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Transesophageal Echocardiographic Assessment of Left Ventricular Mass

Weiner, Menachem M. MD; Kahn, Ronald A. MD; Evans, Adam S. MD

doi: 10.1213/ANE.0000000000000778
Cardiovascular Anesthesiology: Echo Didactics
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From the Department of Anesthesiology, Icahn School of Medicine at Mount Sinai, New York, New York.

Accepted for publication March 12, 2015.

Funding: None.

The authors declare no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website.

Reprints will not be available from the authors.

Address correspondence to Menachem M. Weiner, MD, Department of Anesthesiology, The Mount Sinai Medical Center, One Gustave L. Levy Pl., Box 1010, New York, NY 10029. Address e-mail to menachem.weiner@mountsinai.org.

A 65-year-old man with severe mitral regurgitation attributable to bileaflet prolapse is scheduled to undergo mitral valve repair. On his preoperative transesophageal echocardiography, a left ventricular mass of 156 g/m2 is noted.

Left ventricular geometry can be classified into 4 distinct patterns based on wall thickness, cavity size, and mass: normal, concentric hypertrophy, eccentric hypertrophy, and concentric remodeling (Fig. 1).1 Concentric hypertrophy results from pressure overload states such as aortic stenosis and hypertension and results in an increase in wall thickness and muscle mass of the left ventricular (LV) without comparative dilation of the LV chamber. Eccentric hypertrophy results from volume overload states such as aortic or mitral regurgitation and leads to an increase in muscle mass with comparative dilation of the LV chamber. Thus, both pressure and volume overload states can result in increased LV mass (LVM). The differentiation of patients with increased LVM into concentric versus eccentric hypertrophy requires calculation of relative wall thickness (see formula subsequently and Table 1). Concentric remodeling refers to a state of increased wall thickness without an increase in overall muscle mass and is generally a precursor to concentric hypertrophy. These entities are distinct from the asymmetric hypertrophy found in disorders such as hypertrophic obstructive cardiomyopathy in which only the septal portion of the LV becomes hypertrophic.

Figure 1

Figure 1

Table 1

Table 1

LVM equals the product of LV wall volume and the density of the myocardium (1.04 g/mL). LV myocardial wall volume is assessed by subtracting intracavitary LV volume (what is enclosed by the endocardium) from the volume enclosed by the epicardium.2 Relative wall thickness is a parameter based on wall thickness and cavity size at end-diastole. It is calculated with the following formula3:

A relative wall thickness >0.42 is considered elevated. A patient with normal LVM but increased relative wall thickness would be categorized as having concentric remodeling.

Although most echocardiographers are familiar with the implications of LV hypertrophy, particularly concentric hypertrophy, many are still unaware of the importance of LVM. Whether a patient has increased LVM has been shown in multiple studies to be superior to any particular pattern of LV geometry in prediction of cardiac morbidity and mortality and overcomes the limitations of a 1-dimensional wall thickness measurement.4,5 Although cardiac magnetic resonance imaging is the reference standard for the measurement of LVM, because it does not require geometric assumptions about the LV or dependency on adequate acoustic windows, echocardiography has long been at the forefront in the determination LVM as a result of its low cost and easier availability.2 It has been shown to be reproducible, to have good correlation with cardiac magnetic resonance imaging, and, most importantly, to have good cardiovascular event prediction ability.6

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SIGNIFICANCE OF LVM AS A PREDICTOR OF OUTCOMES AND IMPLICATIONS FOR CARDIAC SURGERY

According to the law of Laplace, LV wall stress = (LV radius × pressure)/(2 × LV wall thickness). Thus, in patients with ventricular pressure or volume overload, LVM increases as the result of an adaptive mechanism to help limit systolic wall stress. The increase in wall thickness preserves left ventricular ejection fraction.7 Although this is initially compensatory, epidemiological studies have long recognized that increased LVM itself is actually a form of “target-organ damage”2 that contributes to the eventual development of cardiovascular disease and subsequent cardiovascular morbidity and mortality independent of conventional risk factors such as hypertension and diabetes.8 Increased LVM has also been associated with diastolic dysfunction9 with concentric hypertrophy showing the greatest impairment whereby the ratio of early diastolic transmitral flow to transmitral flow occurring with atrial contraction is decreased.10 At what point this transition from an adaptive to a maladaptive response occurs remains elusive.2 Furthermore, pathological increases in LVM need to be differentiated from benign increases as may be associated with physical training. The “Athlete’s heart,” as it is now known, is a physiological adaptive increase in both LV chamber size and wall thickness, most pronounced in endurance-trained athletes, which often meets the echocardiographic criteria for eccentric hypertrophy. However, it can be differentiated from pathological forms in that it does not cause diastolic dysfunction and is reversible with short periods of training cessation.11 Despite the importance given to LVM in epidemiological studies, its use is restricted in daily clinical practice and its role has not been firmly established.2

Perioperative implications of increased LVM in all types of cardiac surgery have recently been reported.12–14 Increased LVM leads to a reduction in coronary flow reserve. This, coupled with the increase in myocardial oxygen consumption, can affect myocardial preservation during cardiac surgery. Such patients require special attention to perioperative management, especially optimization of cardioprotection and both intracardiac and intravascular volume status as a result of altered pressure/volume relationships. Increased LVM is a risk factor for greater in-hospital mortality and morbidity, including arrhythmias, respiratory failure, and congestive heart failure after cardiac surgery.13,14

Preoperative categorization of LVM as mild, moderate, or severe has been shown to provide prognostic information independent of other predictors.14,15 In a study at our institution, we found LVM to be a strong independent predictor of perioperative mortality and of clinically significant postoperative atrial and ventricular arrhythmias after adult cardiac surgery. Furthermore, earlier timing of cardiac surgery for both symptomatic and asymptomatic patients with elevated LVM leads to greater regression of the increased LVM and improved recovery of LV function.16 Thus, the incorporation of LVM into the guidelines for the timing of aortic valve replacement and mitral valve repair has been advocated.12,16

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TRANSESOPHAGEAL ECHOCARDIOGRAPHY ASSESSMENT OF LVM

American Society of Echocardiography(ASE) guidelines3 recommend the estimation of LVM based on the geometric assumption of the LV as the shape of an American football (a prolate ellipsoid of revolution, a 3-dimensional [3-D] figure formed by revolving an ellipse around its major axis resulting in its polar axis being twice than the equatorial diameter [i.e., major:minor axis ratio of 2:1]) and uses linear measurements of the LV short-axis dimensions.2 This can be accomplished using either 2-dimensional or M-mode measurements. The ASE-recommended linear formula3 uses inferolateral (InferoLateral Wall Thickness at end-diastole [ILWTd]) and anteroseptal wall (AnteroSeptal Wall Thickness at end-diastole [ASWTd]) thicknesses and LV internal diameter (Left Ventricular Internal Diameter at end-diastole [LVIDd]) at end-diastole (all measured in centimeters):

The calculations necessary for determination of LVM are incorporated into many echocardiographic software systems. The formula can also be programmed into a spreadsheet for easy use in the operating room. This formula requires precise identification of the interfaces because even small errors are magnified when cubed in the formula. Although the ASE convention has in the past been used to measure the distance between the leading edges of the structures, refinements in image processing, particularly the use of harmonic imaging, now allow improved image resolution for measurement of the actual visualized thicknesses and to measure chamber dimensions from endocardium to endocardium.3 Care must be taken to exclude trabeculations and spaces to measure from the actual endocardial border. Although endocardial border definition is rarely an issue with the use of transesophageal echocardiography (TEE), the use of contrast agents may aid in cases of obese patients or those with subdiaphagmatic air, in which the images may be suboptimal. M-mode measurements are limited by the beam orientation being frequently off-axis, and thus 2-dimensional echocardiographic images are more precise and this has become the standard mode of calculation. The ASE recommends measuring ILWTd and ASWTd from the standard transgastric midpapillary short-axis view (Fig. 2A).3 LVIDd is best measured from either the standard midesophageal 2-chamber view (Fig. 2B) or the standard transgastric 2-chamber view (Fig. 2C), depending on which image is of higher quality.3 It is measured at the junction of the basal and middle thirds of the LV (just above the tips of the papillary muscles) on a line perpendicular to the long axis of the ventricle. When unable to obtain these views in a way that adequately shows the true major and minor axes of the LV, LVIDd can be measured from the transgastric midpapillary short-axis view measuring from endocardium to endocardium (Fig. 2A). Reference values as recommended by ASE are provided in Table 2. However, it must be noted that LVM values obtained using TEE are greater by an average of 6 g/m2 as a result of minor differences found in inferolateral wall thickness on TEE.17 The calculation of LVM in cases of both eccentric hypertrophy and concentric hypertrophy are shown in Video 1 (Supplemental Digital Content, http://links.lww.com/AA/B127 and Fig. 3, which is a copy of the freeze frames from the video).

Table 2

Table 2

Figure 2

Figure 2

Figure 3

Figure 3

Although the linear method described previously is the one currently recommended by the ASE, other 2-dimensional echocardiographic methods have been used. Both the area-length formula and the truncated ellipsoid model use myocardial area measurements at the midpapilary muscle level rather than linear measurements.3 These measurements are more cumbersome than the linear measurements, and there is a lack of long-term follow-up information using them, because nearly all studies have used the linear method.2

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DIFFERENT METHODS FOR INDEXING LVM

Although there is strong agreement that LVM needs to be indexed to take into account physiological variations related to body size, controversy exists as to the best method.18 Indexing to body surface area was the initial and most widely used method, but it appears to underestimate the prevalence of increased LVM in overweight patients.19 Current promising methods of indexing involve dividing LVM by height raised to the power of 1.7 or 2.7.18,20 The exponent is necessary to attempt to approximate lean body mass.2 The final determination of which method is best will require further outcome studies comparing the methods in diverse populations.21

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FUTURE ECHOCARDIOGRAPHIC DIRECTIONS

Three-dimensional echocardiographic assessment of LVM has the potential to be more accurate and reduce intra- and interobserver variability by eliminating the need for geometric assumptions and modeling.22,23 Using 3-D echocardiography, myocardial volume is determined by placing points at specific anatomic sites including the mitral annulus and apex. The computer software uses them to create surface models through automated endocardial and epicardial border detection that may then be adjusted manually if necessary.23 This will be especially helpful in patients with asymmetric LV shape. Tracing errors remain an unresolved issue. The papillary muscles are not included in LV myocardial volume. Although 3-D transthoracic echocardiography quantification of LVM has been shown to be accurate and reproducible, TEE is rarely able to obtain adequate images that include the entire LV apex and the full thickness of its walls including the epicardium on which to perform 3-D LVM assessment. Furthermore, no validation studies using TEE-derived 3-D measurements of LVM have been performed, and it remains a research tool at this point.

In conclusion, calculation of LVM can be easily performed in the operating room and provides significant prognostic value as it relates to postoperative outcomes.

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TEACHING POINTS

  • Increased LVM is found in both concentric and eccentric hypertrophy geometrical patterns of the left ventricle and has been linked to prognosis.
  • LVM (g) can be readily calculated by the equation LVM = 0.8 × (1.04 [{LVIDd + ILWTd + ASWTd}3 − {LVIDd}3]) + 0.6. The formula can be programmed into a spreadsheet for easy use in the operating room. The normal range is 88–224 g for a man and 67–162 g for a woman. There is strong agreement that it is necessary to index LVM to body size. Several methods have been proposed.
  • Relative wall thickness has value but only if considered alongside LVM. It can be calculated using the formula: (2 × ILWTd)/LVIDd and allows categorization of patients with increased LVM into concentric versus eccentric hypertrophy. A relative wall thickness >0.42 is considered increased and is found in either normal LVM (concentric remodeling) or concentric LV hypertrophy.
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DISCLOSURES

Name: Menachem M. Weiner, MD.

Contribution: This author helped design the study, conduct the study, analyze the data, and prepare the manuscript.

Attestation: Menachem M. Weiner approved the final manuscript.

Name: Ronald A. Kahn, MD

Contribution: This author helped conduct the study, analyze the data, and prepare the manuscript.

Attestation: Ronald A. Kahn approved the final manuscript.

Name: Adam S. Evans, MD

Contribution: This author helped conduct the study, analyze the data, and prepare the manuscript.

Attestation: Adam S. Evans approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.

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