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The importance of a shared definition of left ventricular hypertrophy: The case of obese women
IJCA-23894; No of Pages 3 International Journal of Cardiology xxx (2016) xxx–xxx
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
The importance of a shared definition of left ventricular hypertrophy: The case of obese women Luca Alessandro Gondoni ⁎, Anna Maria Titon, Mariella Montano, Ferruccio Nibbio, Gianandrea Bertone Unit of Cardiac Rehabilitation, Ospedale San Giuseppe, IRCCS Istituto Auxologico Italiano, Via Cadorna, 90, 28824, Piancavallo di Oggebbio, Verbania, Italy
a r t i c l e
i n f o
Article history: Received 12 January 2016 Received in revised form 28 September 2016 Accepted 5 November 2016 Available online xxxx Keywords: Obesity Left ventricular hypertrophy Echocardiography
a b s t r a c t Background: Left ventricular hypertrophy (LVH) is a risk factor for all-cause mortality. Left ventricular (LV) mass is usually indexed for normalizing the value to the patients phenotype and a correction by body surface area (BSA) is widely utilized being the only approved one according to the last echocardiography guidelines. However indexing LV mass by BSA may cause an underestimation of LVH prevalence in obese subjects and many authors have utilized in the obese subset of patients a correction by height2.7. The aim of our study was to quantify the number of obese patients who, despite having an increased LV mass, fall in the range of normality because they do not reach the LVH cutoff according to the new guidelines. Methods: We reviewed the echocardiograms of 384 white women free from cardiovascular disease. Ninety-six patients (25%) were obese: among them 42 had mild obesity and 54 had moderate or severe obesity. Results: In the obese group, the prevalence of LVH using the absolute LV mass value was similar to the one obtained with the height2.7 correction while a significant smaller number of patients had LVH according to BSA correction. Our study confirms that the method used for correcting LV mass significantly influences the diagnosis of LVH in a non-selected female population: using body surface area underestimates the prevalence of LVH as compared to allometric measures in the obese subset of patients. Conclusion: We recommend that height2.7 be used for LV mass correction in obese patients. © 2016 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Left ventricular hypertrophy (LVH) is a risk factor for sudden death and all-cause mortality in various categories of patients [1]. Echocardiography is the more widely used method for studying left ventricular (LV) mass: as a rule, a correction for body size should be made for normalizing the value of the mass to the patients' phenotype. Various methods may be utilized for that purpose: the most frequently adopted one is a correction by body surface area (BSA): however indexing LV mass by BSA may cause an underestimation of LVH prevalence in obese subjects who have, obviously, a greater BSA as compared to normal weight subjects. To avoid this pitfall many authors have utilized in the obese subset of patients an allometric correction, namely height2.7 [2,3], that correlates well with lean body mass, which is one of the main determinants of LV size and is less strictly related to BMI. Unfortunately the new guidelines on chamber quantification, endorsed by both the American and European Echocardiography Societies, forget to consider the possibility of using height for correction [4] thus seeming ⁎ Corresponding author. E-mail addresses: [email protected] (L. Alessandro Gondoni), [email protected] (A.M. Titon), [email protected] (M. Montano), [email protected] (F. Nibbio), [email protected] (G. Bertone).
inconsistent with the European Guidelines for the management of arterial hypertension [5] that suggest the possibility to use height correction in overweight and obese subjects “in order to scale LV mass to body size and avoid under-diagnosis of LVH”. Since obesity is not a marginal problem and affects a significant proportion of the western population [6], cardiologists have to ask themselves which one is the correct method for defining LVH. The aim of our study was to quantify the number of obese patients who, despite having an increased LV mass, fall in the range of normality because they do not reach the LVH cutoff according to the new guidelines. 2. Patients and methods We reviewed the studies of a group of patients who underwent an echocardiogram for various purposes. The study population consisted of 384 white women. None was affected with cardiovascular disease nor had left ventricular dysfunction. Two-dimensional echocardiographic parameters were obtained with a GE Vivid 7 instrument (GE Medical Systems, Milwaukee, Wisconsin USA). The examinations were conducted with the patient in the left lateral recumbent position during quiet respiration. Parasternal long axis was used for evaluating left ventricular (LV) dimension with a
http://dx.doi.org/10.1016/j.ijcard.2016.11.032 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032
2
L. Alessandro Gondoni et al. / International Journal of Cardiology xxx (2016) xxx–xxx
multifrequency sector transducer set on ideal frequency to obtain optimal imaging. For LV mas calculation we measured end-diastolic diameter (LVEDD), interventricular septum (IVSD) and posterior wall (LVPWD) thickness both at end-diastole (for each parameter an average of three measurements was used). Left ventricular mass was calculated by the Devereux formula [7], i.e. 0.8 × (1.04 × (left ventricular diameter + septum + posterior wall)3 × (left ventricular diameter)3 + 0.6).
Table 2 describes the values of LV mass in our patients according to the correction method.
LV mass absolute value
LV mass/BSA
LV mass/height2.7
2.1. Statistical analysis
Normal/overweight Obese Total Normal/overweight Obese Total Normal/overweight Obese Total
N
Mean ± SD
P
288 96 384 288 96 384 288 96 384
127 ± 28 169 ± 43 138 ± 37 76 ± 16 86 ± 19 79 ± 17 35 ± 8 47 ± 12 38 ± 11
b0.001
b0.001
b0.001
LV = left ventricular; BSA = Body surface area.
Continuous variables are expressed as mean ± standard deviation and categorical variables are expressed as number and percentage. We studied LV mass as absolute value and we corrected it both by BSA and by height2.7. The cut off values above which LVH was diagnosed were the following: for the absolute value of LV mass N 162 g; for LV mass/BSA N 95 g/m2; for LV mass/height2.7 N 44 g/m2.7. Statistical analysis has been performed with SPSS 23.0 package (SPSS Inc. Chicago IL, USA).
3. Results In the study population mean age was 46.5 ± 8.4 years, mean height 161.8 ± 5.9 cm, mean weight 70.2 ± 16.5 kg, and mean BMI 26.8 ± 6.2 kg/m2. Ninety patients (23%) were overweight, while 96 (25%) were obese: among them 42 had mild obesity and the remaining 54 had moderate or severe obesity. The results of mass calculation are shown in Tables 1, and 2. If we considered together the non-obese group (BMI b 30) and compared it to all obese subjects the results did not change: the prevalence of LVH using the absolute LV mass value was quite similar to the one obtained with the height correction (55 and 60% respectively) while only 28% of the obese had LVH according to BSA correction. On the contrary, no significant differences emerged when dealing with the non-obese group and the prevalence of LVH ranged from 10 to 11%, independent of the correction method. Put the other way around, we found that, in the non-obese group, the correction by BSA moved 4 patients from normal to LVH and 7 patients from LVH to normal while in the same group, when using the correction by height2.7 the changes were slightly greater and 10 patients were moved from normal to LVH and 9 moved from LVH to normal. Things changed when we looked at the obese group: using the BSA correction moved 26 patients (27.1%) from LVH to normal, while no patients moved from normal to LVH; using the height2.7 method 8 patients moved from normal to LVH while 3 moved from LVH to normal. As we already knew LV mass was directly and strongly related to BMI (P b 0.001; R = 0.599) (Fig. 1). Interestingly, BSA is significantly related to LV mass (P b 0.001; R = 0.564) while height 2.7 it is not (P = 0.245; R = 0.060). BMI has a weak, albeit significant, relation with h2.7 (P = 0.035; R = −0.108) while it has a very strong relation with BSA (P b 0.001; R = 0.834).
4. Discussion Our study confirms that the method used for correcting LV mass significantly influences the diagnosis of LVH in a non-selected white female population. Several papers have already showed that BSA correction underestimates LVH in obesity [8] even if the prognostic value of LVH remains, independently of the method which is used [9]. Obviously the issue has a practical relevance considering the very high prevalence of obesity worldwide. Therefore we think that a clear definition of the methodology that is used for calculating LVH is mandatory. We can look at our results in two different ways: we can state that our data clearly reaffirm that the correction by body surface area underestimates LVH in obese subjects or else we can say that, using an allometric correction, overestimates it. However this second possibility seems unlikely, since the percentage of patients with LVH using the absolute value of LV mass resembles that of the allometric correction. To confirm this point we have demonstrated that using height2.7 could introduce both an overestimate and an underestimate of LVH in the obese population, but using BSA only produces an underestimate. On the contrary, both correction methods, as well as the use of the absolute value, purport similar results in non-obese subjects. We therefore have to face a methodological problem that has clearly an arithmetical basis, but might have clinically relevant consequences. Looking at the whole picture introduces further complications: indeed we have also to keep in mind that LVH is strongly associated with BMI [3,10] because obese have a higher LV mass independent of the method used for correction. The choice of the indexation method introduces a bias: the use of BSA, which is directly related to LV mass, as a correction factor attenuates the prevalence of LVH in obese, markedly decreasing the effect of body size on LV mass, while using height2.7 (which, on the contrary, has no significant relation to LV mass) reflects more closely the increase of absolute values of LV mass in obese. Beyond mathematical considerations, the biological meaning of LVH in obese patients should be questioned: is LVH a risk factor also in obese? Or else obese must “necessarily” have a larger LV size for hemodynamic and biochemical reasons and we should therefore think that the increase in LV mass is a sort of physiologic hypertrophy? Nearly 77% of the variation in left ventricular mass can be explained by three factors: lean body mass, LV stroke volume, and abdominal
Table 1 describes the prevalence of left ventricular hypertrophy, calculated with different methods, in the different BMI categories. Method
LV mass absolute value LV mass/BSA LV mass/height2.7
Left ventricular hypertrophy All (384)
BMI b25 (198)
BMI 25–30 (90)
BMI 30–35 (42)
BMI N35 (54)
84 (21.9%) 55 (14.3%) 90 (23.4%)
14 (7%) 17 (9%) 12 (6%)
17 (19%) 11 (12%) 20 (22%)
16 (38%) 10 (24%) 18 (43%)
37 (69%) 17 (32%) 40 (74%)
LV = left ventricular; BSA = Body surface area; BMI = body mass index.
Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032
L. Alessandro Gondoni et al. / International Journal of Cardiology xxx (2016) xxx–xxx
3
It is evident that we still lack a “perfect” indexation method. We would strongly recommend that height2.7, independently of the method utilized for LV mass calculation, be used for LV mass correction at least in obese patients.
References
Fig. 1. Relation of left ventricular mass to body mass index.
visceral fat mass, with fat free mass (FFM) as the single main contributing factor [11]. To explain LV remodeling in obese, the coexistence of both hemodynamic and non-hemodynamic mechanisms has to be considered; for the purpose of the discussion of our findings we can overlook the metabolic issues and keep the focus on the hemodynamic picture. Obese have a predominant volume overload associated with pressure overload even in the absence of hypertension. As Alpert showed already in 1993 [12,13], the modifications in ventricular structure related to altered hemodynamics and loading conditions is peculiar to the obesity condition: obesity causes an increase in total blood volume and cardiac output (and we must remember that stroke volume is one of the determinant of LV mass), to cope with the increased tissue demand. This will lead to left ventricular dilation for volume overload and increased preload, and therefore to an increased left ventricular wall stress which, over the long term, may eventually cause LVH. LVH has a prognostic relevance in all patients irrespective if they are obese or not: we therefore have to define it clearly, taking into account the peculiarity of the obese subjects. In this regard probably the best method of indexation could be FFM. However FFM is complex to calculate correctly and therefore is not routinely measured. Height could be a surrogate of FFM, being the main factor which contributes to the magnitude of FFM across most of the lifespan [14]. On the contrary using only BSA seems not acceptable in the category of obese patients.
[1] M.P. Turakhia, N.B. Schiller, M.A. Whooley, Prognostic significance of increased left ventricular mass index to mortality and sudden death in patients with stable coronary heart disease (from the Heart and Soul Study), Am. J. Cardiol. 102 (2008) 1131–1135. [2] G. De Simone, R.B. Devereux, A.P. Maggioni, M. Gorini, O. de Divitiis, P. Verdecchia, Different normalizations for body size and population attributable risk of left ventricular hypertrophy: the MAVI study, Am. J. Hypertens. 18 (2005) 1288–1293. [3] L.R. Peterson, A.D. Waggoner, K.B. Schechtman, Alterations in left ventricular structure and function in young healthy obese women. Assessment by echocardiography and tissue Doppler imaging, J. Am. Coll. Cardiol. 43 (2004) 1399–1404. [4] R.M. Lang, L.P. Badano, V. Mor-Avi, J. Afilalo, A. Armstrong, L. Ernande, F.A. Flachskampf, E. Foster, S.A. Goldstein, T. Kuznetsova, P. Lancellotti, D. Muraru, M.H. Picard, E.R. Rietzschel, L. Rudski, K.T. Spencer, W. Tsang, J.U. Voigt, Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging, Eur. Heart J. Cardiovasc. Imaging 16 (2015) 233–271. [5] The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC), 2013 ESH/ ESC guidelines for the management of arterial hypertension, J. Hypertens. 31 (2013) 1281–1357. [6] C.L. Ogden, M.D. Carroll, C.D. Fryar, K.M. Flegal, Prevalence of obesity among adults and youth: United States, 2011–2014, NCHS Data Brief 219 (Nov 2015) 1–8. [7] R.B. Devereux, N. Reichek, Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method, Circulation 55 (1977) 613–618. [8] G. De Simone, S.R. Daniels, R.B. Devereux, R.A. Meyer, M.J. Roman, O. de Divitiis, R.H. Alderman, Left ventricular mass in normotensive children and adults: assessment of allometric relations and impact of overweight, J. Am. Coll. Cardiol. 20 (1992) 1251–1260. [9] Y. Liao, R.S. Cooper, R. Durazo-Arvizu, G.A. Mensah, J.K. Ghali, Prediction of mortality risk by different methods of indexation for left ventricular mass, J. Am. Coll. Cardiol. 29 (1997) 641–647. [10] C.Y. Wong, T. O'Moore-Sullivan, R. Leano, N. Byrne, E. Beller, T.H. Marwick, Alterations of left ventricular myocardial characteristics associated with obesity, Circulation 110 (19) (Nov 9 2004) 3081–3087. [11] O.J. Rider, J.M. Francis, M.K. Ali, J. Byrne, K. Clarke, S. Neubauer, S.E. Petersen, Determinants of left ventricular mass in obesity; a cardiovascular magnetic resonance study, J. Cardiovasc. Magn. Reson. 11 (2009) 9. [12] M.A. Alpert, M.W. Hashimi, Obesity and the heart, Am. J. Med. Sci. 306 (1993) 117–123. [13] M.A. Alpert, Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome, Am. J. Med. Sci. 321 (2001) 225–236. [14] Z. Wang, J. Zhang, Z. Ying, S.B. Heymsfield, New insights into scaling of fat-free mass to height across children and adults, Am. J. Hum. Biol. 24 (2012) 648–653.
Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
The importance of a shared definition of left ventricular hypertrophy: The case of obese women Luca Alessandro Gondoni ⁎, Anna Maria Titon, Mariella Montano, Ferruccio Nibbio, Gianandrea Bertone Unit of Cardiac Rehabilitation, Ospedale San Giuseppe, IRCCS Istituto Auxologico Italiano, Via Cadorna, 90, 28824, Piancavallo di Oggebbio, Verbania, Italy
a r t i c l e
i n f o
Article history: Received 12 January 2016 Received in revised form 28 September 2016 Accepted 5 November 2016 Available online xxxx Keywords: Obesity Left ventricular hypertrophy Echocardiography
a b s t r a c t Background: Left ventricular hypertrophy (LVH) is a risk factor for all-cause mortality. Left ventricular (LV) mass is usually indexed for normalizing the value to the patients phenotype and a correction by body surface area (BSA) is widely utilized being the only approved one according to the last echocardiography guidelines. However indexing LV mass by BSA may cause an underestimation of LVH prevalence in obese subjects and many authors have utilized in the obese subset of patients a correction by height2.7. The aim of our study was to quantify the number of obese patients who, despite having an increased LV mass, fall in the range of normality because they do not reach the LVH cutoff according to the new guidelines. Methods: We reviewed the echocardiograms of 384 white women free from cardiovascular disease. Ninety-six patients (25%) were obese: among them 42 had mild obesity and 54 had moderate or severe obesity. Results: In the obese group, the prevalence of LVH using the absolute LV mass value was similar to the one obtained with the height2.7 correction while a significant smaller number of patients had LVH according to BSA correction. Our study confirms that the method used for correcting LV mass significantly influences the diagnosis of LVH in a non-selected female population: using body surface area underestimates the prevalence of LVH as compared to allometric measures in the obese subset of patients. Conclusion: We recommend that height2.7 be used for LV mass correction in obese patients. © 2016 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Left ventricular hypertrophy (LVH) is a risk factor for sudden death and all-cause mortality in various categories of patients [1]. Echocardiography is the more widely used method for studying left ventricular (LV) mass: as a rule, a correction for body size should be made for normalizing the value of the mass to the patients' phenotype. Various methods may be utilized for that purpose: the most frequently adopted one is a correction by body surface area (BSA): however indexing LV mass by BSA may cause an underestimation of LVH prevalence in obese subjects who have, obviously, a greater BSA as compared to normal weight subjects. To avoid this pitfall many authors have utilized in the obese subset of patients an allometric correction, namely height2.7 [2,3], that correlates well with lean body mass, which is one of the main determinants of LV size and is less strictly related to BMI. Unfortunately the new guidelines on chamber quantification, endorsed by both the American and European Echocardiography Societies, forget to consider the possibility of using height for correction [4] thus seeming ⁎ Corresponding author. E-mail addresses: [email protected] (L. Alessandro Gondoni), [email protected] (A.M. Titon), [email protected] (M. Montano), [email protected] (F. Nibbio), [email protected] (G. Bertone).
inconsistent with the European Guidelines for the management of arterial hypertension [5] that suggest the possibility to use height correction in overweight and obese subjects “in order to scale LV mass to body size and avoid under-diagnosis of LVH”. Since obesity is not a marginal problem and affects a significant proportion of the western population [6], cardiologists have to ask themselves which one is the correct method for defining LVH. The aim of our study was to quantify the number of obese patients who, despite having an increased LV mass, fall in the range of normality because they do not reach the LVH cutoff according to the new guidelines. 2. Patients and methods We reviewed the studies of a group of patients who underwent an echocardiogram for various purposes. The study population consisted of 384 white women. None was affected with cardiovascular disease nor had left ventricular dysfunction. Two-dimensional echocardiographic parameters were obtained with a GE Vivid 7 instrument (GE Medical Systems, Milwaukee, Wisconsin USA). The examinations were conducted with the patient in the left lateral recumbent position during quiet respiration. Parasternal long axis was used for evaluating left ventricular (LV) dimension with a
http://dx.doi.org/10.1016/j.ijcard.2016.11.032 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032
2
L. Alessandro Gondoni et al. / International Journal of Cardiology xxx (2016) xxx–xxx
multifrequency sector transducer set on ideal frequency to obtain optimal imaging. For LV mas calculation we measured end-diastolic diameter (LVEDD), interventricular septum (IVSD) and posterior wall (LVPWD) thickness both at end-diastole (for each parameter an average of three measurements was used). Left ventricular mass was calculated by the Devereux formula [7], i.e. 0.8 × (1.04 × (left ventricular diameter + septum + posterior wall)3 × (left ventricular diameter)3 + 0.6).
Table 2 describes the values of LV mass in our patients according to the correction method.
LV mass absolute value
LV mass/BSA
LV mass/height2.7
2.1. Statistical analysis
Normal/overweight Obese Total Normal/overweight Obese Total Normal/overweight Obese Total
N
Mean ± SD
P
288 96 384 288 96 384 288 96 384
127 ± 28 169 ± 43 138 ± 37 76 ± 16 86 ± 19 79 ± 17 35 ± 8 47 ± 12 38 ± 11
b0.001
b0.001
b0.001
LV = left ventricular; BSA = Body surface area.
Continuous variables are expressed as mean ± standard deviation and categorical variables are expressed as number and percentage. We studied LV mass as absolute value and we corrected it both by BSA and by height2.7. The cut off values above which LVH was diagnosed were the following: for the absolute value of LV mass N 162 g; for LV mass/BSA N 95 g/m2; for LV mass/height2.7 N 44 g/m2.7. Statistical analysis has been performed with SPSS 23.0 package (SPSS Inc. Chicago IL, USA).
3. Results In the study population mean age was 46.5 ± 8.4 years, mean height 161.8 ± 5.9 cm, mean weight 70.2 ± 16.5 kg, and mean BMI 26.8 ± 6.2 kg/m2. Ninety patients (23%) were overweight, while 96 (25%) were obese: among them 42 had mild obesity and the remaining 54 had moderate or severe obesity. The results of mass calculation are shown in Tables 1, and 2. If we considered together the non-obese group (BMI b 30) and compared it to all obese subjects the results did not change: the prevalence of LVH using the absolute LV mass value was quite similar to the one obtained with the height correction (55 and 60% respectively) while only 28% of the obese had LVH according to BSA correction. On the contrary, no significant differences emerged when dealing with the non-obese group and the prevalence of LVH ranged from 10 to 11%, independent of the correction method. Put the other way around, we found that, in the non-obese group, the correction by BSA moved 4 patients from normal to LVH and 7 patients from LVH to normal while in the same group, when using the correction by height2.7 the changes were slightly greater and 10 patients were moved from normal to LVH and 9 moved from LVH to normal. Things changed when we looked at the obese group: using the BSA correction moved 26 patients (27.1%) from LVH to normal, while no patients moved from normal to LVH; using the height2.7 method 8 patients moved from normal to LVH while 3 moved from LVH to normal. As we already knew LV mass was directly and strongly related to BMI (P b 0.001; R = 0.599) (Fig. 1). Interestingly, BSA is significantly related to LV mass (P b 0.001; R = 0.564) while height 2.7 it is not (P = 0.245; R = 0.060). BMI has a weak, albeit significant, relation with h2.7 (P = 0.035; R = −0.108) while it has a very strong relation with BSA (P b 0.001; R = 0.834).
4. Discussion Our study confirms that the method used for correcting LV mass significantly influences the diagnosis of LVH in a non-selected white female population. Several papers have already showed that BSA correction underestimates LVH in obesity [8] even if the prognostic value of LVH remains, independently of the method which is used [9]. Obviously the issue has a practical relevance considering the very high prevalence of obesity worldwide. Therefore we think that a clear definition of the methodology that is used for calculating LVH is mandatory. We can look at our results in two different ways: we can state that our data clearly reaffirm that the correction by body surface area underestimates LVH in obese subjects or else we can say that, using an allometric correction, overestimates it. However this second possibility seems unlikely, since the percentage of patients with LVH using the absolute value of LV mass resembles that of the allometric correction. To confirm this point we have demonstrated that using height2.7 could introduce both an overestimate and an underestimate of LVH in the obese population, but using BSA only produces an underestimate. On the contrary, both correction methods, as well as the use of the absolute value, purport similar results in non-obese subjects. We therefore have to face a methodological problem that has clearly an arithmetical basis, but might have clinically relevant consequences. Looking at the whole picture introduces further complications: indeed we have also to keep in mind that LVH is strongly associated with BMI [3,10] because obese have a higher LV mass independent of the method used for correction. The choice of the indexation method introduces a bias: the use of BSA, which is directly related to LV mass, as a correction factor attenuates the prevalence of LVH in obese, markedly decreasing the effect of body size on LV mass, while using height2.7 (which, on the contrary, has no significant relation to LV mass) reflects more closely the increase of absolute values of LV mass in obese. Beyond mathematical considerations, the biological meaning of LVH in obese patients should be questioned: is LVH a risk factor also in obese? Or else obese must “necessarily” have a larger LV size for hemodynamic and biochemical reasons and we should therefore think that the increase in LV mass is a sort of physiologic hypertrophy? Nearly 77% of the variation in left ventricular mass can be explained by three factors: lean body mass, LV stroke volume, and abdominal
Table 1 describes the prevalence of left ventricular hypertrophy, calculated with different methods, in the different BMI categories. Method
LV mass absolute value LV mass/BSA LV mass/height2.7
Left ventricular hypertrophy All (384)
BMI b25 (198)
BMI 25–30 (90)
BMI 30–35 (42)
BMI N35 (54)
84 (21.9%) 55 (14.3%) 90 (23.4%)
14 (7%) 17 (9%) 12 (6%)
17 (19%) 11 (12%) 20 (22%)
16 (38%) 10 (24%) 18 (43%)
37 (69%) 17 (32%) 40 (74%)
LV = left ventricular; BSA = Body surface area; BMI = body mass index.
Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032
L. Alessandro Gondoni et al. / International Journal of Cardiology xxx (2016) xxx–xxx
3
It is evident that we still lack a “perfect” indexation method. We would strongly recommend that height2.7, independently of the method utilized for LV mass calculation, be used for LV mass correction at least in obese patients.
References
Fig. 1. Relation of left ventricular mass to body mass index.
visceral fat mass, with fat free mass (FFM) as the single main contributing factor [11]. To explain LV remodeling in obese, the coexistence of both hemodynamic and non-hemodynamic mechanisms has to be considered; for the purpose of the discussion of our findings we can overlook the metabolic issues and keep the focus on the hemodynamic picture. Obese have a predominant volume overload associated with pressure overload even in the absence of hypertension. As Alpert showed already in 1993 [12,13], the modifications in ventricular structure related to altered hemodynamics and loading conditions is peculiar to the obesity condition: obesity causes an increase in total blood volume and cardiac output (and we must remember that stroke volume is one of the determinant of LV mass), to cope with the increased tissue demand. This will lead to left ventricular dilation for volume overload and increased preload, and therefore to an increased left ventricular wall stress which, over the long term, may eventually cause LVH. LVH has a prognostic relevance in all patients irrespective if they are obese or not: we therefore have to define it clearly, taking into account the peculiarity of the obese subjects. In this regard probably the best method of indexation could be FFM. However FFM is complex to calculate correctly and therefore is not routinely measured. Height could be a surrogate of FFM, being the main factor which contributes to the magnitude of FFM across most of the lifespan [14]. On the contrary using only BSA seems not acceptable in the category of obese patients.
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Please cite this article as: L. Alessandro Gondoni, et al., The importance of a shared definition of left ventricular hypertrophy: The case of obese women, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.11.032