| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2000;35:6.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From Copenhagen County University Hospital (K.W., H.I., J.R.), Glostrup, Denmark; The New York Hospital-Cornell Medical Center (J.N.B., M.J.R., R.B.D.), New York, NY; Rush Presbyterian St. Lukes Medical Center (P.R.L.), Chicago, Ill; Haukeland Hospital (E.G.), Bergen, Norway; Sahlgrenska University Hospital-Östra (B.D.), Göteborg, Sweden; Helsinki University Central Hospital (T.A.), Helsinki, Finland; and Veterans Administration Hospital (V.P.), Washington, DC.
Correspondence to Dr Kristian Wachtell, Laboratory of Cardiology, Department of Medicine, Copenhagen County University Hospital, Glostrup, DK-2600 Glostrup, Denmark. E-mail wachtell{at}dadlnet.dk
| Abstract |
|---|
|
|
|---|
Key Words: echocardiography electrocardiography hypertrophy, left ventricular hypertension, essential
| Introduction |
|---|
|
|
|---|
The relation between LVMI and RWT seems important in view of the fact that several studies have shown that stratification by different geometric patterns gives valuable information concerning morbidity and mortality. In these studies, subjects with concentric hypertrophy (ie, increased RWT and LVMI) had the highest incidence of cardiovascular events and death, those with eccentric hypertrophy or concentric remodeling had intermediate rates, and those with normal LV geometry had the least complications.2 6 12 15 16 17 18 However, studies have used a variety of partition values (PVs) for LV mass and RWT to identify LV hypertrophy and geometric remodeling. To date, no study has evaluated the effect of the different indexation methods and PVs for LV hypertrophy and concentric geometry on the distributions of abnormal geometric patterns in a large hypertensive population. The present study compares the impact of various methods of indexing LV mass and calculating RWT on the distributions and correlates of abnormal LV geometric patterns in a large series of subjects with stage I to III hypertension.19
| Methods |
|---|
|
|
|---|
11% of the overall 9194 LIFE participants. In the LIFE
echocardiography study, 2-dimensional and M-mode
echocardiograms were obtained at baseline.22 The study was
carried out in selected echocardiography centers in
Denmark, Finland, Great Britain, Iceland, Norway, Sweden, and the
United States. Before enrollment in the study, all subjects had a
screening ECG that defined LV hypertrophy, a criterion for
enrollment in the LIFE study, by either gender-adjusted Cornell voltage
duration criteria, calculated as (SV3+RaVL
[+6 mm for women])xQRS
2440 mmxms, or Sokolow-Lyon
voltage criteria, calculated as
SV1+RV5/RV6>38
mm. 20 Patients with an aortic valve pressure gradient
>20 mm Hg, symptomatic heart failure, or LV ejection
fraction <40% were excluded from the study. The composite ECG
criterion used for LIFE recruitment was based on results of previous
studies in our laboratory23 24 25 anticipated to have
94% to 96% specificity and 45% to 50% sensitivity. Pilot data
suggested that anatomic LV hypertrophy would be present
in
18% to 22% of hypertensive patients free of the several
exclusion criteria for the LIFE study (lack of severe LV dysfunction,
heart failure, or angina requiring therapy with
angiotensin-converting enzyme inhibitors,
angiotensin II receptor blockers, or ß-blockers,
myocardial infarction or stroke in the past 6 months, or blood pressure
that rose to >200 mm Hg systolic or 115 mm Hg
diastolic during a run-in period of placebo treatment).
Taken together, these estimates yielded projections indicating that
from 62% to 78% of LIFE patients would have anatomic LV
hypertrophy detectable by echocardiography.
After a run-in period that documented eligible levels of clinic
arterial pressure during 14±9 days of placebo treatment,
subjects underwent baseline evaluation. Arterial blood
pressure was also measured by arm-cuff sphygmomanometer at the end of
the echocardiographic examination, after subjects had
been resting supine in a dimly lit room for
30 minutes.
Echocardiographic Methods and Performance
Protocol
Echocardiographic procedures for the present
study were designed with regard to the special difficulties of
performing objective skill-dependent cardiac tests in a multicenter
trial and were based on previously used procedures.26 27 28
Standardized examinations included 2-dimensional guided M-mode
echocardiograms and selected 2-dimensional and Doppler
recordings. Study performance and interpretation
focused on selected measures of LV mass and geometry, global and
regional systolic LV function, and diastolic
filling, maximizing the yield of reliable data to answer specific study
questions.
Before initiation of the study, formal training sessions were held at The New York Hospital-Cornell Medical Center or Ullevål University Hospital, Oslo, Norway; these training sessions combined didactic teaching of selected relevant aspects of echocardiography, the specific protocol, and hands-on training in performing echocardiograms according to the study protocol. Studies were performed with high-quality commercially available echocardiograms equipped with 3.0- to 3.5-MHz and 2.0- to 2.5-MHz probes and VHS or Super-VHS video recorders. To facilitate performance of standardized quantifiable echocardiograms, examining tables with special cutouts were used. Recordings were made from the parasternal window by a standardized protocol to record at least 10 consecutive beats of 2-dimensional and M-mode recordings of the LV internal diameter and wall thicknesses at or just below the tips of the anterior mitral leaflet in both long-axis and short-axis views, with long-axis views of the mitral valve, color Doppler flow recordings to search for mitral and aortic regurgitation, and M-mode and 2-dimensional short-axis and long-axis views of the aortic valve and the left atrium. The apical acoustic window was used to record at least 10 cycles of 2- and 4-chamber images to assess LV wall motion and color flow or pulsed Doppler recording to identify mitral and aortic regurgitation. Studies were sent to The New York Hospital-Cornell University Medical Center for blinded interpretation by experienced technicians and physicians.
Echocardiographic Measurements
Correct orientation of planes for imaging and Doppler
recording was verified as previously
described.26 28 Measurements were made blindly by using
computerized review stations (Digisonics, Inc) equipped with NTSC or
PAL standard VCRs and digitizing tablet and monitor screen
overlay for calibration and performance of measurements. LV
internal dimension and interventricular septal and
posterior wall thicknesses were measured at end diastole
and end systole for up to 3 cycles by recommendation of the American
Society of Echocardiography.29 When
optimal orientation of the LV views could not be obtained, as is common
in subjects who are overweight or over age 60, correctly oriented
2-dimensional linear dimension measurements were made by the
leading-edge convention of the American Society of
Echocardiography.30
Calculation of Derived Variables
End-diastolic LV dimensions were used to calculate
LV mass by a formula shown to yield LV mass values closely related
(r=0.90) to necropsy measurements,31 with
excellent interstudy reproducibility (
=0.93), in a separate series
of 183 hypertensive patients.32 LV mass indexation was
performed by a variety of different methods and PVs for men and women:
Values of LV mass/BSA were 116 g/m2 for men and
104 g/m2 for women,6 27 125
g/m2 for men and 110 g/m2
for women,33 131 g/m2 for men and
100 g/m2 for women,34 or 125
g/m2 for men and women.2 4 Values of
LV mass/height were 143 g/m for men and 102 g/m for
women34 or 126 g/m for men and 105 g/m for
women.10 Values of LV mass/height2.7
were 51 g/m2.7 for men and women10
or 49.2 g/m2.7 for men and 46.7
g/m2.7 for women.10 BSA was
calculated by using the Du Bois formula35 :
0.007184x(weight [kg])0.425x(height
[cm])0.725. Overweight was identified by body
mass index >27.8 kg/m2 in men and 27.3
kg/m2 in women.36 RWT was calculated
as either 2xposterior wall thickness in diastole/LV
internal diameter (RWT1)13 or as
(interventricular septal+posterior wall thickness)/LV
internal diameter (RWT2).14
Increased RWT was present when this ratio of
RWT1 exceeded 0.43, which represents the
97.5th percentile in normal subjects37 or when
RWT2 exceeded 0.45,14 which
represents the 96th percentile in our normal
subjects.37 Disproportionate interventricular
septal thickening was present if interventricular
septal thickness/posterior wall thickness was
1.5.38 All
normal values were checked in our database of an apparently normal
population (n=362) from New York.37
Normal geometry was present when LVMI and RWT were normal, whereas normal LVMI and increased RWT identified concentric remodeling. Increased LVMI but normal RWT identified eccentric LV hypertrophy, and increases of both variables identified concentric LV hypertrophy.12
Statistics
Microsoft Access 97 (Microsoft Corp) and SPSS software version
8.0 (SPSS, Inc) were used for data management and statistical
analysis. Data are presented as mean±SD or frequency
in percent. Differences between 2 groups were assessed by unpaired
Student t test; comparison among multiple groups was
performed by ANOVA with the Scheffé post hoc test. Differences in
prevalences between subgroups were compared by
2 statistics. Univariate relations
between variables were assessed by Pearson correlation
coefficients. Independent correlates of continuous measures of LV
structure and function were identified by linear regression
analysis using an enter procedure with assessment of
collinearity diagnostics. A 2-tailed value of
P<0.05 was considered statistically significant.
| Results |
|---|
|
|
|---|
|
LV Measurements
Mean systolic endocardial function was in the normal range
with fractional shortening of 33±6%; LV ejection fraction was
61±8%. Compared with data from a large previously studied population
of apparently normal adults,37 LIFE subjects had greater
interventricular septal thickness (1.16±0.13 versus
0.89±0.12 cm), posterior wall thickness (1.07±0.16 versus 0.82±0.12
cm), LV end-diastolic dimension (5.29±0.57 versus
4.89±0.45 cm), end-systolic dimension (3.55±0.62 versus
3.08±0.38 cm), LV mass (234.7±54.1 versus 146.1±38.1 g), LV mass/BSA
(124.0±26.7 versus 78.6±15.9 g/m2), LV
mass/height2.7 (56.6±13.8 versus 34.5±7.2
g/m2.7), and RWT (0.41±0.06 versus 0.35±0.07)
(all P<0.001). Disproportionate
interventricular septal thickening was an uncommon finding,
occurring in 0.2% of LIFE subjects and in none of the apparently
normal adults (P=NS).
LV Geometric Patterns
Overall, the prevalence of echocardiographic LV
hypertrophy by our primary gender-specific PVs of 104
g/m2 in women and 116 g/m2
in men was 71%, within the range of 62% to 78% to be expected from
previous studies comparing ECG and anatomic evidence of LV
hypertrophy. Distributions of abnormal geometric patterns
are presented in Table 2 with the
use of RWT1 assessment and Table 3 with the use of
RWT2 assessment. Some form of abnormal geometry
was present in 63% to 86% of LIFE subjects when
RWT1 was used (Table 2), depending on LV
mass PV criteria. Slightly lower prevalences (61% to 84%) were found
when RWT2 and the same LV mass PVs were used
(Table 3).
|
|
Depending on the method of LV mass indexation and the PV used, LV hypertrophy was present in 42% to 77% of subjects. With use of RWT1 (Table 2), the most common geometric abnormality was eccentric hypertrophy (28% to 51%), with concentric hypertrophy present in 19% to 26% and concentric remodeling present in 8% to 20%. For individual PVs using RWT1, concentric LV hypertrophy was the second most common geometric abnormality with use of an LV mass/BSA PV of 116/104 g/m2, an LV mass/height PV of 126/105 g/m, and gender-specific criteria for LV mass/height2.7. When other PVs were used to detect LV hypertrophy, normal LV geometry and, in one instance, concentric LV remodeling were more common than concentric hypertrophy. Comparative data from our reference population37 revealed that 5% to 8% had abnormal LV geometry with use of various LV mass indexation methods and PVs together with RWT1. LV mass/BSA PV of 125/125 g/m2 gave the least separation, and LV mass/height PV of 126/105 g/m gave the highest separation of abnormal geometry prevalence between normal adults and LIFE subjects (Table 2). Classification of LV geometry in subjects with RWT2 calculated as interventricular septal+posterior wall thickness)/LV internal dimension produced slightly lower prevalences of abnormal LV geometric patterns (Table 3).
Comparison of LV geometric patterns by gender (Table 4) produced nearly identical distributions of LV geometric patterns in women and men for LV mass/BSA PVs of 116/104 and 125/110 g/m2 and LV mass/height2.7 PV of 51 g/m2.7. LV mass/BSA PV of 131/100 g/m2, LV mass/height PV of 143/102 g/m, and LV mass/height2.7 PV of 49.2/46.7 g/m2.7 produced significantly higher prevalences of eccentric and concentric hypertrophy and lower prevalences of normal LV geometry and concentric remodeling in women than in men.
|
Patients were cross-classified as having LV hypertrophy by
use of gender-specific criteria for either LV mass/BSA (
116 and
104
g/m2) or LV mass/height2.7
(
49.2 and
46.7 g/m2.7), by both or by
neither, to identify 2 concordant and 2 discordant groups (Table 5). LV mass was highest in the group with
LV hypertrophy by both sets of criteria, lowest in the
group without hypertrophy by either criterion, and
intermediate in the groups with LV hypertrophy by only 1
criterion. Subjects included only by LV mass/BSA had significantly
higher systolic and diastolic blood pressure than
did those included only by LV mass/height2.7.
Patients with LV hypertrophy by LV
mass/height2.7 were significantly overweight,
whereas patients included only by LV mass/BSA had, on average, ideal
body weight.
|
| Discussion |
|---|
|
|
|---|
70% had LV hypertrophy by our primary LV mass/BSA
criteria27 and the remainder had LV mass in the normal
range. Echocardiographic measurements of LV wall thickness and mass have facilitated research on the range and determinants of LV mass in normal individuals7 10 11 28 39 40 41 42 43 44 45 and on the prognostic implications of LV hypertrophy.1 2 3 4 5 6 10 15 16 17 18 Different methods have been used to calculate and index LV mass and to calculate RWT, but only a few studies have systematically assessed the impact of the use of different methods.7 10 33 46 The present study, in a large population of patients with moderate to severe hypertension as manifested by elevated blood pressure levels, ECG evidence of target organ involvement, and the prevalence of clinical cardiovascular disease,20 21 reveals wide ranges of the prevalence of LV hypertrophy (from 42% to 78%) and of normal LV geometry (from 15% to 40%) depending on the choice of criteria (Tables 2 and 3). One important factor in causing this variability, noted in a previous study,33 is the reciprocal relation between sensitivity and specificity that is shown in Table 2. All approaches to detection of abnormal LV geometry (ie, concentric remodeling and eccentric or concentric hypertrophy) had negative predictive values between 92% and 95% in apparently normal adults and positive predictive values of 63% to 86% in LIFE patients. However, even with criteria that had the highest negative predictive values for LV hypertrophy, the large majority of LIFE patients had LV hypertrophy or concentric remodeling. In addition, eccentric LV hypertrophy was consistently the most common geometric abnormality. In combination with any method of LV mass indexation and the use of any PV to recognize LV hypertrophy, use of RWT2 caused a shift in the prevalence of LV geometric patterns from concentric remodeling and hypertrophy to normal geometry and eccentric hypertrophy (Table 3). This occurred because the RWT2 method used a higher PV (0.45 versus 0.43). In addition, the prevalence of abnormal geometry was, on average, slightly lower using RWT2 than RWT1.
One notable result of the present study is that some but not other
criteria for abnormal LV geometry resulted in unequal distribution of
geometric patterns between men and women. The indices that gave the
most similar distribution of LV geometric patterns in men and women
were LV mass/BSA PV of 116/104 or 125/110 g/m2
and LV mass/height2.7 PV of 51/51 or 49.2/46.7
g/m2.7, the first and last of which had been
chosen a priori for main analyses of the LIFE
echocardiography study. Other criteria, including
LV mass/BSA PV of 131/100 g/m2 and LV mass/height
PV of 143/102 g/m gave substantially higher prevalences of LV
hypertrophy in women. A higher prevalence of LV
hypertrophy in women by these PVs had already been reported
by Levy et al34 in the Framingham population. Only 1
criterion (LV mass/BSA PV 125/125 g/m2) resulted
in higher prevalence of LV geometric abnormality in men. The finding of
concentric LV remodeling in
10% of LIFE patients indicates that an
appreciable proportion of hypertensive patients selected on the basis
of the ECG features and other criteria used for enrollment in the
present study have an LV geometric pattern that constitutes a
"false-positive" diagnosis with respect to LV
hypertrophy but is itself associated with an adverse
prognosis.2 15 16 18
By examining the concordance and discordance between the presence of LV hypertrophy by gender-specific criteria based on indexation of LV mass for BSA or height2.7, we found discordant groups, constituting 10% of LIFE patients, that had LV hypertrophy by only 1 criterion. One notable result was that those in whom hypertrophy was identified by the LV mass/height2.7 criterion were significantly more obese and had moderate hypertension, whereas those identified only by LV mass/BSA were of approximately ideal body weight and more severely hypertensive than those in the concordant groups with or without LV hypertrophy by both criteria. We found no significant difference in associated abnormalities, including serum creatinine levels, prevalence of diabetes, angina, previous myocardial infarction or cerebral stroke, or the presence of peripheral arterial disease, suggesting no great difference in clinical outcome among these groups. Although the present study will not have results concerning the impact of LV indexatation and PVs on the prediction of morbidity and mortality until the end of the LIFE trial,20 21 the prospective design and large number of subjects in the LIFE echocardiography study will, in due time, give us valuable information concerning clinical outcome.
In conclusion, some form of LV geometric remodeling was present in 62% to 82% of patients, with eccentric LV hypertrophy as the most common geometric abnormality with the use of any method of LV mass indexation and PV (28% to 51%). The mode of calculation of RWT did not substantially affect results. Patients with hypertrophy by only LV mass/height2.7 PV of 49.2/46.7 g/m2.7 were more obese, whereas those identified by only LV mass/BSA with PV of 116/104 g/m2 were less obese and more hypertensive than those in the 2 concordant groups with or without LV hypertrophy by both criteria.
| Acknowledgments |
|---|
Received May 25, 1999; first decision July 20, 1999; accepted August 12, 1999.
| References |
|---|
|
|
|---|
2. 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;114:345352.
3.
Liao Y, Cooper RS, McGee DL, Mensah GA, Ghali JK. The
relative effects of left ventricular
hypertrophy, coronary artery disease, and
ventricular dysfunction on survival among black adults.
JAMA. 1995;273:15921597.
4. Casale PN, Devereux RB, Milner M, Zullo G, Harshfield GA, Pickering TG, Laragh JH. Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Ann Intern Med. 1986;105:173178.
5. Devereux RB, de Simone G, Koren MJ, Roman MJ, Laragh JH. Left ventricular mass as a predictor of development of hypertension. Am J Hypertens. 1991;4:603S607S.[Medline] [Order article via Infotrieve]
6. Ghali JK, Liao Y, Simmons B, Castaner A, Cao G, Cooper RS. The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease. Ann Intern Med. 1992;117:831836.
7. de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol. 1992;20:12511260.[Abstract]
8. Lauer MS, Okin PM, Anderson KM, Levy D. Impact of echocardiographic left ventricular mass on mechanistic implications of exercise testing parameters. Am J Cardiol. 1995;76:952956.[Medline] [Order article via Infotrieve]
9.
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;23:600606.
10. de Simone G, Devereux RB, Daniels SR, Koren MJ, Meyer RA, Laragh JH. Effect of growth on variability of left ventricular mass: assessment of allometric signals in adults and children and their capacity to predict cardiovascular risk. J Am Coll Cardiol. 1995;25:10561062.[Abstract]
11. Daniels SR, Kimball TR, Morrison JA, Khoury P, Meyer RA. Indexing left ventricular mass to account for differences in body size in children and adolescents without cardiovascular disease. Am J Cardiol. 1995;76:699701.[Medline] [Order article via Infotrieve]
12. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, Vargiu P, Simongini I, Laragh JH. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19:15501558.[Abstract]
13. Reichek N, Devereux RB. Reliable estimation of peak left ventricular systolic pressure by M-mode echographic-determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients. Am Heart J. 1982;103:202209.[Medline] [Order article via Infotrieve]
14. Verdecchia P, Porcellati C, Zampi I, Schillaci G, Gatteschi C, Battistelli M, Bartoccini C, Borgioni C, Ciucci A. Asymmetric left ventricular remodeling due to isolated septal thickening in patients with systemic hypertension and normal left ventricular masses. Am J Cardiol. 1994;73:247252.[Medline] [Order article via Infotrieve]
15. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Bartoccini C, Santucci A, Santucci C, Reboldi G, Porcellati C. Adverse prognostic significance of concentric remodeling of the left ventricle in hypertensive patients with normal left ventricular mass. J Am Coll Cardiol. 1995;25:871878.[Abstract]
16. Krumholz HM, Larson M, Levy D. Prognosis of left ventricular geometric patterns in the Framingham Heart Study. J Am Coll Cardiol. 1995;25:879884.[Abstract]
17. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Santucci A, Santucci C, Reboldi G, Porcellati C. Prognostic value of left ventricular mass and geometry in systemic hypertension with left ventricular hypertrophy. Am J Cardiol. 1996;78:197202.[Medline] [Order article via Infotrieve]
18.
Ghali JK, Liao Y, Cooper RS. Influence of left
ventricular geometric patterns on prognosis in patients
with or without coronary artery disease. J Am Coll
Cardiol. 1998;31:16351640.
19.
Joint National Committee on Detection, Evaluation, and
Treatment of High Blood Pressure. The Fifth Report of the Joint
National Committee on Detection, Evaluation, and Treatment of High
Blood Pressure (JNC V). Arch Intern Med. 1993;153:154183.
20. Dahlof B, Devereux RB, de Faire U, Fyhrquist F, Hedner T, Ibsen H, Julius S, Kjeldsen S, Kristianson K, Lederballe-Petersen O, Omvik P, Nieminen MS, Oparil S, Wedel H. The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension Study. Am J Hypertens. 1997;10:705713.[Medline] [Order article via Infotrieve]
21.
Dahlof B, Devereux RB, Julius S, Kjeldsen SE, Beevers
G, de Faire U, Fyhrquist F, Hedner T, Ibsen H, Kristianson K, et al.
Characteristics of 9194 patients with left ventricular
hypertrophy: the LIFE study. Hypertension. 1998;32:989997.
22. Devereux RB, Bella JN, Dahlof B, Gerdts E, Nieminen MS, Nielsen JR, Papademetriou V. Left ventricular geometry and function in hypertensive patients with ECG left ventricular hypertrophy: the LIFE trial. J Am Coll Cardiol. 1998;31(suppl A):376A. Abstract.
23. 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;20:11801186.[Abstract]
24. 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;25:417423.[Abstract]
25. Okin PM, Roman MJ, Devereux RB, Kligfield P. Electrocardiographic identification of left ventricular hypertrophy: test performance in relation to definition of hypertrophy and presence of obesity. J Am Coll Cardiol. 1996;27:124131.[Abstract]
26. Devereux RB, Roman MJ. Evaluation of cardiac function and vascular structure and function by echocardiography and other noninvasive techniques. In: Laragh JH, Brenner BM, ed. Hypertension: Pathophysiology, Diagnosis, and Management. 2nd ed. New York, NY: Raven Press Ltd; 1995:19691985.
27. Devereux RB, Dahlof B, Levy D, Pfeffer MA. Comparison of enalapril versus nifedipine to decrease left ventricular hypertrophy in systemic hypertension (the PRESERVE trial). Am J Cardiol. 1996;78:6165.[Medline] [Order article via Infotrieve]
28.
Devereux RB, Roman MJ, de Simone G, OGrady MJ,
Paranicas M, Yeh JL, Fabsitz RR, Howard BV. Relations of left
ventricular mass to demographic and
hemodynamic variables in American Indians: the
Strong Heart Study. Circulation. 1997;96:14161423.
29.
Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations
regarding quantitation in M-mode echocardiography:
results of a survey of echocardiographic measurements.
Circulation. 1978;58:10721083.
30. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux RB, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman NH, Tajik AJ. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989;2:358367.[Medline] [Order article via Infotrieve]
31. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986;57:450458.[Medline] [Order article via Infotrieve]
32.
Palmieri V, Dahlöf B, DeQuattro V, Sharpe N,
Bella JN, de Simone G, Paranicas M, Fishman D, Devereux RB. Reliability
of echocardiographic assessment of left ventricular structure and
function: The Preserve Study. J Am Coll Cardiol. 1999;34:16251632.
33. Hammond IW, Devereux RB, Alderman MH, Lutas EM, Spitzer MC, Crowley JS, Laragh JH. The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension. J Am Coll Cardiol. 1986;7:639650.[Abstract]
34. Levy D, Savage DD, Garrison RJ, Anderson KM, Kannel WB, Castelli WP. Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol. 1987;59:956960.[Medline] [Order article via Infotrieve]
35. Du Bois D, Du Bois E. A formula to estimate the approximate surface area if height and weight be known. Arch Intern Med. 1916;17:863871.
36. National Institutes of Health Consensus Development Conference. Health implications of obesity. Ann Intern Med. 1985;103(pt 2):9771077.
37. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Association of carotid atherosclerosis and left ventricular hypertrophy. J Am Coll Cardiol. 1995;25:8390.[Abstract]
38. Doi YL, McKenna WJ, Gehrke J, Oakley CM, Goodwin JF. M mode echocardiography in hypertrophic cardiomyopathy: diagnostic criteria and prediction of obstruction. Am J Cardiol. 1980;45:614.[Medline] [Order article via Infotrieve]
39. Dannenberg AL, Levy D, Garrison RJ. Impact of age on echocardiographic left ventricular mass in a healthy population (the Framingham Study). Am J Cardiol. 1989;64:10661068.[Medline] [Order article via Infotrieve]
40.
Gardin JM, Siscovick D, Anton Culver H, Lynch JC, Smith
VE, Klopfenstein HS, Bommer WJ, Fried L, OLeary D, Manolio TA. Sex,
age, and disease affect echocardiographic left
ventricular mass and systolic function in the
free-living elderly: the Cardiovascular Health Study.
Circulation. 1995;91:17391748.
41. Shub C, Klein AL, Zachariah PK, Bailey KR, Tajik AJ. Determination of left ventricular mass by echocardiography in a normal population: effect of age and sex in addition to body size. Mayo Clin Proc. 1994;69:205211.[Medline] [Order article via Infotrieve]
42. Devereux RB, Lutas EM, Casale PN, Kligfield P, Eisenberg RR, Hammond IW, Miller DH, Reis G, Alderman MH, Laragh JH. Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Coll Cardiol. 1984;4:12221230.[Abstract]
43. Savage DD, Garrison RJ, Kannel WB, Levy D, Anderson SJ, Stokes J III, Feinleib M, Castelli WP. The spectrum of left ventricular hypertrophy in a general population sample: the Framingham Study. Circulation. 1987;75(suppl I, pt 2):I-26I-33.
44. Hammond IW, Devereux RB, Alderman MH, Laragh JH. Relation of blood pressure and body build to left ventricular mass in normotensive and hypertensive employed adults. J Am Coll Cardiol. 1988;12:9961004.[Abstract]
45. Jones EC, Devereux RB, OGrady MJ, Schwartz JE, Liu JE, Pickering TG, Roman MJ. Relation of hemodynamic volume load to arterial and cardiac size. J Am Coll Cardiol. 1997;29:13031310.[Abstract]
46. Liao Y, Cooper RS, Durazo-Arvizu R, Mensah GA, Ghali JK. Prediction of mortality risk by different methods of indexation for left ventricular mass. J Am Coll Cardiol. 1997;29:641647.[Abstract]
This article has been cited by other articles:
![]() |
N. Reichek, R. B. Devereux, R. A. Rocha, R. Hilkert, D. Hall, D. Purkayastha, and B. Pitt Magnetic Resonance Imaging Left Ventricular Mass Reduction With Fixed-Dose Angiotensin-Converting Enzyme Inhibitor-Based Regimens in Patients With High-Risk Hypertension Hypertension, October 1, 2009; 54(4): 731 - 737. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Dimopoulos, F. Nicosia, P. Donati, P. Prometti, M. De Vecchi, R. Zulli, and V. Grassi QT Dispersion and Left Ventricular Hypertrophy in Elderly Hypertensive and Normotensive Patients Angiology, October 1, 2008; 59(5): 605 - 612. [Abstract] [PDF] |
||||
![]() |
E. Gerdts, P. M. Okin, G. de Simone, D. Cramariuc, K. Wachtell, K. Boman, and R. B. Devereux Gender Differences in Left Ventricular Structure and Function During Antihypertensive Treatment: The Losartan Intervention for Endpoint Reduction in Hypertension Study Hypertension, April 1, 2008; 51(4): 1109 - 1114. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. J. Meyers, T. H. Mosley, E. Fox, E. Boerwinkle, D. K. Arnett, R. B. Devereux, and S. L.R. Kardia Genetic Variations Associated With Echocardiographic Left Ventricular Traits in Hypertensive Blacks Hypertension, May 1, 2007; 49(5): 992 - 999. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Persson, E. Lonn, M. Edner, L. Baruch, C. C. Lang, J. J. Morton, J. Ostergren, R. S. McKelvie, and for the Investigators of the CHARM Echocardiograph Diastolic Dysfunction in Heart Failure With Preserved Systolic Function: Need for Objective Evidence: Results From the CHARM Echocardiographic Substudy-CHARMES J. Am. Coll. Cardiol., February 13, 2007; 49(6): 687 - 694. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. S. Vasan Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations Circulation, May 16, 2006; 113(19): 2335 - 2362. [Full Text] [PDF] |
||||
![]() |
A. Morganti Randomized Clinical Trials on Surrogate End Points: Are They Useful for Evaluating Cardiovascular and Renal Disease Protection in Hypertension? The Case for Yes J. Am. Soc. Nephrol., April 1, 2006; 17(4_suppl_2): S141 - S144. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Wachtell, M. Lehto, E. Gerdts, M. H. Olsen, B. Hornestam, B. Dahlof, H. Ibsen, S. Julius, S. E. Kjeldsen, L. H. Lindholm, et al. Reply J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1585 - 1586. [Full Text] [PDF] |
||||
![]() |
S.-H. Hank Juo, M. R. Di Tullio, H.-F. Lin, T. Rundek, B. Boden-Albala, S. Homma, and R. L. Sacco Heritability of Left Ventricular Mass and Other Morphologic Variables in Caribbean Hispanic Subjects: The Northern Manhattan Family Study J. Am. Coll. Cardiol., August 16, 2005; 46(4): 735 - 737. [Full Text] [PDF] |
||||
![]() |
M. H. Drazner, D. L. Dries, R. M. Peshock, R. S. Cooper, C. Klassen, F. Kazi, D. Willett, and R. G. Victor Left Ventricular Hypertrophy Is More Prevalent in Blacks Than Whites in the General Population: The Dallas Heart Study Hypertension, July 1, 2005; 46(1): 124 - 129. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Wachtell, M. Lehto, E. Gerdts, M. H. Olsen, B. Hornestam, B. Dahlof, H. Ibsen, S. Julius, S. E. Kjeldsen, L. H. Lindholm, et al. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: The Losartan Intervention For End point reduction in hypertension (LIFE) study J. Am. Coll. Cardiol., March 1, 2005; 45(5): 712 - 719. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Glorioso, F. Filigheddu, P. P. Parpaglia, A. Soro, C. Troffa, G. Argiolas, and P. Mulatero 11{beta}-Hydroxysteroid dehydrogenase type 2 activity is associated with left ventricular mass in essential hypertension Eur. Heart J., March 1, 2005; 26(5): 498 - 504. [Abstract] [Full Text] [PDF] |
||||
![]() |
G S Bleumink, A F C Schut, M C J M Sturkenboom, J A M J L Janssen, J C M Witteman, C M van Duijn, A Hofman, and B H C. Stricker A promoter polymorphism of the insulin-like growth factor-I gene is associated with left ventricular hypertrophy Heart, February 1, 2005; 91(2): 239 - 240. [Full Text] [PDF] |
||||
![]() |
G. de Simone, S. R. Daniels, T. R. Kimball, M. J. Roman, C. Romano, M. Chinali, M. Galderisi, and R. B. Devereux Evaluation of Concentric Left Ventricular Geometry in Humans: Evidence for Age-Related Systematic Underestimation Hypertension, January 1, 2005; 45(1): 64 - 68. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Nunez, D. K. Arnett, E. J. Benjamin, P. R. Liebson, T. N. Skelton, H. Taylor, and M. Andrew Optimal Threshold Value for Left Ventricular Hypertrophy in Blacks: The Atherosclerosis Risk in Communities Study Hypertension, January 1, 2005; 45(1): 58 - 63. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. B. Devereux, K. Wachtell, E. Gerdts, K. Boman, M. S. Nieminen, V. Papademetriou, J. Rokkedal, K. Harris, P. Aurup, and B. Dahlof Prognostic Significance of Left Ventricular Mass Change During Treatment of Hypertension JAMA, November 17, 2004; 292(19): 2350 - 2356. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Zakynthinos, Ch. Pierutsakos, K. Konstantinidis, S. Zakynthinos, and D. Papadogiannis Losartan Reduces Left Ventricular Hypertrophy Proportionally to Blood Pressure Reduction in Hypertensives, but Does Not Affect Diastolic Cardiac Function Angiology, November 1, 2004; 55(6): 669 - 678. [Abstract] [PDF] |
||||
![]() |
E. Zakynthinos, Ch. Pierutsakos, K. Konstantinidis, S. Zakynthinos, and D. Papadogiannis Losartan Reduces Left Ventricular Hypertrophy Proportionally to Blood Pressure Reduction in Hypertensives, but Does Not Affect Diastolic Cardiac Function Angiology, November 1, 2004; 55(6): 669 - 678. [Abstract] [PDF] |
||||
![]() |
R. B. Devereux, B. Dahlof, E. Gerdts, K. Boman, M. S. Nieminen, V. Papademetriou, J. Rokkedal, K. E. Harris, J. M. Edelman, and K. Wachtell Regression of Hypertensive Left Ventricular Hypertrophy by Losartan Compared With Atenolol: The Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Trial Circulation, September 14, 2004; 110(11): 1456 - 1462. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. B. J. Mancini, B. Dahlof, and J. Diez Surrogate Markers for Cardiovascular Disease: Structural Markers Circulation, June 29, 2004; 109(25_suppl_1): IV-22 - IV-30. [Full Text] [PDF] |
||||
![]() |
M. L. Muiesan, M. Salvetti, C. Monteduro, B. Bonzi, A. Paini, S. Viola, P. Poisa, D. Rizzoni, M. Castellano, and E. Agabiti-Rosei Left Ventricular Concentric Geometry During Treatment Adversely Affects Cardiovascular Prognosis in Hypertensive Patients Hypertension, April 1, 2004; 43(4): 731 - 738. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Pitt, N. Reichek, R. Willenbrock, F. Zannad, R. A. Phillips, B. Roniker, J. Kleiman, S. Krause, D. Burns, and G. H. Williams Effects of Eplerenone, Enalapril, and Eplerenone/Enalapril in Patients With Essential Hypertension and Left Ventricular Hypertrophy: The 4E-Left Ventricular Hypertrophy Study Circulation, October 14, 2003; 108(15): 1831 - 1838. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. M. Okin, R. B. Devereux, R. R. Fabsitz, E. T. Lee, J. M. Galloway, and B. V. Howard Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the strong heart study J. Am. Coll. Cardiol., October 16, 2002; 40(8): 1395 - 1400. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Wachtell, V. Palmieri, M. H. Olsen, E. Gerdts, V. Papademetriou, M. S. Nieminen, G. Smith, B. Dahlof, G. P. Aurigemma, and R. B. Devereux Change in Systolic Left Ventricular Performance After 3 Years of Antihypertensive Treatment: The Losartan Intervention for Endpoint (LIFE) Study Circulation, July 9, 2002; 106(2): 227 - 232. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Gerdts, L. Oikarinen, V. Palmieri, J. E. Otterstad, K. Wachtell, K. Boman, B. Dahlof, and R. B. Devereux Correlates of Left Atrial Size in Hypertensive Patients With Left Ventricular Hypertrophy: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study Hypertension, March 1, 2002; 39(3): 739 - 743. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Zoccali, F. A. Benedetto, F. Mallamaci, G. Tripepi, G. Giacone, A. Cataliotti, G. Seminara, B. Stancanelli, and L. S. Malatino Prognostic Impact of the Indexation of Left Ventricular Mass in Patients Undergoing Dialysis J. Am. Soc. Nephrol., December 1, 2001; 12(12): 2768 - 2774. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Laviades, N. Varo, and J. Diez Transforming Growth Factor {beta} in Hypertensives With Cardiorenal Damage Hypertension, October 1, 2000; 36(4): 517 - 522. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Wachtell, J. N. Bella, J. Rokkedal, V. Palmieri, V. Papademetriou, B. Dahlof, T. Aalto, E. Gerdts, and R. B. Devereux Change in Diastolic Left Ventricular Filling After One Year of Antihypertensive Treatment: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study Circulation, March 5, 2002; 105(9): 1071 - 1076. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |