.Although sufficient data linking risk and cardiacchamber sizes exist for several parameters (i.e.,EF, LV size, LA volume); risk data are lacking formany other parameters. Unfortunately, this approachcontinues to have several limitations. Thefirst obstacle is how to best define ‘‘risk’’. Thecutoffs suggested for a single parameter varybroadly for the risk of death, myocardial infarction(MI), atrial fibrillation etc. In addition, much of therisk literature applies to specific populations (post-MI, elderly), and not general cardiovascular riskreadily applicable to consecutive patients studiedin an echocardiography laboratory. Lastly, althoughhaving data specifically related to risk isideal, it is not clear that this is necessary. Perhapscardiac risk rises inherently as echocardiographicparameters become more abnormal. This has beenshown for several echocardiographic parameters(LA dimension, wall thickness, LV size and LV mass)which, when partitioned based on populationestimates, demonstrated graduated risk, which isoften non-linear.11

Lastly cutoffs values may be determined fromexpert opinion. Although scientifically least rigorous,this method takes into account the collectiveexperience of having read and measured tens ofthousands of echocardiograms.No single methodology could be used for allparameters. The tables of cutoffs represent a consensusof a panel of experts using a combination ofthe methods described above (Table 2). The consensusvalues are more robust for some parametersthan others and future research may redefine thecutoff values. Despite the limitations, these partitionvalues represent a leap forward towards thestandardization of clinical echocardiography.

Quantification of the left ventricleLeft ventricular dimensions, volumes and wallthicknesses are echocardiographic measurementswidely used in clinical practice and research.12,13

LV size and performance are still frequently visuallyestimated. However, qualitative assessmentof LV size and function may have significant inter-observer variability and is a function of interpreterskill. Therefore, it should regularly becompared to quantitative measurements, especiallywhen different views qualitatively suggestdifferent degrees of LV dysfunction. Similarly, itis also important to cross-check quantitative datausing the ‘‘eye-ball’’ method, to avoid overemphasison process-related measurements, which attimes may depend on structures seen in a singlestill-frame. It is important to account for the integrationover time of moving structures seen in oneplane, and the integration of three-dimensionalspace obtained from viewing a structure in multipleorthogonal planes. Methods for quantitationof LV size, mass and function using two-dimensionalimaging have been validated.14e17

There are distinct advantages and disadvantagesto each of the accepted quantitativemethods (Table 3). For example, linear LV measurementshave been widely validated in the managementof valvular heart disease, but maymisrepresent dilatation and dysfunction in patientswith regional wall motion abnormalitiesdue to coronary artery disease. Thus, laboratoriesshould be familiar with all available techniquesand peer review literature and should apply themon a selective basis.General principles for linear andvolumetric LV measurementsTo obtain accurate linear measurements of interventricularseptal and posterior wall thicknessesand LV internal dimension, recordings should be made from the parasternal long-axisacoustic window. It is recommended that LV internaldiameters (LVIDd and LVIDs, respectively)and wall thicknesses be measured at the level ofthe LV minor axis, approximately at the mitralvalve leaflet tips. These linear measurements canbe made directly from 2D images or using 2DtargetedM-mode echocardiography.By virtue of their high pulse rate, M-moderecordings have excellent temporal resolutionand may complement 2-D images in separatingstructures such as trabeculae adjacent to theposterior wall, false tendons on the left side ofthe septum, and tricuspid apparatus or moderatorband on the right side of the septum from theadjacent endocardium. However, it should berecognized that even with 2D guidance, it maynot be possible to align the M-mode cursor perpendicularto the long axis of the ventricle which ismandatory to obtain a true minor axis dimension

measurement. Alternatively, chamber dimensionand wall thicknesses can be acquired from theparasternal short-axis view using direct 2D measurementsor targeted M-mode echocardiographyprovided that the M-mode cursor can be positionedperpendicular to the septum and LV posterior wall.A 2D method, useful for assessing patients withcoronary artery disease has been proposed. Whenusing this method, it is recommended that LVinternal diameters (LVIDd and LVIDs, respectively)and wall thicknesses be measured at the level ofthe LV minor dimension, at the mitral chordaelevel. These linear measurements can also bemade directly from 2D images or using 2D-targetedM-mode echocardiography. Direct 2D minor axismeasurements at the chordae level intersect theinterventricular septum below the left ventricularoutflow tract,2,5,18 and thus provides a global assessmentin a symmetrically contracting LV, andalso evaluates basal regional function in a chamberwith regional wall motion abnormalities. Thedirect 2D minor axis dimensions are smaller thanthe M-mode measurements with the upper limitsof normal of LVIDd being 5.2 cm vs 5.5 cm andthe lower limits of normal for fractional shorteningbeing 0.18 vs 0.25. Normal systolic and diastolicmeasurements reported for this parameter are4.7 G 0.4 cm and 3.3 G 0.5 cm, respectively.2,18 LVID and septal and posterior wall thicknesses(SWT and PWT, respectively) are measured at enddiastole(d) and end-systole (s) from 2-D or M-moderecordings,1,2 preferably on several cardiac cycles(Fig. 1).1,2 Refinements in image processing haveallowed improved resolution of cardiac structures.Consequently, it is now possible to measure the actualvisualized thickness of the ventricular septumand other chamber dimensions as defined by theactual tissueeblood interface, rather than the distancebetween the leading edge echoes which hadpreviously been recommended.5 Use of 2-D echoderivedlinear dimensions overcomes the commonproblem of oblique parasternal images resultingin overestimation of cavity and wall dimensionsfrom M mode. If manual calibration of images isrequired, 6 cm or larger distances should be usedto minimize errors due to imprecise placement ofcalibration points.In order to obtain volumetric measurements themost important views for 2-D quantitation are themid-papillary short-axis view and the apical fourandtwo-chamber views. Volumetric measurementsrequire manual tracing of the endocardial border.The papillary muscles should be excluded from thecavity in the tracing. Accurate measurementsrequire optimal visualization of the endocardialborder in order to minimize the need for extrapolation.It is recommended that the basal border ofthe LV cavity area be delineated by a straight lineconnecting the mitral valve insertions at the lateraland septal borders of the annulus on the fourchamber

view and the anterior and inferior annularborders on the two-chamber view.End-diastole can be defined at the onset of theQRS, but is preferably defined as the framefollowing mitral valve closure or the frame in thecardiac cycle in which the cardiac dimension islargest. In sinus rhythm, this follows atrial contraction.End-systole is best defined as the framepreceding mitral valve opening or the time in thecardiac cycle in which the cardiac dimension issmallest in a normal heart. In the two-chamberview, mitral valve motion is not always clearlydiscernible and the frames with the largest andsmallest volumes should be identified as enddiastoleand end-systole, respectively.The recommended TEE views for measurementof LV diameters are the mid esophageal twochamberview (Fig. 2) and the transgastric (TG)two- chamber views (Fig. 3). LV diameters aremeasured from the endocardium of the anteriorwall to the endocardium of the inferior wall ina line perpendicular to the long-axis of the ventricleat the junction of the basal and middle thirdsof the long-axis. The recommended TEE view formeasurement of LV wall thicknesses is the TGmid short-axis view (Fig. 4). With TEE, the longaxisdimension of the LV is often foreshortened inthe mid-esophageal four-chamber and long-axisFigure 1views; therefore the mid-esophageal two-chamberview is preferred for this measurement. Care mustbe made to avoid foreshortening TEE views, by recordingthe image plane which shows the maximumobtainable chamber size, finding the anglefor diameter measurement which is perpendicularto the long-axis of that chamber, then measuringthe maximum obtainable short-axis diameter.Calculation of left ventricular massIn clinical practice, LV chamber dimensions arecommonly used to derive measures of LV systolicfunction, whereas in epidemiologic studies andtreatment trials, the single largest application ofechocardiography has been the estimation of LVmass in populations and its change with antihypertensivetherapy.13,19 All LV mass algorithms,whether utilizing M-mode, 2-D or 3-D echocardiographicmeasurements, are based upon subtractionof the LV cavity volume from the volumeenclosed by the LV epicardium to obtain LV muscleor ‘‘shell’’ volume. This shell volume is then convertedto mass by multiplying by myocardial density.Hence, quantitation of LV mass requiresaccurate identification of interfaces between thecardiac blood pool and endocardium and betweenepicardium and pericardium.To date, most LV mass calculations have beenmade using linear measurements derived from 2-DtargetedM-mode or, more recently, from 2-Dlinear LV measurements.20 The ASE recommended

formula for estimation of LV mass from LV linear dimensions (validated with necropsy r ¼ 0.90,p < 0.00121) is based on modeling the LV as aprolate ellipse of revolution:LV mass ¼ 0:8_ð1:04½ðLVIDdþPWTdþSWTdÞ3_ðLVIDdÞ3_Þþ0:6 gThis formula is appropriate for evaluating patientswithout major distortions of LV geometry,e.g., patients with hypertension. Since this formularequires cubing primary measurements, evensmall errors in these measurements are magnified.Calculation of relative wall thickness (RWT) by theformula, (2 _ PWTd)/LVIDd, permits categorizationof an increase in LV mass as either concentric(RWT _ 0.42) or eccentric (RWT _ 0.42) hypertrophyand allows identification of concentricremodeling (normal LV mass with increased RWT)(Fig. 5).22

The most commonly employed 2-D methods formeasuring LV mass are based on the areaelengthformula and the truncated ellipsoid model, asdescribed in detail in the 1989 ASE document onLV quantitation.2 Both methods were validated inthe early 1980s in animal models and by comparingpre-morbid echocardiograms with measured LVweight at autopsy in humans. Both methods relyon measurements of myocardial area at the midpapillarymuscle level. The epicardium is tracedto obtain the total area (A1) and the endocardiumis traced to obtain the cavity area (A2). Myocardial area (Am) is computed as the difference:Am ¼ A1 _ A2. Assuming a circular area, the radiusis computed (b ¼ A2/p) and a mean wall thickness(t) derived (Fig. 6). Left ventricular mass can becalculated by one of the two formulae shown inFig. 6. In the presence of extensive regional wallmotion abnormalities (e.g. myocardial infarction),the biplane Simpson’s method may be used,although this method is dependent on adequateendocardial and epicardial definition of the LVwhich often is challenging from this window. Mostlaboratories obtain the measurement at enddiastoleand exclude the papillary muscles in tracingthe myocardial area.TEE evaluation of LV mass is also highly accurate,but has minor systematic differences in LVposterior wall thickness. In particular LV massderived from TEE wall thickness measurements ishigher by an average of 6 g/m2.8Left ventricular systolic function: linearand volumetric measurementMany echocardiographic laboratories rely on Mmodemeasurements or linear dimensions derivedfrom the two-dimensional image for quantification.Linear measurements from M-mode and 2-Dimages have proven to be reproducible with lowintra- and inter-observer variability.20,23e26 Althoughlinear measures of LV function are problematicwhen there is a marked regional

difference in function, in patients with uncomplicatedhypertension, obesity or valvular diseases,such regional differences are rare in the absenceof clinically recognized myocardial infarction.Hence fractional shortening and its relationshipto end-systolic stress often provide useful informationin clinical studies.27 The previously usedTeichholz or Quinones methods of calculating LVejection fraction from LV linear dimensions mayresult in inaccuracies due to the geometric assumptionsrequired to convert a linear measurementto a 3-D volume.28,29 Accordingly, the useof linear measurements to calculate LV EF is notrecommended for clinic practice.Contraction of muscle fibers in the LV midwallmay better reflect intrinsic contractility thancontraction of fibers at the endocardium. Calculationof midwall, rather than endocardial fractionalshortening is particularly useful in revealingunderlying systolic dysfunction in the setting ofconcentric hypertrophy.30 Mid-wall fractionalshortening (MWFS) may be computed from linearmeasures of diastolic and systolic cavity sizes and wall thicknesses based on mathematicalmodels,30,31 according to the following formulas:Inner shell ¼ _hLVIDdþSWTd=2þPWTd=2_3

_LVIDd3 þLVIDs3_1=3

_LVIDsThe most commonly used 2-D measurement forvolume measurements is the biplane method ofdiscs (modified Simpson’s rule) and is the currentlyrecommended method of choice by consensus ofthis committee (Fig. 7). The principle underlyingthis method is that the total LV volume is calculatedfrom the summation of a stack of elliptical discs.The height of each disc is calculated as a fraction(usually one-twentieth) of the LV long axis basedon the longer of the two lengths from the twoandfour-chamber views. The cross-sectional areaof the disk is based on the two diameters obtainedfrom the two- and four-chamber views. When twoadequate orthogonal views are not available, a singleplane can be used and the area of the disc isthen assumed to be circular. The limitations ofusing a single plane are greatest when extensivewall motion abnormalities are present.An alternative method to calculate LV volumeswhen apical endocardial definition precludes accuratetracing is the areaelength method wherethe LV is assumed to be bullet-shaped (Fig. 6). Themid LV cross-sectional area is computed by planimetryin the parasternal short-axis view andthe length of the ventricle taken from the midpoint of the annulus to the apex in the apicalfour-chamber view. These measurements are repeated at end-diastole and end-systole and thevolume is computed according to the formula:volume ¼ [5(area)(length)] O 6. The most widelyused parameter for indexing volumes is the bodysurface area (BSA) in m2.

The end-diastolic and end-systolic volumes(EDV, ESV) are calculated by either of the twomethods described above and the ejection fractionis calculated as follows:Ejection fraction ¼ ðEDV_ESVÞ=EDVPartition values for recognizing depressed LVsystolic function in Table 6 follow the conventionalpractice of using the same cut-offs in women andmen; however, emerging echocardiographic and MRIdata suggests that LV ejection fraction and otherindices are somewhat higher in apparently normalwomen than in men.32,33 Quantitation of LV volumesusing TEE is challenging due to difficulties inobtaining a non-foreshortened LV cavity from theesophageal approach. However when carefullyacquired, direct comparisons between TEE andTTE volumes and ejection fraction have shownminor or no significant differences.8,9

Reference values for left ventricularmeasurements (Tables 4e6)Reference values for LV linear dimensions havebeen obtained from an ethnically diverse populationof 510 normal-weight, normotensive, non-diabeticwhite, African-American and American-Indianadults without recognized cardiovascular disease(unpublished data). The populations from whichthese data has been derived have been describedin detail previously.20,34e36 Reference values forvolumetric measurements have also been obtainedin a normal adult population.37

Normal values for LV mass differ between menand women even when indexed for body surfacearea (Table 4). The best method for normalizing LVmass measurements in adults is still debated.While body surface area (BSA) has been most oftenemployed in clinical trials, this method will underestimatethe prevalence of LV hypertrophy in overweightand obese individuals. The ability to detectLV hypertrophy related to obesity as well as tocardiovascular diseases is enhanced by indexingLV mass for the power of its allometric or growthrelation with height (height2.7). Data are inconclusiveas to whether such indexing of LV mass mayimprove or attenuate prediction of cardiovascularevents. Of note, the reference limits for LV massin Table 4 are lower than those published insome previous echocardiographic studies, yet are virtually identical to those based on direct necropsymeasurement and cutoff values used in clinicaltrials.19,20,36,38,39 Although some prior studieshave suggested racial differences in LV mass measurement,the consensus of the literature availableindicates that no significant differencesexist between clinically normal black and whitesubjects. In contrast, a recent study has shownracial-ethnic differences in left ventricular structurein hypertensive adults.40 Although the sensitivity,specificity and predictive value of LV wall thicknessmeasurements for detection of LV hypertrophy

are lower than for calculated LV mass, it issometimes easiest in clinical practice to identifyLV hypertrophy by measuring an increased LVposterior and septal thickness.41

The use of LV mass in children is complicated bythe need for indexing the measurement relative topatient body size. The intent of indexing is toaccount for normal childhood growth of lean bodymass without discounting the pathologic effects ofoverweight and obesity. In this way, an indexed LVmass measurement in early childhood can bedirectly compared to a subsequent measurementduring adolescence and adulthood. Dividing LVmass by height raised to a power of 2.5e3.0 isthe most widely accepted indexing method inolder children and adolescents since it correlatesbest to indexing LV mass to lean body mass.42 Currentlyan intermediate value of 2.7 is generallyused.43,44 In younger children (<8 years), themost ideal indexing factor remains an area of research,but height raised to a power of 2.0 appearsto be the most appropriate.45

Three-dimensional assessmentof volume and massThree-dimensional chamber volume and mass areincompletely characterized by one-dimensional ortwo-dimensional approaches, which are based ongeometric assumptions. While these inaccuracieshave been considered inevitable and of minorclinical importance in the past, in most situationsaccurate measurements are required, particularlywhen following the course of a disease with serialexaminations. Over the last decade, several threedimensionalechocardiographic techniques becameavailable to measure LV volumes and mass.46e59

These can be conceptually divided into techniques,which are based on off-line reconstructionfrom a set of 2-D cross-sections, or on-line dataacquisition using a matrix array transducer, alsoknown as real-time 3-D echocardiography. Afteracquisition of the raw data, calculation of LVvolumes and mass requires identification of endocardial borders (and for mass epicardial border)using manual or semi-automated algorithms.These borders are then processed to calculatethe cavity or myocardial volume by summation ofdiscs54,56 or other methods.46e48

Regardless of which acquisition or analysismethod is used, 3-D echocardiography does notrely on geometric assumptions for volume/masscalculations and is not subject to plane positioningerrors, which can lead to chamber foreshortening.Studies comparing 3-D echocardiographic LV volumesor mass to other gold-standards such asmagnetic resonance imaging, have confirmed 3-Dechocardiography to be accurate. Compared tomagnetic resonance data, LV and RV volumescalculated from 3-D echocardiography showedsignificantly better agreement (smaller bias), lower

scatter and lower intra- and inter-observer variabilitythan 2-D echocardiography.46,54,57,60 Thesuperiority of 3-D echocardiographic LV mass calculationsover values calculated from M-mode derivedor 2-D echocardiography has been convincinglyshown.55,57,59 Right ventricular volume and masshave also been measured by 3-D echocardiographywith good agreement with magnetic resonancedata.58,61 Current limitations include the requirementof regular rhythm, relative inferior imagequality of real-time 3-D echocardiography comparedto 2-D images, and the time necessary foroff-line data analysis. However, the greater numberof acquired data points, the lack of geometricassumptions, increasingly sophisticated 3-D imageand measurements solutions offset theselimitations.Regional left ventricular functionIn 1989, the American Society of Echocardiographyrecommended a 16 segment model for LVsegmentation.2 This model consists of six segmentsat both basal and mid-ventricular levels and foursegments at the apex (Fig. 8). The attachment ofthe right ventricular wall to the left ventricle definesthe septum, which is divided at basal andmid LV levels into anteroseptum and inferoseptum.Continuing counterclockwise, the remaining segmentsat both basal and mid ventricular levelsare labeled as inferior, inferolateral, anterolateraland anterior. The apex includes septal, inferior,lateral, and anterior segments. This model hasbecome widely utilized in echocardiography. Incontrast, nuclear perfusion imaging, cardiovascularmagnetic resonance and cardiac computedtomography have commonly used a larger numberof segments.In 2002, the American Heart Association WritingGroup on Myocardial Segmentation and Registrationfor Cardiac Imaging, in an attempt to establishsegmentation standards applicable to all typesof imaging, recommended a 17-segment model(Fig. 8).62 This differs from the previous 16-segment model predominantly by the addition ofa 17th segment, the ‘‘apical cap.’’ The apicalcap is the segment beyond the end of the LVcavity. Refinements in echocardiographic imaging,including harmonics and contrast imaging arebelieved to permit improved imaging of the apex.Either model is practical for clinical applicationyet sufficiently detailed for semi-quantitativeanalysis. The 17-segment model should be predominantlyused for myocardial perfusion studies oranytime efforts are made to compare betweenimaging modalities. The 16-segment model isappropriate for studies assessing wall motionabnormalities as the tip of the normal apex(segment 17) does not move.The mass and size of the myocardium asassessed at autopsy is the basis for determiningTable 6 Reference limits and values and partition values of left ventricular function

Women MenReferencerangeMildlyabnormalModeratelyabnormalSeverelyabnormalReferencerangeMildlyabnormalModeratelyabnormalSeverelyabnormalLinear methodEndocardialfractionalshortening (%)27e45 22e26 17e21 _16 25e43 20e24 15e19 _14Midwallfractionalshortening (%)15e23 13e14 11e12 _10 14e22 12e13 10e11 _102-D methodEjectionfraction (%)‡55 45e54 30e44 <30 ‡55 45e54 30e44 <30Values in bold are recommended and best validated.the distribution of segments. Sectioned into basal,mid ventricular and apical thirds, perpendicular tothe LV long-axis, with the mid ventricular thirddefined by the papillary muscles, the measuredmyocardial mass in adults without cardiac diseasewas 43% for the base, 36% for the mid cavity and21% for the apex.63 The 16-segment model closelyapproximates this, creating a distribution of 37.5%for both the basal and mid portions and 25% for theapical portion. The 17-segment model createsa distribution of 35.3%, 35.3% and 29.4% for thebasal, mid and apical portions (including the apicalcap) of the heart, respectively.Variability exists in the coronary artery bloodsupply to myocardial segments. Nevertheless, thesegments are usually attributed to the three majorcoronary arteries are shown in the TTE G distributionsof Fig. 9.62

Since the 1970s, echocardiography has beenused for the evaluation of LV regional wall motionduring infarction and ischemia.64e66 It is recognizedthat regional myocardial blood flow andregional LV systolic function are related overa wide range of blood flows.67 Although regionalwall motion abnormalities at rest may not beseen until the luminal diameter stenosis exceeds85%, with exercise, a coronary lesion of 50% can resultin regional dysfunction. It is recognized thatechocardiography can overestimate the amountof ischemic or infarcted myocardium, as wallmotion of adjacent regions may be affected bytethering, disturbance of regional loading conditions

and stunning.68 Therefore, wall thickeningas well as motion should be considered. Moreover,it should be remembered that regional wall motionabnormalities may occur in the absence of coronaryartery disease.It is recommended that each segment be analyzedindividually and scored on the basis of itsmotion and systolic thickening. Ideally, the functionof each segment should be confirmed in multipleviews. A segment which is normal or hyperkineticis assigned a score of 1, hypokinesis ¼ 2, akinesis(negligible thickening) ¼ 3, dyskinesis (paradoxicalsystolic motion) ¼ 4, and aneurysmal (diastolicdeformation) ¼ 5.1 Wall motion score index can bederived as a sum of all scores divided by the numberof segments visualized.Assessment of LV remodeling and the useof echocardiography in clinical trialsLeft ventricular remodeling describes the processby which the heart changes its size, geometry andfunction over time. Quantitative 2-D transthoracicFigure 8 Segmental analysis of LV walls based on schematic views, in a parasternal short and long axis orientation,at three different levels. The ‘‘apex segments’’ are usually visualized from apical four-chamber, apical two- andthree-chamber views. The apical cap can only be appreciated on some contrast studies. A 16 segment model canbe used, without the apical cap, as described in an ASE 1989 document.2 A 17 segment model, including the apicalcap, has been suggested by the American Heart Association Writing Group on Myocardial Segmentation and Registrationfor Cardiac Imaging.62

echocardiography enables characterization of LVremodeling that occurs in normal subjects and ina variety of heart diseases. LV remodeling may bephysiological when the heart increases in size butmaintains normal function during growth, physicaltraining and pregnancy. Several studies have demonstratedthat both isometric and isotonic exercisecause remodeling of the left and right ventricularchamber sizes and wall thicknesses.69e73 Thesechanges in the highly-trained, elite ‘‘athletehearts’’ are directly related to the type and durationof exercise and have been characterized echocardiographically.With isometric exercise, adisproportionate increase occurs in LV mass comparedto the increase in LV diastolic volume resultingin significantly greater wall thickness to cavitysize ratio (h/R ratio) than take place in normalnon-athletic subjects with no change in ejectionphase indices of LV contractile function.69e73 Thisphysiologic hypertrophic remodeling of the athleteheart is reversible with cessation of endurancetraining and is related to the total increase inlean body weight70 and triggered by enhanced cardiacsympathetic activity.74 Remodeling may becompensatory in chronic pressure overload due tosystemic hypertension or aortic stenosis resultingin concentric hypertrophy (increased wall thickness,normal cavity volume and preserved ejection

fraction) (Fig. 5). Compensatory LV remodelingalso occurs in chronic volume overload associatedwith mitral or aortic regurgitation, which inducesa ventricular architecture characterized by eccentrichypertrophy, LV chamber dilatation and initiallynormal contractile function. Pressure andvolume overload may remain compensated by appropriatehypertrophy which normalizes wallstress such that hemodynamics and ejection fractionremain stable long term. However, in somepatients chronically increased afterload cannotbe normalized indefinitely and the remodelingprocess becomes pathologic.Transition to pathologic remodeling is heraldedby progressive ventricular dilatation, distortion ofcavity shape and disruption of the normal geometryof the mitral annulus and subvalvular apparatusresulting in mitral regurgitation. The additionalvolume load from mitral regurgitation escalatesthe deterioration in systolic function and developmentof heart failure. LV dilatation begets mitralregurgitation and mitral regurgitation begets furtherLV dilatation, progressive remodeling andcontractile dysfunction.Changes in LV size and geometry due to hypertension(Fig. 5) reflect the dominant underlyinghemodynamic alterations associated with bloodpressure elevation.22,75 The pressure-overloadpattern of concentric hypertrophy is uncommonin otherwise healthy hypertensive individuals andis associated with high systolic blood pressureand high peripheral resistance. In contrast, eccentric LV hypertrophy is associated with normal peripheralresistance but high cardiac index consistentwith excess circulating blood volume. Concentricremodeling (normal LV mass with increased relativewall thickness) is characterized by high peripheralresistance, low cardiac index, andincreased arterial stiffness.76,77

A unique form of remodeling occurs followingmyocardial infarction due to the abrupt loss ofcontracting myocytes.22,78 Early expansion of theinfarct zone is associated with early LV dilatationas the increased regional wall stress is redistributedto preserve stroke volume. The extent ofearly and late post-infarction remodeling is determinedby a number of factors, including size andlocation of infarction, activation of the sympatheticnervous system, and up-regulation of therenin/angiotensin/aldosterone system and natriureticpeptides. Between one-half and one-thirdof post-infarction patients experience progressivedilatation79,80 with distortion of ventricular geometryand secondary mitral regurgitation. Mitralregurgitation further increases the propensity fordeterioration in LV function and development ofcongestive heart failure. Pathologic LV remodelingis the final common pathway to heart failure,whether the initial stimulus is chronic pressure orchronic volume overload, genetically determined

cardiomyopathy or myocardial infarction. The etiologyof LV dysfunction in approximately two thirdsof the 4.9 million patients with heart failure in theUSA is coronary artery disease.81

While LV remodeling in patients with chronicsystemic hypertension, chronic valvular regurgitationand primary cardiomyopathies has been described,the transition to heart failure is less wellknown because the time course is so prolonged. Bycontrast, the time course from myocardial infarctionto heart failure is shorter and has been clearlydocumented.The traditional quantitative echocardiographicmeasurements recommended to evaluate LV remodelingincluded estimates of LV volumes eitherfrom biplane or single plane images as advocatedby the American Society of Echocardiography.Although biplane and single-plane volume estimationsare not interchangeable, both estimates areequally sensitive for detecting time-dependent LVremodeling and deteriorating contractile function.77 LV volumes and derived ejection fractionhave been demonstrated to predict adversecardiovascular events at follow-up, includingdeath, recurrent infarction, heart failure, ventriculararrhythmias and mitral regurgitation innumerous post-infarction and heart failuretrials.78e81 This committee recommends the useof quantitative estimation of LV volumes, LVEF,LV mass and shape as (described in the respectivesections above) to follow LV remodeling induced byphysiologic and pathologic stimuli. In addition,these measurements provide prognostic informationincremental to that of baseline clinicaldemographics.Quantification of the RV and RVOTThe normal right ventricle (RV) is a complexcrescent-shaped structure wrapped around theleft ventricle and is incompletely visualized inany single 2-D echocardiographic view. Thus,accurate assessment of RV morphology and functionrequires integration of multiple echocardiographicviews, including the parasternal long andshort-axis views, the RV inflow view, the apicalfour-chamber and the subcostal views. Whilemultiple methods for quantitative echocardiographicRV assessment have been described, inclinical practice assessment of RV structure andfunction remains mostly qualitative. Nevertheless,numerous studies have recently emphasized theimportance of RV function in the prognosis ofa variety of cardio-pulmonary diseases suggestingthat more routine quantification of RV functionis warranted under most clinical circumstances.Compared to the left ventricle, the right ventricleis a thin-walled structure under normalconditions. The normal right ventricle is accustomedto a low pulmonary resistance and hencelow afterload; thus, normal RV pressure is low and

right ventricular compliance high. The right ventricleis therefore sensitive to changes in afterload,and alterations in RV size and function areindicators of increased pulmonary vascular resistanceand load transmitted from the left-sidedchambers. Elevations in RV afterload in adults aremanifested acutely by RV dilatation and chronicallyby concentric RV hypertrophy. In addition,intrinsic RV abnormalities, such as infarction or RVdysplasia82 can cause RV dilatation or reduced RVwall thickness. Thus, assessment of RV size andwall thickness is integral to the assessment of RVfunction.Right ventricular free wall thickness, normallyless than 0.5 cm, is measured using either M-modeor 2-D imaging. Although RV free wall thickness canbe assessed from the apical and parasternal longaxisviews, the subcostal view measured at thepeak of the R wave at the level of the tricuspidvalve chordae tendinae provides less variationand closely correlates with RV peak systolic pressure(Fig. 10).75 Care must be taken to avoid over measurement due to the presence of epicardial fatdeposition as well as coarse trabeculations withinthe right ventricle.Qualitative assessment of RV size is easilyaccomplished from the apical four-chamber view(Fig. 11). In this view, RV area or mid cavity diametershould be smaller than that of the left ventricle.In cases of moderate enlargement, the RVcavity area is similar to that of the LV and it mayshare the apex of the heart. As RV dilation progresses,the cavity area will exceed that of the LVand the RV will be ‘‘apex forming’’. Quantitativeassessment of RV size is also best performed inthe apical four-chamber view. Care must be takento obtain a true non-foreshortened apical fourchamberview, oriented to obtain the maximumRV dimension, prior to making these measurements.Measurement of the mid-cavity and basalRV diameter in the apical four-chamber view atend-diastole is a simple method to quantify RVsize (Fig. 11). In addition, RV longitudinal diametercan be measured from this view. Table 7 providesnormal RV dimensions from the apical four-chamberview.76,80,83

Right ventricular size may be assessed may beassessed with TEE in the mid-esophageal fourchamberview (Fig. 12). The mid-esophagealfour- chamber view, which generally parallelswhat is obtainable from the apical four-chamberview, should originate at the mid-left atrial leveland pass through the LV apex with the multiplaneangle adjusted to maximize the tricuspid annulusdiameter, usually between 10 and 20 degrees.Right ventricular systolic function is generallyestimated qualitatively in clinical practice. Whenthe evaluation is based on a qualitative assessment,the displacement of the tricuspid annulusshould be observed. In systole, the tricuspid

annulus will normally descend toward the apex1.5e2.0 cm. Tricuspid annular excursion of lessthan 1.5 cm has been associated with poor prognosisin a variety of cardiovascular diseases.84 Althougha number of techniques exist for accuratequantitation, direct calculation of RV volumesand ejection fraction remains problematic giventhe complex geometry of the right ventricle andthe lack of standard methods for assessing RVvolumes. Nevertheless, a number of echocardiographictechniques may be used to assess RV function.Right ventricular fractional area change (FAC)measured in the apical four-chamber view is a simplemethod for assessment of RV function that hascorrelated with RV ejection fractions measured byMRI (r ¼ 0.88) and has been related to outcome ina number of disease states.81,85 Normal RV areasand fractional area changes are shown in Table 8.Additional assessment of the RV systolic functionincludes tissue imaging of tricuspid annularFigure 10 Methods of measuring right ventricular wallthickness (arrows) from an M-mode echo (left) and asubcostal transthoracic echo (right).Figure 11velocity or right ventricular index of myocardialperformance (Tei Index).86

The RV outflow tract (RVOT) extends from theanterosuperior aspect of the right ventricle to thepulmonary artery, and includes the pulmonaryvalve. It is best imaged from the parasternallong-axis view angled superiorly, and the parasternalshort-axis at the base of the heart. It canadditionally be imaged from the subcostal long andtransverse windows as well as the apical window.Measurement of the RV outflow tract is mostaccurate from the parasternal short-axis (Fig. 13)just proximal to the pulmonary valve. Mean RVOTmeasurements are shown in Table 7.75 With TEE,the mid-esophageal RV inflow-outflow view usuallyprovides the best image of the RVOT just proximalto the pulmonary valve (Fig. 14).Quantification of LA/RA sizeThe left atrium (LA) fulfills three major physiologicroles that impact on LV filling and performance.The left atrium acts as a contractile pump thatdelivers 15e30% of the LV filling, as a reservoir thatcollects pulmonary venous return during ventricularsystole and as a conduit for the passage ofstored blood from the LA to the LV during earlyventricular diastole.87 Increased left atrial size isassociated with adverse cardiovascular outcomes.88e90 An increase in atrial size most commonlyis related to increased wall tension due to increasedfilling pressure.91,92 Although increasedfilling volumes can cause an increase in LA size,the adverse outcomes associated with increaseddimension and volume are more strongly associatedwith increased filling pressure. Relationshipsexist between increased left atrial size and the incidenceof atrial fibrillation and stroke,93e101 risk

of overall mortality after MI,102,103 and the risk ofdeath and hospitalization in subjects with dilatedcardiomyopathy.104e108 LA enlargement is a markerof both the severity and chronicity of diastolicdysfunction and magnitude of LA pressureelevation.88,91,92

Table 7 Reference limits and partition values of right ventricular and pulmonary artery size76

ReferencerangeMildlyabnormalModeratelyabnormalSeverelyabnormalRV dimensionsBasal RV diameter (RVD#1) (cm) 2.0e2.8 2.9e3.3 3.4e3.8 _3.9Mid RV diameter (RVD#2) (cm) 2.7e3.3 3.4e3.7 3.8e4.1 _4.2Base-to-apex length (RVD#3) (cm) 7.1e7.9 8.0e8.5 8.6e9.1 _9.2RVOT diametersAbove aortic valve (RVOT#1) (cm) 2.5e2.9 3.0e3.2 3.3e3.5 _3.6Above pulmonic valve (RVOT#2) (cm) 1.7e2.3 2.4e2.7 2.8e3.1 _3.2PA diameterBelow pulmonic valve (PA#1) (cm) 1.5e2.1 2.2e2.5 2.6e2.9 _3.0Figure 12The LA size is measured at the end-ventricularsystole when the LA chamber is at its greatestdimension. While recording images for computingLA volume, care should be taken to avoid foreshorteningof the LA. The base of the LA should beat its largest size indicating that the imaging planepasses through the maximal short-axis area. TheLA length should also be maximized ensuringalignment along the true long-axis of the LA.When performing planimetry the LA, the confluencesof the pulmonary veins and LA appendageshould be excluded.With TEE, the LA frequently cannot fit in itsentirety into the image sector. Measurements of LAvolume from this approach cannot be reliablyperformed however; LA dimension can beestimated combining measurements from differentimaging planes.LA linear dimensionThe LA can be visualized from multiple echocardiographicviews from which several potential LAdimensions can be measured. However, the largevolume of prior clinical and research work used theM-mode or 2-D derived anteroposterior (AP) lineardimension obtained from the parasternal long-axisview making this the standard for linear LAmeasurement (Fig. 15).93,95,96,98,104,105 The conventionfor M-mode measurement is to measurefrom the leading edge of the posterior aortic wallto the leading edge of the posterior LA wall. However, to avoid the variable extent of spacebetween the LA and aortic root, the trailing edgeof the posterior aortic is recommended.Although these linear measurements have beenshown to correlate with angiographic measurementsand have been widely used in clinical

practice and research, they inaccurately representtrue LA size.109,110 Evaluation of the LA in the APdimension assumes that a consistent relationshipis maintained between the AP dimension and allother LA dimensions as the atrium enlarges, whichis often not the case.111,112 Expansion of the leftatrium in the AP dimension may be constrainedby the thoracic cavity between the sternumand the spine. Predominant enlargement in thesuperior-inferior and medial-lateral dimensionswill alter LA geometry such that the AP dimensionmay not be representative of LA size. For thesereasons, AP linear dimensions of the left atriumas the sole measure of left atrial size may be misleadingand should be accompanied by left atrialvolume determination in both clinical practiceand research.LA volume measurementsWhen LA size is measured in clinical practice,volume determinations are preferred over lineardimensions because they allow accurate assessmentof the asymmetric remodeling of the LAchamber.111 In addition, the strength of therelationship between cardiovascular disease isstronger for LA volume than for LA linear dimensions.97,113 Echocardiographic measures of LA volumehave been compared with cine-computedtomography, biplane contrast ventriculographyand MRI.109,114e116 These studies have showneither good agreement or a tendency for echocardiographicmeasurements to underestimate comparativeLA volumes.The simplest method for estimating LA volume isthe cube formula, which assumes that the LAvolume is that of a sphere with a diameter equalto the LA antero-posterior dimension. However,this method has proven to be inferior to othervolume techniques.109,111,117 Left atrial volumesare best calculated using either an ellipsoid modelor Simpson’s rule.88,89,97,101,102,109e111,115e117

The ellipsoid model assumes that the LA can beadequately represented as a prolate ellipse witha volume of 4p/3(L/2)(D1/2)(D2/2), where L is thelong-axis (ellipsoid) and D1 and D2 are orthogonalshort-axis dimensions. LA volume can be estimatedusing this biplane dimension-length formula bysubstituting the LA antero-posterior diameteracquired from the parasternal long-axis as D1, LAmedial-lateral dimension from the parasternalshort-axis as D2 and the LA long-axis from the apicalfour-chamber for L.117e119 Simplified methodsusing non-orthogonal linear measurements forFigure 14 Measurement of the right ventricular outflow tract at the pulmonic valve annulus (RVOT2), and at andmain pulmonary artery from the midesophageal RV inflow-outflow view.Figure 15estimation of LA volume have been proposed.113

Volume determined using linear dimensions isvery dependent on careful selection of the locationand direction of the minor axis dimensions

and has been shown to significantly underestimateLA volume.117

In order to estimate the LA minor axis dimensionof the ellipsoid more reliably, the long-axis LA areascan be traced and a composite dimension derived.This dimension takes into account the entire LAborder, rather than a single linear measurement.When long-axis-area is substituted for minor axisdimension, the biplane areaelength formula isused: 8(A1)(A2)/3p(L), where A1 and A2 representthe maximal planimetered LA area acquired fromthe apical four- and two-chamber-views, respectively.The length (L) remains the LA long-axislength determined as the distance of the perpendicularline measured from the middle of the planeof the mitral annulus to the superior aspect of theleft atrium (Fig. 16). In the areaelength formulathe length (L) is measured in both the four- andtwo-chamber views and the shortest of these twoL measurements is used in the formula.The areaelength formula can be computed froma single plane, typically the apical four-chamber,by assuming A1 ¼A2, such that volume ¼ 8(A1)2/3p(L).120 However, this method makes geometricassumptions that may be inaccurate. In older subjectsthe diaphragm lifts the cardiac apex upwardwhich increases the angle between ventricle andatrium. Thus the apical four-chamber view willcommonly intersect the atria tangentially in oldersubjects and result in underestimation of volumeusing a single plane technique. Since the majorityof prior research and clinical studies have used thebiplane areaelength formula, it is the recommendedellipsoid method (Figs. 15 and 16).LA volume may also be measured using Simpson’srule, similar to its application for LV measurements,which states that the volume of a geometricalfigure can be calculated from the sum of thevolumes of smaller figures of similar shape. Mostcommonly, Simpson’s algorithm divides the LA intoa series of stacked oval disks whose height is h andwhose orthogonal minor and major axes are D1 andD2 (method of disks). The volume of the entireleft atrium can be derived from the sum of the volume of the individual disks. Volume ¼ p/4(h)P(D1)(D2). The formula is integrated with theaid of a computer and the calculated volumeprovided by the software package online (Fig. 17).The use of the Simpson’s method in this wayrequires the input of biplane LA planimetry toderive the diameters. Optimal contours should beobtained orthogonally around the long-axis of theleft atrium using TTE apical views. Care should betaken to exclude the pulmonary veins from the LAtracing. The inferior border should be representedby the plane of the mitral annulus. A single planemethod of disks could be used to estimate LAvolume by assuming the stacked disks are circularV ¼ p/4(h)P(D1).2 However, as noted above, thismakes the assumption that the LA width in the apical

two- and four-chamber are identical, which isoften not the case and therefore this formula isnot preferred.Three-dimensional echocardiography shouldprovide the most accurate evaluation of LA volumeand has shown promise, however to date noconsensus exists on the specific method that shouldbe used for data acquisition and there is nocomparison with established normal values.121e123

Normal values of LA measurementsThe non-indexed LA linear measurements aretaken from a Framingham Heart Study cohort of1099 subjects between the ages of 20 and45 years old who were not obese, were of averageheight and were without cardiovascular disease(Table 9).11 Slightly higher values have beenreported in a cohort of 767 subjects withoutcardiovascular disease in which obesity and heightwere not exclusion criteria.113 Both body sizeand aging have been noted to influence LAsize.10,87,113 There are also gender differences inLA size, however, these are nearly completely accountedfor by variation in body size.87,113,120,124

The influence of subject size on LA size is typicallycorrected by indexing to some measure of bodysize. In fact, from childhood onward the indexedatrial volume changes very little.125 Several indexingmethods have been proposed, such as height,weight, estimated lean body mass and body surfacearea.10,113 The most commonly used convention,and that recommended by this committee,is indexing LA size by dividing by body surfacearea.Normal indexed LA volume has been determinedusing the preferred biplane techniques (areaelength or method of disks) in a number of studiesinvolving several hundred patients to be22 G 6 ml/m2.88,120,126,127 Absolute LA volume hasalso been reported however in clinical practiceindexing to body surface area accounts for variationsin body size and should therefore be used.As cardiac risk and LA size are closely linked,Figuremore importantly than simply characterizing thedegree of LA enlargement, normal referencevalues for LA volume allow prediction of cardiacrisk. There are now multiple peer reviewed articleswhich validate the progressive increase inrisk associated with having LA volumes greaterthan these normative values.89,97,99e103,106e108,128

Consequently, indexed LA volume measurementsshould become a routine laboratory measure sinceit reflects the burden and chronicity of elevated LVfilling pressure and is a strong predictor ofoutcome.Right atriumMuch less research and clinical data are availableon quantifying right atrial size. Although the RAcan be assessed from many different views, quantificationof RA size is most commonly performed

from the apical four-chamber view. The minor axisdimension should be taken in a plane perpendicularto the long-axis of the RA and extends from thelateral border of the RA to the interatrial septum.Normative values for the RA minor axis are shownin Table 9.80,129 Although RA dimension may varyby gender, no separate reference values for maleand females can be recommended at this time.Although, limited data are available for RAvolumes, assessment of RA volumes would bemore robust and accurate for determination ofRA size than linear dimensions. As there are nostandard orthogonal RA views to use an apicalbiplane calculation, the single plane areaelengthand method of discs formulae have been applied toRA volume determination in several small studies.120,130,131 We believe there is too little peer reviewedvalidated literature to recommend normalRA volumetric values at this time. However, limiteddata on small number of normal subjectsrevealed that indexed RA volumes are similar toLA normal values in men (21 ml/m2) but appearto be slightly smaller in women.120

Quantification of the aorta and IVCAortic measurementsRecordings should be made from the parasternallong-axis acoustic window to visualize the aorticroot and proximal ascending aorta. Two-dimensionalimages should be used to visualize the LVoutflow tract and the aortic root should be recordedin different views in varying intercostalspaces and at different distances from the leftsternal border. Right parasternal views, recorded Table 9Reference limits and partition values for left atrial dimensions/volumesWomen MenReferenceRangeMildlyAbnormalModeratelyAbnormalSeverelyAbnormalReferenceRangeMildlyAbnormalModeratelyAbnormalSeverelyAbnormalAtrial dimensionswith the patient in a right lateral decubitusposition are also useful. Measurements are usuallytaken at: (1) aortic valve annulus (hinge point ofaortic leaflets); (2) the maximal diameter in thesinuses of Valsalva; and (3) sinotubular junction(transition between the sinuses of Valsalva and thetubular portion of the ascending aorta).Views used for measurement should be thosethat show the largest diameter of the aortic root.

When measuring the aortic diameter, it is particularlyimportant, to use the maximum obtainableshort-axis diameter measured perpendicular to thelong-axis of the vessel in that view. Some expertsfavor inner edge-to-inner edge techniques tomatch those used by other methods of imagingthe aorta, such as MRI and CT scanning. Howeverthe normative data for echocardiography wereobtained using the leading edge technique(Fig. 18). Advances in ultrasound instrumentationwhich have resulted in improved image resolutionshould minimize the difference between thesemeasurement methods.Reliability of aortic root measurements bythis method yielded an intra-class correlationcoefficient of 0.79 (p < 0.001) in a study of 183hypertensive patients (unpublished data). Twodimensionalaortic diameter measurements arepreferable to M-mode measurements, as cyclicmotion of the heart and resultant changes inM-mode cursor location relative to the maximumdiameter of the sinuses of Valsalva result insystematic underestimation (by w2 mm) of aorticdiameter by M-mode in comparison to the 2-Daortic diameter.132 The aortic annular diameter ismeasured between the hinge points of the aorticvalve leaflets (inner edgeeinner edge) in the parasternalor apical long-axis views that reveal thelargest aortic annular diameter with color flowmapping to clarify tissueeblood interfaces ifnecessary.132

The thoracic aorta can be better imaged usingTEE than, as most of it is in the near field of thetransducer. The ascending aorta can be seen inlong-axis, using the mid-esophageal aortic valvelong-axis view at about 130 degrees and the midesophagealascending aorta long-axis view. Theshort-axis view of the ascending aorta is obtainedusing the mid-esophageal views at about 45 degrees.For measurements of the descending aorta,short-axis views at about 0 degrees, and long-axisviews at about 90 degrees, can be recorded fromthe level of the diaphragm up to the aortic arch(Fig. 19). The arch itself and origins of two of thegreat vessels can be seen in most patients. Thereis a ‘‘blind spot’’ in the upper ascending aortaand the proximal arch that is not seen by TEEdue to the interposed tracheal bifurcation.Identification of aortic root dilatationAortic root diameter at the sinuses of Valsalva isrelated most strongly to body surface area andage. Therefore, body surface area may be used topredict aortic root diameter in three age-strata:<20 years, 20e40 and >40 years, by publishedequations.132 Aortic root dilatation at the sinusesof Valsalva is defined as an aortic root diameterabove the upper limit of the 95% confidence intervalof the distribution in a large reference population.132 Aortic dilatation can be easily detected byplotting observed aortic root diameter versus body

surface area on previously-published nomograms(Fig. 20).132 Aortic dilatation is strongly associatedwith the presence and progression of aortic regurgitation133

and with the occurrence of aorticdissection.134 The presence of hipertensión appears to have minimal impact on aortic rootdiameter at the sinuses of Valsalva133,135 but isassociated with enlargement of more distal aorticsegments.135

Evaluation of the inferior vena cavaExamination of the inferior vena cava (IVC) fromthe subcostal view should be included as part ofthe routine TTE examination. It is generally agreedthat the diameter of the inferior vena cava shouldbe measured with the patient in the left decubitusposition at 1.0e2.0 cm from the junction with theright atrium, using the long-axis view. For accuracy,this measurement should be made perpendicularto the IVC long-axis. The diameter of theinferior vena cava decreases in response to inspirationwhen the negative intrathoracic pressureleads to an increase in right ventricular fillingfrom the systemic veins. The diameter of the IVCand the percent decrease in the diameter duringinspiration correlate with right atrial pressure.The relationship has been called the ‘‘collapsibilityindex’’.136 Evaluation of the inspiratory responseoften requires a brief ‘‘sniff’’ as normalinspiration may not elicit this response.The normal IVC diameter is <1.7 cm. There isa 50% decrease in the diameter when the rightatrial pressure is normal (0e5 mmHg). A dilatedIVC (>1.7 cm) with normal inspiratory collapse(_50%) is suggestive of a mildly elevated RA pressure(6e10 mmHg). When the inspiratory collapse is <50%, the RA pressure is usually between 10 and15 mmHg. Finally, a dilated IVC without any collapsesuggests a markedly increased RA pressureof >15 mmHg. In contrast, a small IVC (usually<1.2 cm) with spontaneous collapse often is seenin the presence of intravascular volumedepletion.137

There are several additional conditions to beconsidered in evaluating the inferior vena cava.Athletes have been shown to have dilated inferiorvena cavae with normal collapsibility index. Studies137,138

have found that the mean IVC diameter inathletes was 2.31 G 0.46 compared to 1.14 G 0.13in aged-matched normals. The highest diameterswere seen in highly trained swimmers.One study showed that a dilated IVC in themechanically ventilated patient did not alwaysindicate a high right atrial pressure. However,a small IVC (<1.2 cm) had a 100% specificity fora RA pressure of less than 10 mmHg with a low sensitivity.139 A more recent study suggested thatthere was a better correlation when the IVC diameterwas measured at end-expiration and enddiastoleusing M-mode echocardiography.140

The use of the inferior vena cava size and

dynamics is encouraged for estimation of the rightatrial pressure. This estimate should be used inestimation of the pulmonary artery pressure basedon the tricuspid regurgitant jet velocity.AcknowledgmentsThe authors wish to thank Harvey Feigenbaum,MD, and Nelson B. Schiller for their careful reviewand thoughtful comments.References1. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendationsregarding quantitation in M-mode echocardiography:results of a survey of echocardiographic measurements.Circulation 1978;58:1072e83.2. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R,Feigenbaum H, et al. Recommendations for quantitationof the left ventricle by two-dimensional echocardiography.American Society of Echocardiography Committee on Standards,Subcommittee on Quantitation of Two-DimensionalEchocardiograms. J Am Soc Echocardiogr 1989;2:358e67.3. Hirata K, Watanabe H, Beppu S, Muro T, Teragaki M,Yoshiyama M, et al. Pitfalls of echocardiographic measurementin tissue harmonic imaging: in vitro and in vivo study.J Am Soc Echocardiogr 2002;15:1038e44.4. McGavigan AD, Dunn FG, Goodfield NE. Secondary harmonicimaging overestimates left ventricular mass compared tofundamental echocardiography. Eur J Echocardiogr 2003;4:178e81.5. FeigenbaumH, ArmstrongW, Ryan T. Feigenbaum’s echocardiography.6th ed. Philadelphia (PA): Lippincott, Williamsand Wilkins; 2005.6. Mulvagh SL, DeMaria AN, Feinstein SB, Burns PN,Kaul S, Miller JG, et al. Contrast echocardiography:current and future applications. J Am Soc Echocardiogr2000;13:331e42.7. Nahar T, Croft L, Shapiro R, Fruchtman S, Diamond J,Henzlova M, et al. Comparison of four echocardiographictechniques for measuring left ventricular ejection fraction.Am J Cardiol 2000;86:1358e62.8. Colombo PC, Municino A, Brofferio A, Kholdarova L,Nanna M, Ilercil A, et al. Cross-sectional multiplane transesophagealechocardiographic measurements: comparisonwith standard transthoracic values obtained in the samesetting. Echocardiography 2002;19:383e90.9. Hozumi T, Shakudo M, Shah PM. Quantitation of left ventricularvolumes and ejection fraction by biplane transesophagealechocardiography. Am J Cardiol 1993;72:356e9.10. Vasan RS, Levy D, Larson MG, Benjamin EJ. Interpretationof echocardiographic measurements: a call for standardization.Am Heart J 2000;139:412e22.11. Vasan RS, Larson MG, Levy D, Evans JC, Benjamin EJ.Distribution and categorization of echocardiographic measurementsin relation to reference limits: the FraminghamHeart Study: formulation of a height- and sex-specificclassification and its prospective validation. Circulation1997;96:1863e73.12. Devereux RB, Roman MJ. Evaluation of cardiac and vascularstructure by echocardiography and other noninvasivetechniques. In: Laragh JH, Brenner BM, editors. Hypertension:pathophysiolog, diagnosis, treatment. 2nd ed. NewYork: Raven Press; 1995. p. 1969e85.13. Gottdiener JS, Bednarz J, Devereux R, Gardin J, Klein A,Manning WJ, et al. American Society of Echocardiographyrecommendations for use of echocardiography in clinicaltrials. J Am Soc Echocardiogr 2004;17:1086e119.14. Wyatt HL, Heng MK, Meerbaum S, Hestenes JD, Cobo JM,Davidson RM, et al. Cross-sectional echocardiography. I.Analysis of mathematic models for quantifying mass ofthe left ventricle in dogs. Circulation 1979;60:1104e13.15. Reichek N, Helak J, Plappert T, Sutton MS, Weber KT. Anatomicvalidation of left ventricular mass estimates fromclinical two-dimensional echocardiography: initial results.Circulation 1983;67:348e52.

16. Helak JW, Reichek N. Quantitation of human left ventricularmass and volume by two-dimensional echocardiography:in vitro anatomic validation. Circulation 1981;63:1398e407.17. Schiller NB, Skioldebrand CG, Schiller EJ, Mavroudis CC,Silverman NH, Rahimtoola SH, et al. Canine left ventricularmass estimation by two-dimensional echocardiography.Circulation 1983;68:210e6.18. Triulzi MO, Gillam LD, Gentile F, Newell J, Weyman A. Normaladult cross-sectional echocardiographic values: Lineardimensions and chamber areas. Echocardiography 1984;1:403e26.19. Devereux RB, Wachtell K, Gerdts E, Boman K,Nieminen MS, Papademetriou V, et al. Prognostic significanceof left ventricular mass change during treatmentof hypertension. JAMA 2004;292:1e7.20. Ilercil A, O’Grady MJ, Roman MJ, Paranicas M, Lee ET,Welty TK, et al. Reference values for echocardiographicmeasurements in urban and rural populations of differingethnicity: the Strong Heart Study. J Am Soc Echocardiogr2001;14:601e11.21. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E,Sachs I, et al. Echocardiographic assessment of left ventricularhypertrophy: comparison to necropsy findings.Am J Cardiol 1986;57:450e822. Ganau A, Devereux RB, Roman MJ, de Simone G,Pickering TG, Saba PS, et al. Patterns of left ventricularhypertrophy and geometric remodeling in essential hypertension.J Am Coll Cardiol 1992;19:1550e8.23. Devereux RB, de Simone G, Pickering TG, Schwartz JE,Roman MJ. Relation of left ventricular midwall functionto cardiovascular risk factors and arterial structure andfunction. Hypertension 1998;31:929e36.24. Palmieri V, Dahlof B, DeQuattro V, Sharpe N, Bella JN, deSimone G, et al. Reliability of echocardiographic assessmentof left ventricular structure and function: the PRESERVEstudy: Prospective Randomized Study EvaluatingRegression of Ventricular Enlargement. J Am Coll Cardiol1999;34:1625e32.25. Nidorf SM, Picard MH, Triulzi MO, Thomas JD, Newell J,King ME, et al. New perspectives in the assessment ofcardiac chamber dimensions during development andadulthood. J Am Coll Cardiol 1992;19:983e8.26. Pearlman JD, Triulzi MO, King ME, Newell J, Weyman AE.Limits of normal left ventricular dimensions in growthand development: analysis of dimensions and variance inthe two-dimensional echocardiograms of 268 normalhealthy subjects. J Am Coll Cardiol 1988;12:1432e41.27. Lang RM, Borow KM, Neumann A, Janzen D. Systemicvascular resistance: an unreliable index of left ventricularafterload. Circulation 1986;74:1114e23.28. Quinones MA, Waggoner AD, Reduto LA, Nelson JG,Young JB, Winters Jr WL, et al. A new, simplified andaccurate method for determining ejection fraction withtwo-dimensional echocardiography. Circulation 1981;64:744e53.29. Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems inechocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absenceof asynergy. Am J Cardiol 1976;37:7e11.30. de Simone G, Devereux RB, Roman MJ, Ganau A, Saba PS,Alderman MH, et al. Assessment of left ventricular functionby the midwall fractional shortening/end-systolicstress relation in human hypertension. J Am Coll Cardiol1994;23:1444e51.31. Shimizu G, Zile MR, Blaustein AS, Gaasch WH. Left ventricularchamber filling and midwall fiber lengthening inpatients with left ventricular hypertrophy: overestimationof fiber velocities by conventional midwall measurements.Circulation 1985;71:266e72.32. Celentano A, Palmieri V, Arezzi E, Mureddu GF, Sabatella M,Di MG, et al. Gender differences in left ventricular chamberand midwall systolic function in normotensive and hypertensiveadults. J Hypertens 2003;21:1415e23.33. Gerdts E, Zabalgoitia M, Bjornstad H, Svendsen TL,

Devereux RB. Gender differences in systolic left ventricularfunction in hypertensive patients with electrocardiographicleft ventricular hypertrophy (the LIFE study). AmJ Cardiol 2001;87:980e3.34. Devereux RB, Roman MJ, de Simone G, O’Grady MJ,Paranicas M, Yeh JL, et al. Relations of left ventricularmass to demographic and hemodynamic variables in AmericanIndians: the Strong Heart Study. Circulation 1997;96:1416e23.35. Devereux RB, Bella JN, Palmieri V, Oberman A,Kitzman DW, Hopkins PN, et al. Left ventricular systolicdysfunction in a biracial sample of hypertensive adults:The Hypertension Genetic Epidemiology Network (HyperGEN) Study. Hypertension 2001;38:417e23.36. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB.Association of carotid atherosclerosis and left ventricularhypertrophy. J Am Coll Cardiol 1995;25:83e90.37. Wahr DW, Wang YS, Schiller NB. Left ventricular volumesdetermined by two-dimensional echocardiography in anormal adult population. J Am Coll Cardiol 1983;1:863e8.38. de Simone G, Daniels SR, Devereux RB, Meyer RA,Roman MJ, de Divitiis O, et al. Left ventricular mass andbody size in normotensive children and adults: assessmentof allometric relations and impact of overweight. J AmColl Cardiol 1992;20:1251e60.39. Devereux RB, Palmieri V, Sharpe N, De QV, Bella JN, et al.Effects of once-daily angiotensin-converting enzyme inhibitionand calcium channel blockade-based antihypertensivetreatment regimens on left ventricular hypertrophyand diastolic filling in hypertension: the prospective randomizedenalapril study evaluating regression of ventricularenlargement (preserve) trial. Circulation 2001;104:1248e54.40. Kizer JR, Arnett DK, Bella JN, Paranicas M, Rao DC,Province MA, et al. Differences in left ventricular structurebetween black and white hypertensive adults: the HypertensionGenetic Epidemiology Network study. Hypertension2004;43:1182e8.41. Devereux RB, Casale PN, Kligfield P, Eisenberg RR, Miller D,Campo E, et al. Performance of primary and derived Mmodeechocardiographic measurements for detection ofleft ventricular hypertrophy in necropsied subjects andin patients with systemic hypertension, mitral regurgitationand dilated cardiomyopathy. Am J Cardiol 1986;57:1388e93.42. Malcolm DD, Burns TL, Mahoney LT, Lauer RM. Factorsaffecting left ventricular mass in childhood: the MuscatineStudy. Pediatrics 1993;92:703e9.43. Daniels SR, Meyer RA, Liang YC, Bove KE. Echocardiographicallydetermined left ventricular mass index in normalchildren, adolescents and young adults. J Am Coll Cardiol1988;12:703e8.44. Daniels SR, Kimball TR, Morrison JA, Khoury P, Meyer RA.Indexing left ventricular mass to account for differencesin body size in children and adolescents without cardiovasculardisease. Am J Cardiol 1995;76:699e701.45. de SG, Devereux RB, Daniels SR, Koren MJ, Meyer RA,Laragh JH. Effect of growth on variability of left ventricularmass: assessment of allometric signals in adults andchildren and their capacity to predict cardiovascularrisk. J Am Coll Cardiol 1995;25:1056e62.46. Gopal AS, Keller AM, Rigling R, King Jr DL, King DL. Leftventricular volume and endocardial surface area bythree-dimensional echocardiography: comparison withtwo-dimensional echocardiography and nuclear magneticresonance imaging in normal subjects. J Am Coll Cardiol1993;22:258e70.47. Handschumacher MD, Lethor JP, Siu SC, Mele D, Rivera JM,Picard MH, et al. A new integrated system for threedimensionalechocardiographic reconstruction: developmentand validation for ventricular volume withapplication in human subjects. J Am Coll Cardiol 1993;21:743e53.48. Jiang L, Vazquez de Prada JA, Handschumacher MD,

Vuille C, Guererro JL, Picard MH, et al. Quantitativethree-dimensional reconstruction of aneurysmal left ventricles.In vitro and in vivo validation. Circulation 1995;91:222e30.49. King DL, Harrison MR, King Jr DL, Gopal AS, Martin RP,DeMaria AN. Improved reproducibility of left atrialand left ventricular measurements by guided threedimensionalechocardiography. J Am Coll Cardiol 1992;20:1238e45.50. Kuhl HP, Franke A, Frielingsdorf J, Flaskamp C, Krebs W,Flachskampf FA, et al. Determination of left ventricularmass and circumferential wall thickness by three-dimensionalreconstruction: in vitro validation of a new methodthat uses a multiplane transesophageal transducer. J AmSoc Echocardiogr 1997;10:107e19.51. Roelandt JR, Ten Cate FJ, Vletter WB, Taams MA. Ultrasonicdynamic three-dimensional visualization of the heartwith a multiplane transesophageal imaging transducer.J Am Soc Echocardiogr 1994;7:217e29.52. Sheikh K, Smith SW, von Ramm O, Kisslo J. Real-time,three-dimensional echocardiography: feasibility and initialuse. Echocardiography 1991;8:119e25.53. Wollschlager H, Zeiher AM, Geibel A, Kasper W, Just H,Wollschlager S. Transespohogeal echo computer tomography:computational reconstruction of any desired view ofthe beating heart. In: Hanrath P, Uebis R, Krebs W, editors.Cardiovascular imaging by ultrasound. Dordrecht: Kluwer;1993.54. Buck T, Hunold P, Wentz KU, Tkalec W, Nesser HJ, Erbel R.Tomographic three-dimensional echocardiographic determinationof chamber size and systolic function in patientswith left ventricular aneurysm: comparison to magneticresonance imaging, cineventriculography, and two-dimensionalechocardiography. Circulation 1997;96:4286e97.55. Kuhl HP, Franke A, Merx M, Hoffmann R, Puschmann D,Hanrath P. Rapid quantification of left ventricular functionand mass using transoesophageal three-dimensional echocardiography:validation of a method that uses long-axiscutplanes. Eur J Echocardiogr 2000;1:213e21.56. Nosir YF, Fioretti PM, Vletter WB, Boersma E, Salustri A,Postma JT, et al. Accurate measurement of left ventricularejection fraction by three-dimensional echocardiography.A comparison with radionuclide angiography. Circulation1996;94:460e6.57. Gopal AS, Schnellbaecher MJ, Shen Z, Boxt LM, Katz J,King DL. Freehand three-dimensional echocardiographyfor determination of left ventricular volume and mass inpatients with abnormal ventricles: comparison with magneticresonance imaging. J Am Soc Echocardiogr 1997;10:853e61.58. Shiota T, Jones M, Chikada M, Fleishman CE,Castellucci JB, Cotter B, et al. Real-time three-dimensionalechocardiography for determining right ventricularstroke volume in an animal model of chronic right ventricularvolume overload. Circulation 1998;97:1897e900.59. Mor-Avi V, Sugeng L, Weinert L, MacEneaney P, Caiani EG,Koch R, et al. Fast measurement of left ventricular masswith real-time three-dimensional echocardiography: comparisonwith magnetic resonance imaging. Circulation2004;110:1814e8.60. Jiang L, Siu SC, Handschumacher MD, Luis GJ, Vazquez dePrada JA, King ME, et al. Three-dimensional echocardiography.In vivo validation for right ventricular volume andfunction. Circulation 1994;89:2342e50.61. Jiang L, Vazquez de Prada JA, Handschumacher MD,Guererro JL, Vlahakes GJ, King ME, et al. Three-dimensionalechocardiography: in vivo validation for right ventricularfree wall mass as an index of hypertrophy. J AmColl Cardiol 1994;23:1715e22.62. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S,Laskey WK, et al. Standardized myocardial segmentationand nomenclature for tomographic imaging of the heart:a statement for healthcare professionals from the CardiacImaging Committee of the Council on Clinical Cardiology ofthe American Heart Association. Circulation 2002;105:

539e42.63. Edwards WD, Tajik AJ, Seward JB. Standardized nomenclatureand anatomic basis for regional tomographic analysisof the heart. Mayo Clin Proc 1981;56:479e97.64. Heger JJ, Weyman AE, Wann LS, Dillon JC, Feigenbaum H.Cross-sectional echocardiography in acute myocardialinfarction: detection and localization of regional leftventricular asynergy. Circulation 1979;60:531e8.65. Kerber RE, Abboud FM. Echocardiographic detection ofregional myocardial infarction: an experimental study.Circulation 1973;47:997e1005.66. Weiss JL, Bulkley BH, Hutchins GM, Mason SJ. Two-dimensionalechocardiographic recognition of myocardial injuryin man: comparison with postmortem studies. Circulation1981;63:401e8.67. Ross Jr J. Myocardial perfusion-contraction matching.Implications for coronary heart disease and hibernation.Circulation 1991;83:1076e83.68. Lieberman AN, Weiss JL, Jugdutt BI, Becker LC,Bulkley BH, Garrison JG, et al. Two-dimensional echocardiographyand infarct size: relationship of regional wallmotion and thickening to the extent of myocardial infarctionin the dog. Circulation 1981;63:739e46.69. Fagard R, Aubert A, Lysens R, Staessen J, Vanhees L,Amery A. Noninvasive assessment of seasonal variationsin cardiac structure and function in cyclists. Circulation1983;67:896e901.70. Fisher AG, Adams TD, Yanowitz FG, Ridges JD, Orsmond G,Nelson AG. Noninvasive evaluation of world class athletesengaged in different modes of training. Am J Cardiol 1989;63:337e41.71. Vos M, Hauser AM, Dressendorfer RH, Hashimoto T,Dudlets P, Gordon S, et al. Enlargement of the right heartin the endurance athlete: a two-dimensional echocardiographicstudy. Int J Sports Med 1985;6:271e5.72. Douglas PS, O’Toole ML, Hiller WD, Reichek N. Left ventricularstructure and function by echocardiography in ultraenduranceathletes. Am J Cardiol 1986;58:805e9.73. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P.The upper limit of physiologic cardiac hypertrophy in highlytrained elite athletes. N Engl J Med 1991;324:295e301.74. Neri Serneri GG, Boddi M, Modesti PA, Cecioni I, Coppo M,Padeletti L, et al. Increased cardiac sympathetic activityand insulin-like growth factor-I formation are associatedwith physiological hypertrophy in athletes. Circ Res 2001;89:977e82.75. Matsukubo H, Matsuura T, Endo N, Asayama J, Watanabe T.Echocardiographic measurement of right ventricular wallthickness. A new application of subxiphoid echocardiography.Circulation 1977;56:278e84.76. Foale R, Nihoyannopoulos P, McKenna W, Kleinebenne A,Nadazdin A, Rowland E, et al. Echocardiographic measurementof the normal adult right ventricle. Br Heart J 1986;56:33e44.77. Roman MJ, Ganau A, Saba PS, Pini R, Pickering TG,Devereux RB. Impact of arterial stiffening on left ventricularstructure. Hypertension 2000;36:489e94.78. Picard MH, Wilkins GT, Ray PA, Weyman AE. Natural historyof left ventricular size and function after acute myocardialinfarction. Assessment and prediction by echocardiographicendocardial surface mapping. Circulation 1990;82:484e94.79. St John Sutton M, Pfeffer MA, Moye L, Plappert T,Rouleau JL, Lamas G, et al. Cardiovascular death andleft ventricular remodeling two years after myocardial infarction:baseline predictors and impact of long-term useof captopril: information from the Survival and VentricularEnlargement (SAVE) trial. Circulation 1997;96:3294e9.80. Weyman A. Practices and principles of echocardiography.2nd ed. Philadelphia (PA): Lippincott Williams and Wilkins;1994.81. Zornoff LA, Skali H, Pfeffer MA, St John SM, Rouleau JL,Lamas GA, et al. Right ventricular dysfunction and risk ofheart failure and mortality after myocardial infarction.J Am Coll Cardiol 2002;39:1450e5.

82. Yoerger DM, Marcus F, Sherrill D, Calkins H, Towbin JA,Zareba W, et al. Echocardiographic findings in patientsmeeting task force criteria for arrhythmogenic right ventriculardysplasia: new insights from the multidisciplinarystudy of right ventricular dysplasia. J Am Coll Cardiol2005;45:860e5.83. Schenk P, Globits S, Koller J, Brunner C, Artemiou O,Klepetko W, et al. Accuracy of echocardiographic rightventricular parameters in patients with different endstagelung diseases prior to lung transplantation. J HeartLung Transplant 2000;19:145e54.84. Samad BA, Alam M, Jensen-Urstad K. Prognostic impact ofright ventricular involvement as assessed by tricuspid annularmotion in patients with acute myocardial infarction.Am J Cardiol 2002;90:778e81.85. Maslow AD, Regan MM, Panzica P, Heindel S, Mashikian J,Comunale ME. Precardiopulmonary bypass right ventricularfunction is associated with poor outcome after coronaryartery bypass grafting in patients with severe leftventricular systolic dysfunction. Anesth Analg 2002;95:1507e18. table.86. Severino S, Caso P, Cicala S, Galderisi M, De Simone L,D’Andrea A, et al. Involvement of right ventricle in leftventricular hypertrophic cardiomyopathy: analysis bypulsed Doppler tissue imaging. Eur J Echocardiogr 2000;1:281e8.87. Spencer KT, Mor-Avi V, Gorcsan III J, DeMaria AN,Kimball TR, Monaghan MJ, et al. Effects of aging on leftatrial reservoir, conduit, and booster pump function:a multi-institution acoustic quantification study. Heart2001;85:272e7.88. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Leftatrial volume as a morphophysiologic expression of leftventricular diastolic dysfunction and relation to cardiovascularrisk burden. Am J Cardiol 2002;90:1284e9.89. Tsang TS, Barnes ME, Gersh BJ, Takemoto Y, Rosales AG,Bailey KR, et al. Prediction of risk for first age-relatedcardiovascular events in an elderly population: the incrementalvalue of echocardiography. J Am Coll Cardiol2003;42:1199e205.90. Kizer JR, Bella JN, Palmieri V, et al. Left atrial diameter asan independent predictor of first clinical cardiovascularevents in middle-aged and elderly adults: the strong heartstudy. Am Heart J 2006;151:412e8.91. Simek CL, Feldman MD, Haber HL, Wu CC, Jayaweera AR,Kaul S. Relationship between left ventricular wall thicknessand left atrial size: comparison with other measuresof diastolic function. J Am Soc Echocardiogr 1995;8:37e47.92. Appleton CP, Galloway JM, Gonzalez MS, Gaballa M,Basnight MA. Estimation of left ventricular filling pressuresusing two-dimensional and Doppler echocardiography inadult patients with cardiac disease. Additional value ofanalyzing left atrial size, left atrial ejection fraction andthe difference in duration of pulmonary venous and mitralflow velocity at atrial contraction. J Am Coll Cardiol 1993;22:1972e82.93. Benjamin EJ, D’Agostino RB, Belanger AJ, Wolf PA, Levy D.Left atrial size and the risk of stroke and death. TheFramingham Heart Study. Circulation 1995;92:835e41.94. Bolca O, Akdemir O, Eren M, Dagdeviren B, Yildirim A,Tezel T. Left atrial maximum volume is a recurrence predictorin lone atrial fibrillation: an acoustic quantificationstudy. Jpn Heart J 2002;43:241e8.95. Di Tullio MR, Sacco RL, Sciacca RR, Homma S. Left atrialsize and the risk of ischemic stroke in an ethnically mixedpopulation. Stroke 1999;30:2019e24.96. Flaker GC, Fletcher KA, Rothbart RM, Halperin JL, Hart RG.Clinical and echocardiographic features of intermittentatrial fibrillation that predict recurrent atrial fibrillation.Stroke Prevention in Atrial Fibrillation (SPAF) Investigators.Am J Cardiol 1995;76:355e8.97. Tsang TS, Barnes ME, Bailey KR, Leibson CL, Montgomery SC,Takemoto Y, et al. Left atrial volume: important risk markerof incident atrial fibrillation in 1655 older men and women.

Mayo Clin Proc 2001;76:467e75.98. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographicpredictors of nonrheumatic atrial fibrillation. TheFramingham Heart Study. Circulation 1994;89:724e30.99. Barnes ME, Miyasaka Y, Seward JB, Gersh BJ, Rosales AG,Bailey KR, et al. Left atrial volume in the prediction of firstischemic stroke in an elderly cohort without atrial fibrillation.Mayo Clin Proc 2004;79:1008e14.100. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Risksfor atrial fibrillation and congestive heart failure in patients>/¼65 years of age with abnormal left ventriculardiastolic relaxation. Am J Cardiol 2004;93:54e8.101. Tsang TS, Gersh BJ, Appleton CP, Tajik AJ, Barnes ME,Bailey KR, et al. Left ventricular diastolic dysfunction asa predictor of the first diagnosed nonvalvular atrial fibrillationin 840 elderly men and women. J Am Coll Cardiol2002;40:1636e44.102. Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS,Wright RS, et al. Left atrial volume: a powerful predictorof survival after acute myocardial infarction. Circulation2003;107:2207e12.103. Beinart R, Boyko V, Schwammenthal E, Kuperstein R,Sagie A, Hod H, et al. Long-term prognostic significanceof left atrial volume in acute myocardial infarction. J AmColl Cardiol 2004;44:327e34.104. Modena MG, Muia N, Sgura FA, Molinari R, Castella A,Rossi R. Left atrial size is the major predictor of cardiacdeath and overall clinical outcome in patients with dilatedcardiomyopathy: a long-term follow-up study. Clin Cardiol1997;20:553e60.105. Quinones MA, Greenberg BH, Kopelen HA, Koilpillai C,Limacher MC, Shindler DM, et al. Echocardiographic predictorsof clinical outcome in patients with left ventriculardysfunction enrolled in the SOLVD registry and trials:significance of left ventricular hypertrophy. Studies ofLeft Ventricular Dysfunction. J Am Coll Cardiol 2000;35:1237e44.106. Rossi A, Cicoira M, Zanolla L, Sandrini R, Golia G, Zardini P,et al. Determinants and prognostic value of left atrialvolume in patients with dilated cardiomyopathy. J AmColl Cardiol 1425;2002:40.107. Dini FL, Cortigiani L, Baldini U, Boni A, Nuti R, Barsotti L,et al. Prognostic value of left atrial enlargement in patientswith idiopathic dilated cardiomyopathy and ischemiccardiomyopathy. Am J Cardiol 2002;89:518e23.108. Sabharwal N, Cemin R, Rajan K, Hickman M, Lahiri A,Senior R. Usefulness of left atrial volume as a predictorof mortality in patients with ischemic cardiomyopathy.Am J Cardiol 2004;94:760e3.109. Schabelman S, Schiller NB, Silverman NH, Ports TA. Leftatrial volume estimation by two-dimensional echocardiography.Catheterization Cardiovasc Diagn 1981;7:165e78.110. Wade MR, Chandraratna PA, Reid CL, Lin SL,Rahimtoola SH. Accuracy of nondirected and directedM-mode echocardiography as an estimate of left atrialsize. Am J Cardiol 1987;60:1208e11.111. Lester SJ, Ryan EW, Schiller NB, Foster E. Best method inclinical practice and in research studies to determineleft atrial size. Am J Cardiol 1999;84:829e32.112. Loperfido F, Pennestri F, Digaetano A, Scabbia E,Santarelli P, Mongiardo R, et al. Assessment of left atrialdimensions by cross sectional echocardiography in patientswith mitral valve disease. Br Heart J 1983;50:570e8.113. Pritchett AM, Jacobsen SJ, Mahoney DW, Rodeheffer RJ,Bailey KR, Redfield MM. Left atrial volume as an indexof left atrial size: a population-based study. J Am CollCardiol 2003;41:1036e43.114. Kircher B, Abbott JA, Pau S, Gould RG, Himelman RB,Higgins CB, et al. Left atrial volume determination bybiplane two-dimensional echocardiography: validation bycine computed tomography. Am Heart J 1991;121:864e71.115. Rodevan O, Bjornerheim R, Ljosland M, Maehle J,Smith HJ, Ihlen H. Left atrial volumes assessed by threeandtwo-dimensional echocardiography compared to MRIestimates. Int J Cardiovasc Imaging 1999;15:397e410.

116. Vandenberg BF, Weiss RM, Kinzey J, Acker M, Stark CA,Stanford W, et al. Comparison of left atrial volume bytwo-dimensional echocardiography and cine-computedtomography. Am J Cardiol 1995;75:754e7.117. Khankirawatana B, Khankirawatana S, Porter T. Howshould left atrial size be reported? Comparative assessmentwith use of multiple echocardiographic methods.Am Heart J 2004;147:369e74.118. Hiraishi S, DiSessa TG, Jarmakani JM, Nakanishi T, Isabel-Jones J, Friedman WF. Two-dimensional echocardiographicassessment of left atrial size in children. Am JCardiol 1983;52:1249e57.119. Jessurun ER, van Hemel NM, Kelder JC, Defauw JA,Brutel DLR, Ernst JM, et al. The effect of maze operationson atrial volume. Ann Thorac Surg 2003;75:51e6.120. Wang Y, Gutman JM, Heilbron D, Wahr D, Schiller NB. Atrialvolume in a normal adult population by two-dimensionalechocardiography. Chest 1984;86:595e601.121. Keller AM, Gopal AS, King DL. Left and right atrial volumeby freehand three-dimensional echocardiography: in vivovalidation using magnetic resonance imaging. Eur J Echocardiogr2000;1:55e65.122. Khankirawatana B, Khankirawatana S, Lof J, Porter TR.Left atrial volume determination by three-dimensionalechocardiography reconstruction: validation and applicationof a simplified technique. J Am Soc Echocardiogr2002;15:1051e6.123. Poutanen T, Ikonen A, Vainio P, Jokinen E, Tikanoja T. Leftatrial volume assessed by transthoracic three dimensionalechocardiography and magnetic resonance imaging: dynamicchanges during the heart cycle in children. Heart2000;83:537e42.124. Knutsen KM, Stugaard M, Michelsen S, Otterstad JE.M-mode echocardiographic findings in apparently healthy,non-athletic Norwegians aged 20e70 years. Influence ofage, sex and body surface area. J Intern Med 1989;225:111e5.125. Pearlman JD, Triulzi MO, King ME, Abascal VM, Newell J,Weyman AE. Left atrial dimensions in growth anddevelopment: normal limits for two-dimensional echocardiography.J Am Coll Cardiol 1990;16:1168e74.126. Gutman J, Wang YS, Wahr D, Schiller NB. Normal left atrialfunction determined by 2-dimensional echocardiography.Am J Cardiol 1983;51:336e40.127. Thomas L, Levett K, Boyd A, Leung DY, Schiller NB,Ross DL. Compensatory changes in atrial volumes withnormal aging: is atrial enlargement inevitable? J Am CollCardiol 2002;40:1630e5.128. Losi MA, Betocchi S, Aversa M, Lombardi R, Miranda M,D’Alessandro G, et al. Determinants of atrial fibrillationdevelopment in patients with hypertrophic cardiomyopathy.Am J Cardiol 2004;94:895e900.129. Schnittger I, Gordon EP, Fitzgerald PJ, Popp RL. Standardizedintracardiac measurements of two-dimensional echocardiography.J Am Coll Cardiol 1983;2:934e8.130. DePace NL, Ren JF, Kotler MN, Mintz GS, Kimbiris D,Kalman P. Two-dimensional echocardiographic determinationof right atrial emptying volume: a noninvasive index inquantifying the degree of tricuspid regurgitation. Am JCardiol 1983;52:525e9.131. Kaplan JD, Evans Jr GT, Foster E, Lim D, Schiller NB.Evaluation of electrocardiographic criteria for right atrialenlargement by quantitative two-dimensional echocardiography.J Am Coll Cardiol 1994;23:747e52.132. Roman MJ, Devereux RB, Kramer-Fox R, O’Loughlin J.Two-dimensional echocardiographic aortic root dimensionsin normal children and adults. Am J Cardiol 1989;64:507e12.133. Roman MJ, Devereux RB, Niles NW, Hochreiter C,Kligfield P, Sato N, et al. Aortic root dilatation as a causeof isolated, severe aortic regurgitation. Prevalence, clinicaland echocardiographic patterns, and relation to leftventricular hypertrophy and function. Ann Intern Med1987;106:800e7.

134. Morrison D, Devereux R, Roman MJ. Association of aortic root dilation with aortic dissection: a case-control study.J Am Coll Cardiol 2003:41. Ref Type: Abstract.135. Kim M, Roman MJ, Cavallini MC, Schwartz JE, Pickering TG,Devereux RB. Effect of hypertension on aortic root sizeand prevalence of aortic regurgitation. Hypertension1996;28:47e52.136. Moreno FL, Hagan AD, Holmen JR, Pryor TA, Strickland RD,Castle CH. Evaluation of size and dynamics of the inferiorvena cava as an index of right-sided cardiac function. Am JCardiol 1984;53:579e85.137. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimationof right atrial pressure from the inspiratory collapse ofthe inferior vena cava. Am J Cardiol 1990;66:493e6.138. Goldhammer E, Mesnick N, Abinader EG, Sagiv M. Dilatedinferior vena cava: a common echocardiographic findingin highly trained elite athletes. J Am Soc Echocardiogr1999;12:988e93.139. Jue J, Chung W, Schiller NB. Does inferior vena cava sizepredict right atrial pressures in patients receiving mechanicalventilation? J Am Soc Echocardiogr 1992;5:613e9.140. Bendjelid K, Romand JA, Walder B, Suter PM, Fournier G.Correlation between measured inferior vena cava diameterand right atrial pressure depends on the echocardiographicmethod used in patients who aremechanically ventilated. J Am Soc Echocardiogr 2002;15:944e9.