(Hypertension. 2000;35:13.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Effect of Obesity on Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients
The Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study
From the Division of Cardiology, Department of Medicine, Weill Medical College of Cornell University, New York, NY (P.M.O., R.B.D.); Sahlgrenska University Hospital/Östra, Göteborg, Sweden (S.J., B.D.); and Ullevål University Hospital, Oslo, Norway (S.E.K.).
Correspondence to Peter M. Okin, MD, Weill Medical College of Cornell University, 525 East 68th St, New York, NY 10021. E-mail pokin{at}mail.med.cornell.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract—Obesity may limit sensitivity of ECG voltage criteria for left ventricular hypertrophy (LVH) because of the attenuating effects of increased body mass on precordial voltages. However, obesity is associated with an increased prevalence of anatomic LVH, making more accurate ECG criteria in obese patients a clinical priority. ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria was used to select patients for the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study. Clinical and ECG data were available in 8417 patients (54% women; mean age, 67±7 years); 2519 were overweight and 1573 were obese by gender-specific body mass index criteria. Increased body mass index had significant but directionally opposite effects on ECG LVH by these 2 criteria. Compared with normal-weight patients, obese and overweight patients had lower Sokolow-Lyon voltage and a lower prevalence of ECG LVH by Sokolow-Lyon criteria (10.9% versus 16.2% versus 31.4%; P<0.001). In contrast, obese and overweight patients had higher mean values of the Cornell product and higher prevalences of ECG LVH by this criterion (75.1% versus 69.9% versus 60.7%; P<0.001). After adjustment for age, gender, race, myocardial infarction, and diastolic and pulse pressure with the use of logistic regression analysis, increased body mass remained highly predictive of the presence of ECG LVH. Compared with normal-weight patients, obese patients had a >2-fold higher risk of ECG LVH by the Cornell product but a 4-fold lower risk of ECG LVH by Sokolow-Lyon voltage; overweight status was associated with intermediate risks, with a 151% greater likelihood of ECG LVH by the Cornell product but only 44% of the risk of LVH by Sokolow-Lyon voltage criteria compared with normal-weight individuals. Thus, Sokolow-Lyon voltage criteria underestimate the prevalence of anatomic LVH in the presence of obesity, whereas Cornell product criteria for ECG LVH appear to provide a more accurate measure of LVH in obese and overweight patients.
Key Words: blood pressure • electrocardiography • hypertrophy • obesity
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Increased left ventricular (LV) mass detected by standard 12-lead ECG1 2 and by echocardiography3 4 has been associated with increased morbidity and mortality. However, low sensitivity of standard voltage criteria for detection of LV hypertrophy (LVH) has limited utility of the ECG for identification of patients with LVH.5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Although Cornell voltage criteria modestly improve ECG detection of LVH in hypertensive patients,6 7 the product of Cornell voltage and QRS duration (Cornell voltage-duration product),8 9 an approximation of the area under the QRS,10 appears to further enhance sensitivity of the ECG for LVH while maintaining high specificity. As a consequence, Cornell voltage-duration product criteria were used in combination with Sokolow-Lyon voltage5 to identify hypertensive patients at increased risk of subsequent cardiovascular morbidity and mortality for inclusion in the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study, a prospective trial designed to compare the efficacy of losartan and atenolol in reducing the risk of cardiovascular events.21 22
Obesity has been associated with increases in LV wall thickness, LV mass, and the prevalence of echocardiographic LVH, independent of the impact of blood pressure.23 24 25 26 Conversely, obesity has been shown to decrease sensitivity of precordial lead ECG criteria for LVH, presumably because of the attenuating effects of increased distance of exploring electrodes from the LV and attenuation of QRS amplitudes by interposed tissue.11 14 15 16 17 18 19 20 However, obesity is common in hypertensive patients,23 24 25 26 raising questions regarding the utility of precordial voltage criteria in detecting hypertensive LVH. Moreover, previous studies of the impact of increased body mass on ECG LVH criteria have produced conflicting results with respect to the prevalence of Cornell voltage criteria and have not examined the independent effects of obesity on ECG LVH criteria using multivariable analyses.14 15 16 17 18 19 20 Thus, the present study was undertaken to characterize more fully the relations of Cornell and Sokolow-Lyon voltage and voltage-duration product criteria to body habitus in hypertensive patients.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Protocol
LIFE is a prospective, double-blind, randomized study of 9194 patients with hypertension and ECG LVH testing the hypothesis that incidence of cardiovascular death or nonfatal myocardial infarction or stroke will be decreased by at least an additional 15% by use of losartan versus atenolol.21 22 Study entry and exclusion criteria and clinical protocols have been published21 22 ; body mass index (BMI) was calculated from measured height and weight. On the basis of the second National Health and Nutrition Examination Survey (NHANES II),27 overweight was defined as BMI of 27.8 to 31.0 kg/m2 for men and 27.3 to 32.2 kg/m2 for women; obesity was defined as higher BMI.
Patients were recruited into LIFE on the basis of LVH on a screening ECG read at a central core laboratory.21 22 Based on prior evidence that the product of QRS voltage and duration had the greatest sensitivity at high levels of specificity compared with anatomic and echocardiographic LV mass,8 9 the Cornell voltage-duration product (RaVL+SV3, with 8 mm added in women8 9 ) was used with a threshold value of 2440 mm · ms to identify LVH. After publication in late 1995 of 2 studies suggesting that a smaller gender adjustment was more appropriate12 13 and feedback from field investigators that some otherwise eligible patients had ECG LVH by the insensitive but specific Sokolow-Lyon voltage criteria but not by the Cornell product, the gender adjustment of Cornell voltage was reduced from 8 to 6 mm, and Sokolow-Lyon voltage (SV1+RV5/6) >38 mm was accepted as an alternative ECG eligibility criterion for patients enrolled after April 30, 1996.21
Electrocardiography
Patients enrolled into LIFE had an additional baseline ECG
performed before beginning treatment. All ECGs were interpreted at a
central core laboratory by experienced investigators blinded to
clinical information. QRS duration was measured to the nearest 4 ms,
and R waves in leads aVL, V5, and
V6 and S waves in leads V1
and V3 were measured to the nearest 0.5 mm
(0.05 mV). Cornell and Sokolow-Lyon voltages were calculated as
noted above,5 6 7 and voltage-duration products were
calculated as the product of Cornell or Sokolow-Lyon voltage times
QRS duration.8 9 ECG LVH by Sokolow-Lyon voltage criteria
was defined according to the preselected partition value of 38 mm
for LIFE study eligibility.21 22 ECG LVH by Cornell
voltage criteria was considered present when voltage was 
20
mm in women or 28 mm in men, as initially defined for this
method.6 7 Because patients were recruited into LIFE with
the use of 2 different gender adjustments for Cornell product
calculations,22 ECG LVH according to Cornell product
criteria was defined for this study with the use of previously
determined gender-specific partitions of 1713 mm · ms in
women and 2647 mm · ms in men,9 10 on the
basis of unadjusted voltage measurements. Similarly, for this study ECG
LVH by Sokolow-Lyon product criteria was defined with the use of
previously determined gender-specific partition values of 3224
mm · ms in women and 3674 mm · ms in
men.9 10
Statistical Analysis
Data are presented for normal-weight, overweight, and
obese groups as mean±SD for continuous variables and proportions
for categorical variables. Differences in prevalences between
groups were compared with 
2 analyses.
Mean values of demographic variables were compared with ANOVA; mean
values of ECG measures were compared with 2-way ANOVA to take into
account the known impact of gender on these variables. Mean blood
pressure values were further examined with 2-way ANOVA to compare
differences between patients with and without ECG LVH by weight group.
Mean values of ECG criteria were further compared with ANCOVA to adjust
for baseline differences in age, gender, race, self-reported myocardial
infarction, and diastolic and pulse blood pressure between
groups. The independent contribution of overweight and obese status to
the risk of ECG LVH was determined with logistic regression
analyses. For all tests, a 2-tailed P value <0.05
was required for statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Relation of Clinical Characteristics to Body Habitus
Clinical, demographic, and ECG data were available for analysis in 8417 patients (54% women; mean age, 67±7 years). Obesity was present in 1573 patients (19%), 2519 patients (30%) were overweight, and 4325 patients (51%) had normal BMI values. Clinical characteristics according to BMI group are shown in Table 1. Compared with normal-weight patients, obese and overweight patients were younger, were more likely to be female, and had lower prevalences of self-reported myocardial infarction. Obese patients were more likely to be black than either overweight or normal-weight patients. Mean systolic blood pressure was identical across groups, but increased BMI was associated with higher diastolic blood pressures and consequently lower pulse pressures.
|
Effect of Body Habitus on ECG LVH Criteria
Increased BMI had significant but directionally opposite
associations with mean values and prevalences of ECG LVH according to
Cornell and Sokolow-Lyon voltage and voltage-duration product
criteria (Table 2, Figures 1 and 2).
Compared with normal-weight patients, overweight and obese patients had
lower mean values of Sokolow-Lyon voltage and voltage-duration
product (Table 2) and a decreasing prevalence of ECG LVH by
Sokolow-Lyon voltage (from 31.4% to 16.2% to 10.9%;
P<0.001) and voltage-duration product criteria (from
37.7% to 24.3% to 19.3%; P<0.001) (Figures 1 and 2). In contrast, compared with normal-weight patients,
overweight and obese patients had higher mean values of Cornell voltage
and Cornell product measurements (Table 2), with parallel
higher prevalences of ECG LVH by both voltage (52.0% versus 62.4%
versus 62.3%; P<0.001) and voltage-duration product
criteria (60.7% versus 69.9% versus 75.1%; P<0.001)
(Figures 1 and 2). These differences in mean values
remained significant after adjustment for baseline demographic and
blood pressure differences with the use of ANCOVA.
|
|
|
To determine whether the decreasing frequency of ECG LVH by Sokolow-Lyon voltage and voltage-duration product criteria as BMI increased was associated with identification of a subset of obese patients with more severe hypertension, mean values of systolic blood pressure in normal, overweight, and obese patients were further examined in patients with or without ECG LVH (Table 3). The proportionally fewer patients with ECG LVH by Sokolow-Lyon voltage criteria as body mass increased had proportionally higher mean systolic pressure (P=0.004), as did, to a lesser degree, patients with ECG LVH by Sokolow-Lyon product criteria (P=0.035). In contrast, the increasing proportion of patients with ECG LVH by Cornell voltage or voltage-duration product criteria as body mass increased had similarly elevated systolic pressures across weight groups. Of note, patients with ECG LVH by any of the 4 criteria examined had higher systolic pressures than patients who did not meet these criteria for LVH on their baseline ECGs, and systolic pressure did not vary with increasing obesity among patients with no evidence of ECG LVH (Table 3).
|
The independent contribution of overweight and obesity to the likelihood of ECG LVH was assessed with logistic regression analysis (Table 4). After we controlled for the possible effects of demographic variables and blood pressure on ECG LVH prevalence, increased body mass remained highly predictive of the presence of ECG LVH (Table 4). Compared with normal-weight patients, obese patients had a >2-fold higher risk of ECG LVH by Cornell voltage-duration product criteria and nearly 1.5-fold higher risk of Cornell voltage criteria for LVH. In contrast, obese patients had only 39% of the risk of ECG LVH by Sokolow-Lyon product criteria and merely 25% of the risk of ECG LVH by Sokolow-Lyon voltage compared with normal-weight patients. Overweight status was associated with intermediate risks of ECG LVH: compared with normal-weight patients, the likelihoods of ECG LVH by Cornell voltage and Cornell-product criteria were 135% and 151%, respectively, and the risks of LVH by Sokolow-Lyon voltage and voltage-duration product criteria were 44% and 55%, respectively.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
These findings demonstrate that the prevalence and degree of ECG LVH by Cornell and Sokolow-Lyon criteria in hypertensive patients are strongly affected by obesity. The significantly lower prevalence of LVH by Sokolow-Lyon voltage and voltage-duration product criteria in obese and overweight patients suggests that these criteria may underestimate the presence of anatomic LVH in the presence of obesity. In contrast, the higher prevalence and severity of Cornell product and voltage criteria with greater body mass, paralleling the known association of anatomic LVH with obesity,23 24 25 26 suggest that these criteria provide a more accurate measure of LVH in obese and overweight individuals.
LVH and Obesity
A number of previous studies have examined the relationship of LVH
by ECG criteria to obesity, predominantly finding decreased sensitivity
of precordial lead voltage criteria in overweight
patients.11 14 15 16 17 18 19 20 Levy et al11 found a
negative association between sensitivity of predominantly
precordial lead voltage criteria and quartile of BMI in 4684
subjects from the Framingham Heart Study. Abergel et al16
found sensitivity of Sokolow-Lyon voltage to be significantly lower in
obese hypertensive patients than in nonobese patients but found no
significant differences in sensitivity of Cornell voltage according to
body habitus. Similar effects of obesity on sensitivity of Sokolow-Lyon
voltage and Cornell voltage were found in a study of 212 patients from
our laboratory.17 Among 7543 participants in the Hispanic
Health and Nutrition Examination Survey,19 R-wave
amplitude in V5 was lower in overweight subjects
and both R-wave amplitude in aVL and Cornell voltage were higher in
overweight than normal-weight subjects. However, after adjustment for
the effects of age, QRS axis, gender, and race, obesity was not
independently associated with ECG LVH by Cornell voltage.
The present study extends these observations to a large,
heterogeneous population of hypertensive patients,
demonstrating strong negative associations of obesity with Sokolow-Lyon
voltage and voltage-duration product and equally strong positive
associations of obesity with Cornell voltage and voltage-duration
product, even after the impact of blood pressure and other
clinically relevant variables was taken into account (Table 4). Moreover, among the criteria examined, the Cornell
voltage-duration product identified the highest prevalence of ECG
LVH in obese patients, consistent with the positive impact of
obesity on anatomic LVH.23 24 25 26 In this context, it is
notable that multiplication of Sokolow-Lyon voltage by QRS duration
attenuated the negative relation between obesity and LVH by
Sokolow-Lyon voltage ECG criteria. Given that voltage-duration
product criteria are, in effect, approximations of the area under
the QRS,8 9 10 these findings support previous observations
in a small population that true time-voltage area criteria for ECG LVH
may be less affected by obesity.18 It is intriguing to
note that the Perugia score,1 13 which combines Cornell
voltage, the Romhilt-Estes point score, and the presence or absence of
the "strain" pattern in lateral precordial leads, behaved quite
similarly to Cornell criteria in the present population. ECG LVH by
the Perugia score was present in 70.1% of normal-weight patients,
74.9% of overweight patients, and 75.3% of obese hypertensive
patients (2=26.09, P<0.001 for
trend), suggesting that accuracy of this ECG criterion may also be
relatively independent of obesity.
The decreased prevalence and sensitivity of precordial lead voltage criteria for detecting anatomic LVH in obese patients,11 14 15 16 17 18 19 20 despite the recognized increased prevalence of echocardiographic LVH with higher body mass,23 24 25 26 have been attributed to attenuating effects of increased distance of exploring electrodes from the LV and attenuation of precordial QRS amplitudes by interposed tissue.11 14 15 16 17 18 19 20 28 Horton et al14 demonstrated that Sokolow-Lyon voltage was inversely related to the square of the distance from the anterior chest wall to the mid-LV and that this distance correlated directly with body surface area, suggesting that Sokolow-Lyon voltage varies inversely with increasing body size. Devereux et al15 demonstrated that patients with false-negative Sokolow-Lyon voltage for LVH had both increased body weight and increased distance from the chest wall to the LV compared with patients with true-positive ECG LVH findings. Rautaharju et al28 also found that increasing chest size was associated with lower Sokolow-Lyon voltage and further demonstrated that Cornell voltage increased with greater chest dimension, but they did not examine the relation of increased chest size to body mass.
Although female gender was strongly associated with increased BMI
(Table 1), gender did not play a significant role in the
observed lower prevalence and severity of Sokolow-Lyon criteria with
increasing body mass (Table 4). This finding contrasts with
previous suggestions that breast tissue importantly attenuates
precordial ECG voltages.28 The present findings
are supported by observations by Rautaharju et al28 that,
although increasing breast size was associated with lower Sokolow-Lyon
voltage and greater Cornell voltage, these effects were small in
magnitude (
15 µV for each 1-cm increment in breast size) with
R values <0.10, suggesting that breast size alone accounted
for <1% of ECG amplitude variations.
The association of anatomic LVH with increasing BMI23 24 25 26
and lower sensitivity of many ECG criteria in obese
patients11 14 15 16 17 18 19 20 led investigators to incorporate BMI
into regression equations with ECG voltage in attempts to improve ECG
sensitivity for LVH.12 20 However, further examination
revealed that sensitivity of BMI-adjusted voltage criteria for anatomic
LVH was highly dependent on body habitus, with lower ECG sensitivities
in normal-weight than in obese subjects.17 18 Indeed,
adjusting the Cornell product for BMI, age, and
gender20 in the present population produced
substantially lower prevalences of ECG LVH in normal-weight patients
(18.9%), overweight patients (19.1%), and obese patients (26.1%)
compared with unadjusted Cornell product criteria
(P<0.001) and still left a significant residual association
with increasing BMI group (2=40.35,
P<0.001 for trend). Although anatomic LVH has been linked
to increasing body mass and obesity,23 24 25 26 recent
observations suggest that LV mass is more strongly related to fat-free
body mass than to either adipose mass or BMI, and that normalizing LV
mass for fat-free body mass appears to increase sensitivity for
detection of anatomic LVH.26 The strong positive relation
of fat-free body mass to both total body weight and BMI suggests that
increased fat-free body mass may have similar effects on prevalence and
performance of these ECG criteria. Additional study of the
performance of ECG LVH criteria in relation to fat-free and
adipose body mass is needed.
Implications
The low prevalence of ECG LVH by Sokolow-Lyon voltage and
voltage-duration product criteria in overweight and obese
hypertensive patients suggests that these criteria severely
underestimate the presence of anatomic LVH in these patients. These
findings contrast with the relatively higher sensitivity of
Sokolow-Lyon voltage and product criteria in patients with
eccentric LVH due to valvular heart disease9 10
and the general association of obesity with this geometric pattern of
hypertrophy. Use of voltage-duration products mitigates
the negative impact of increased BMI on prevalence of LVH by
Sokolow-Lyon criteria and increases the association between LVH by
Cornell criteria and increased BMI, suggesting that voltage-duration
products may be the most accurate conventional ECG method to detect
anatomic LVH, independent of body habitus. These findings, as well as
previous studies showing increased accuracy of true time-voltage area
criteria for LVH and the independence of area criteria
performance from the effects of obesity,10 18
suggest that true time-voltage area ECG criteria for LVH will provide
the most stable and accurate test performance, independent of
body habitus. Analyses in the echocardiographic
substudy that enrolled >10% of LIFE patients will provide greater
insight into the impact of obesity on the accuracy of standard ECG
criteria; further study in additional populations will be required to
more fully assess the value of time-voltage area criteria in relation
to body habitus. Because the present study was, by design, limited
to patients with hypertension and target organ damage, further study of
this issue in normotensive and less highly selected hypertensive
patients will be of importance.
|
Acknowledgments |
|---|
This study was supported in part by grant COZ-368 from Merck and Co, Inc (West Point, Pa).
Received July 6, 1999; first decision July 20, 1999; accepted August 19, 1999.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Porcellati C. Prognostic value of a new electrocardiographic method for diagnosis of left ventricular hypertrophy. J Am Coll Cardiol. 1998;31:383–390.
2. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham Study. Ann Intern Med. 1969;71:89–105.
3. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–352.
4. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990;322:1561–1566.[Abstract]
5. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37:161–186.[Medline] [Order article via Infotrieve]
6. Casale PN, Devereux RB, Kligfield P, Eisenberg RR, Miller DH, Chaudhary BS, Phillips MC. Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. J Am Coll Cardiol. 1985;6:572–580.[Abstract]
7.
Casale PN, Devereux RB, Alonso DR, Campo E, Kligfield
P. Improved sex-specific criteria of left ventricular
hypertrophy for clinical and computer interpretation of
electrocardiograms: validation with autopsy findings.
Circulation. 1987;75:565–572.
8. Molloy TJ, Okin PM, Devereux RB, Kligfield P. Electrocardiographic detection of left ventricular hypertrophy by the simple QRS voltage-duration product. J Am Coll Cardiol. 1992;20:1180–1186.[Abstract]
9. Okin PM, Roman MJ, Devereux RB, Kligfield P. Electrocardiographic identification of increased left ventricular mass by simple voltage-duration products. J Am Coll Cardiol. 1995;25:417–423.[Abstract]
10.
Okin PM, Roman MJ, Devereux RB, Pickering TG, Borer JS,
Kligfield P. Time-voltage QRS area of the 12-lead
electrocardiogram: detection of left
ventricular hypertrophy.
Hypertension. 1998;31:937–942.
11.
Levy D, Labib SB, Anderson KM, Christianson JC, Kannel
WB, Castelli WP. Determinants of sensitivity and specificity of
electrocardiographic criteria for left ventricular
hypertrophy. Circulation. 1990;81:815–820.
12. Norman JE, Levy D, Campbell G, Bailey JJ. Improved detection of echocardiographic left ventricular hypertrophy using a new electrocardiographic algorithm. J Am Coll Cardiol. 1993;21:1680–1686.[Abstract]
13. Schillaci G, Verdecchia P, Borgioni C, Ciucci A, Guerrieri M, Zampi I, Battistelli M, Bartoccini C, Porecellata C. Improved electrocardiographic diagnosis of echocardiographic left ventricular hypertrophy. Am J Cardiol. 1995;74:714–719.
14.
Horton JD, Sherber HS, Lakatta EG. Distance correction
for precordial electrocardiographic voltage in estimating left
ventricular mass: an echocardiographic
study. Circulation. 1977;55:509–512.
15.
Devereux RB, Phillips MC, Casale PN, Eisenberg RR,
Kligfield P. Geometric determinants of electrocardiographic left
ventricular hypertrophy.
Circulation. 1983;67:907–911.
16. Abergel E, Tase M, Menard J, Chatellier G. Influence of obesity on the diagnostic value of electrocardiographic criteria for detecting left ventricular hypertrophy. Am J Cardiol. 1996;77:739–744.[Medline] [Order article via Infotrieve]
17. Okin PM, Roman MJ, Devereux RB, Kligfield P. Electrocardiographic identification of left ventricular hypertrophy: test performance in relation to the definition of hypertrophy and the presence of obesity. J Am Coll Cardiol. 1996;27:124–131.[Abstract]
18. Okin PM, Roman MJ, Devereux RB, Kligfield P. Electrocardiographic identification of left ventricular hypertrophy: relationship of test performance to body habitus. J Electrocardiol. 1996;29(suppl):256–261.
19. Rautaharju PM, Zhou SH, Calhoun HP. Ethnic differences in ECG amplitudes in North American white, black, and Hispanic men and women: effect of obesity and age. J Electrocardiol. 1994;27(suppl):20–31.
20. Norman JE, Levy D. Improved electrocardiographic detection of echocardiographic left ventricular hypertrophy: results of a correlated data base approach. J Am Coll Cardiol. 1995;26:1022–1029.[Abstract]
21. Dahlöf B, Devereux R, de Faire U, Fyhrquist F, Hedner T, Ibsen H, Julius S, Kjeldsen S, Kristianson K, Lederballe-Pedersen O, Lindholm LH, Nieminen MS, Omvik P, Oparil S, Wedel H, for the LIFE Study Group. The Losartan Intervention For Endpoint Reduction (LIFE) in Hypertension Study: rationale, design, and methods. Am J Hypertens. 1997;10:705–713.[Medline] [Order article via Infotrieve]
22.
Dahlöf B, Devereux RB, Julius S, Kjeldsen SE,
Beevers G, de Faire U, Fyhrquist F, Hedner T, Ibsen H, Kristianson K,
Lederballe-Pedersen O, Lindholm LH, Nieminen MS, Omvik P, Oparil S,
Wedel H, for the LIFE Study Group. The Losartan Intervention
For Endpoint Reduction (LIFE) in Hypertension Study: baseline
characteristics of 9194 patients with left ventricular
hypertrophy. Hypertension. 1998;32:989–997.
23. Lauer MS, Anderson KM, Levy D. Separate and joint influences of obesity and mild hypertension on left ventricular mass and geometry: the Framingham Heart Study. J Am Coll Cardiol. 1992;19:130–134.[Abstract]
24.
de Simone G, Devereux RB, Roman MJ, Alderman MH, Laragh
JH. Relation of obesity and gender to left ventricular
hypertrophy in normotensive and hypertensive adults.
Hypertension. 1994;23:600–606.
25.
Hense HW, Gneiting B, Muscholl M, Broeckel U, Kuch B,
Doering A, Riegger GAJ, Schunkert H. The associations of body size and
body composition with left ventricular mass: impacts for
indexation in adults. J Am Coll Cardiol. 1998;32:451–457.
26.
Bella JN, Devereux RB, Roman MJ, O’Grady MJ, Welty TK,
Lee ET, Fabsitz RR, Howard BV, for the Strong Heart Study
Investigators. Relations of left ventricular mass to
fat-free and adipose body mass: the Strong Heart Study.
Circulation. 1998;98:2538–2544.
27. National Institutes of Health Consensus Development Panel on the Health Implications of Obesity. Health implications of obesity. Ann Intern Med. 1985;103:1073–1077.
28. Rautaharju PM, Park L, Rautaharju FS, Crow R. A standardized procedure for locating and documenting ECG chest electrode positions: consideration of the effect of breast tissue on ECG amplitudes in women. J Electrocardiol. 1998;31:17–29.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  E. W. Hancock, B. J. Deal, D. M. Mirvis, P. Okin, P. Kligfield, and L. S. Gettes AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part V: Electrocardiogram Changes Associated With Cardiac Chamber Hypertrophy A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology J. Am. Coll. Cardiol., March 17, 2009; 53(11): 992 - 1002. [Full Text] [PDF]
|
|
|
|
 |
|
 E. W. Hancock, B. J. Deal, D. M. Mirvis, P. Okin, P. Kligfield, and L. S. Gettes AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part V: Electrocardiogram Changes Associated With Cardiac Chamber Hypertrophy: A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: Endorsed by the International Society for Computerized Electrocardiology Circulation, March 17, 2009; 119(10): e251 - e261. [Full Text] [PDF]
|
|
|
|
 |
|
 B. M. Mayosi, P. J. Avery, M. Farrall, B. Keavney, and H. Watkins Genome-wide linkage analysis of electrocardiographic and echocardiographic left ventricular hypertrophy in families with hypertension Eur. Heart J., February 2, 2008; 29(4): 525 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Ingelsson, L. M. Sullivan, C. S. Fox, J. M. Murabito, E. J. Benjamin, J. F. Polak, J. B. Meigs, M. J. Keyes, C. J. O'Donnell, T. J. Wang, et al. Burden and Prognostic Importance of Subclinical Cardiovascular Disease in Overweight and Obese Individuals Circulation, July 24, 2007; 116(4): 375 - 384. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Mitsuhashi, H. Yatsuya, K. Tamakoshi, K. Matsushita, R. Otsuka, K. Wada, K. Sugiura, S. Takefuji, Y. Hotta, T. Kondo, et al. Adiponectin Level and Left Ventricular Hypertrophy in Japanese Men Hypertension, June 1, 2007; 49(6): 1448 - 1454. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Salles, C. Cardoso, A. R. Nogueira, K. Bloch, and E. Muxfeldt Importance of the Electrocardiographic Strain Pattern in Patients With Resistant Hypertension Hypertension, September 1, 2006; 48(3): 437 - 442. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. Pontiroli, F. Folli, M. Paganelli, G. Micheletto, P. Pizzocri, P. Vedani, F. Luisi, L. Perego, A. Morabito, and S. Bressani Doldi Laparoscopic Gastric Banding Prevents Type 2 Diabetes and Arterial Hypertension and Induces Their Remission in Morbid Obesity: A 4-year case-controlled study Diabetes Care, November 1, 2005; 28(11): 2703 - 2709. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Perego, P. Pizzocri, D. Corradi, F. Maisano, M. Paganelli, P. Fiorina, M. Barbieri, A. Morabito, G. Paolisso, F. Folli, et al. Circulating Leptin Correlates with Left Ventricular Mass in Morbid (Grade III) Obesity before and after Weight Loss Induced by Bariatric Surgery: A Potential Role for Leptin in Mediating Human Left Ventricular Hypertrophy J. Clin. Endocrinol. Metab., July 1, 2005; 90(7): 4087 - 4093. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verdecchia, G. Carini, A. Circo, E. Dovellini, E. Giovannini, M. Lombardo, P. Solinas, M. Gorini, A. P. Maggioni, and the MAVI Study Group Left ventricular mass and cardiovascular morbidity in essential hypertension: the MAVI study J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1829 - 1835. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verdecchia, C. Porcellati, G. Reboldi, R. Gattobigio, C. Borgioni, T. A. Pearson, and G. Ambrosio Left Ventricular Hypertrophy as an Independent Predictor of Acute Cerebrovascular Events in Essential Hypertension Circulation, October 23, 2001; 104(17): 2039 - 2044. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||