Written by Judith Buckland, RDCS, FASE, MBA and Andrea Fields, MHA, RDCS

Should LV Mass be indexed with Height or BSA?

We recently posted a 2-part blog series on how to calculate LV Mass (LVM) and one of our readers provided some great feedback regarding the impact of height on LVM.  We thought this reader’s comment was worth sharing and answering.

Reader:  Using body surface area to normalize LVM will misclassify obese hypertensive patients and artificially increase the proportion of concentric LV remodeling. As also recommended by EACVI/ASE (Marwick TH et al. J Am Soc Echocardiogr 2015;28:727-54.), using height raised to validated powers (called allometric signals) might be much more appropriate to identify obesity-associated LVH. The most used allometric exponent is 2.7. Normalization of LVM for height in meters raised to the power of 2.7 near doubles the population attributable risk of LVH.

Thank you for sharing this information with our readers.  We also found that article useful in explaining how height factors into LVM.  The article explains how LVM and volumes bear an approximately quadratic relationship with height in men rather than approximately cubic relationship with height in women.  The paper went on to explain the effects of gender on LVM which indicates that after adjustment for blood pressure and anthropometric parameters, LV volume and LVM are higher in men than in women.  These differences persist when values of LVM are corrected for fat-free mass.  This sex difference may explain the surprising lack of consensus in appropriate indexation of LVM, as it impacts the optimal method for indexing LVM for body height.

LVM calculated by the Devereux formula in men and women by height

The graph displays LVM, calculated by the Devereux formula (unidimensional 2D measurements) in healthy patients.

  • The red line represents the body height–LVM relationship in men.
  • The blue line represents the body height–LVM relationship in women.
  • The black line represents the exaggeration of nonlinearity in the height–LVM relationship when the confounding effect of sex is neglected.
  • Using the allometric index 1.7, the body height– LVM relationship in men (red) and women (blue) is parallel and indexation for body height is optimally achieved by height (ht) 1.7 in both sexes.
  • However, when an allometric exponent is computed for males and females considered together (thick black line) without adjustment for gender, there is an exaggeration of nonlinearity in the height–LVM relationship (allometric index 2.7).
  • This has important clinical and epidemiological implications, resulting in marked overestimation of the prevalence of LV hypertrophy in short subjects and a marked underestimation in tall subjects. The appropriate indexation remains an issue of contention.

ASE Comments

In the ASE 2015 Chamber Quantification Guidelines they acknowledged that whether to use height, weight, or BSA as the indexing term remains controversial.

  • Studies suggest that indexing to height raised to allometric powers such as 1.7, 2.13, and 2.7 has advantages over indexing to BSA, especially when attempting to predict events in obese patients.
  • However most large population studies reporting LV mass have indexed to BSA.
  • Calculation of relative wall thickness (RWT) with the formula (2 x PWd)/(LVIDd) permits categorization of an increase in LV mass as either:
    • Concentric hypertrophy (RWT > 0.42)
    • Eccentric hypertrophy (RWT < 0.42)
    • Identification of concentric remodeling (normal LV mass with increased RWT)


ASE Recommendations

The final recommendations from the ASE for LVM states that in normally shaped left ventricle, both M-mode and 2D echocardiographic formulas to calculate LV mass can be used. Normal values for these techniques should be reported indexed to BSA.

  • Reference upper limits of normal LV mass by linear measurements are 95 g/m2 in women and 115 g/m2 in men.
  • Reference upper limits of normal LV mass by 2D measurements are 88 g/m2 in women and 102 g/m2 in men with 2D methods.
  • Because 3DE is the only echocardiographic technique that measures myocardial volume directly, without geometric assumptions regarding LV shape and distribution of wall thickening, this technique is promising and may be used in abnormally shaped ventricles or in patients with asymmetric or localized hypertrophy.
  • Limited upper normal limits of 3D echocardiographic LV mass data are currently available in the literature but are insufficient to substantiate recommendations for reference values


Be aware that there is a relationship of height that is not corrected by indexing by BSA which may result in the overestimation of the prevalence of LV hypertrophy in short subjects and a marked underestimation in tall subjects.  ASE recognizes that indexing to height raised to allometric powers such as 1.7, 2.13, and 2.7 has advantages over indexing to BSA, especially when attempting to predict events in obese patients, however most large population studies reporting LV mass have indexed to BSA.  ASE current recommendations, due to the large database of LVM reporting, currently is to index to BSA.

We love it when our readers provide feedback and education for our readers, so please keep your comments coming!


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  • Marwick, T. H., PhD, Gillebert, T. C., MD, & G. A., MD. (2015). Recommendations on the Use of Echocardiography in Adult Hypertension. JASE,28(7), 1-12. Retrieved March 1, 2017, from http://asecho.org/wordpress/wp-content/uploads/2015/07/2015_Hypertension.pdf
  • Lang, R. M., MD, Badano, L. P., MD, & Mor-Avi, V., PhD. (2015). Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. JASE, 28(1), 1-53. Retrieved March 1, 2017, from http://asecho.org/wordpress/wp-content/uploads/2015/01/ChamberQuantification2015.pdf


left ventricular hypertrophyLVH

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Giovanni de Simone
The definition of the best way to approach the non-ratiometric relation between height (a linear measure) and LVM (a cubic measure) needs further clarifications. There is no doubt that between our approach and the one proposed form pooling Asklepios and MESA study there are two critical differences: one is the age-span and the other is the sex question. When adopting the 1.7 approach in the Strong Heart Study, a cohort with very high prevalence of obesity, hazard and population attributable risk fell to non-significant values (Hypertension. 2011;57:e9-e10). It is clear from our and others' studies that the relation between height and organ size changes in relations to the period of life we consider. Thus, using a single allometric signal for the entire age-span (i.e. 2.7) might at least partially resolve this problem. The other issue is sex. There is no reason to figure out that organ size of males and females have different relations with fat-free mass (of which height is a surrogate). Also in humans we have evidence that the number of cardiomyocytes is not different in girls and boys at the birth, and that sex-specific amount of physiological LVH occurs at the puberty, largely due to differentiation of hormonal pattern and, as a consequence, of body composition (an issue that can largely explain the reported figure (however, in addition, I might show a figure from J Hypertens 2011;29:1431–1438 that visually explains the sex-specific body composition). Our conclusion is that females have more “hypertrophic reserve” than males and, therefore, they require more time to reach harmful levels of LVM (possibly this is one of the reason of their longer life expectation). If this postulate holds true, there is no need to consider separately men and women, despite the consolidated tradition. In addition to the very broad evidence supporting the use of the 2.7 allometric signal, more recently a new cohort study, the European Project On Genes in Hypertension (EPOGH), independent of the groups proposing these different approaches, demonstrated the better ability of this signal to identify CV risk (J Hypertens. 2016 Jun;34(6):1186-94. doi: 10.1097/HJH.0000000000000922). As said in a recent editorial comment in JASE, we are far from the identification of the perfect way to approach this critical marker of risk, but we are all proceeding in the right direction. We need to pay a lot of attention to avoid confusion and, at least in the future, the inconsistency on this issue that can be noted in the two recommendations published in 2015 (Lang and Marwick), which in part reflect this confusion. Anyway, whoever is interested in this topic is invited to come to my talk in Anhaiem at the next AHA scentific sessions.
Thank you so much for your insight. For anyone who would like to hear more on this topic:American Heart Association, Scientific Sessions November 11-15, 2017 Anaheim, California

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