Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2000;35:6-12

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wachtell, K.
Right arrow Articles by Devereux, R. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wachtell, K.
Right arrow Articles by Devereux, R. B.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*High Blood Pressure
Related Collections
Right arrow Hypertrophy

(Hypertension. 2000;35:6.)
© 2000 American Heart Association, Inc.


Scientific Contributions

Impact of Different Partition Values on Prevalences of Left Ventricular Hypertrophy and Concentric Geometry in a Large Hypertensive Population

The LIFE Study

Kristian Wachtell; Jonathan N. Bella; Philip R. Liebson; Eva Gerdts; Björn Dahlöf; Tapio Aalto; Mary J. Roman; Vasilios Papademetriou; Hans Ibsen; Jens Rokkedal; Richard B. Devereux

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. Luke’s 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
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Abstract—Left ventricular (LV) hypertrophy and concentric remodeling have been defined by using a variety of indexation methods and partition values (PVs) for LV mass and relative wall thickness (RWT). The effects of these methods on the distribution of LV geometric patterns in hypertensive subjects remain unclear. Echocardiograms were obtained in 941 patients with stage I to III hypertension and LV hypertrophy by ECG. LV mass was calculated by using different methods of indexation for body size and different PVs to identify hypertrophy: LV mass/body surface area (g/m2) PV for men/women 116/104, 125/110, or 125/125; LV mass/height (g/m) PV 143/102 or 126/105; and LV mass/height2.7 (g/m2.7) PV 51/51 or 49.2/46.7. RWT was calculated by either 2xend-diastolic posterior wall thickness (PWT)/end-diastolic LV internal dimension (LVID) or end-diastolic interventricular septum dimension+end-diastolic PWT/end-diastolic LVID. LV hypertrophy or remodeling was present in 63% to 86% of subjects, and LV hypertrophy was present in 42% to 77%. By any index, eccentric hypertrophy was the common LV geometric pattern. Use of interventricular septum dimension+PWT/LVID to calculate RWT slightly increased the prevalence of normal geometry and eccentric hypertrophy compared with the use of 2xPWT/LVID. Subjects with LV hypertrophy identified by only LV mass/height2.7 PV 49.2/46.7 were more obese, whereas those identified by only LV mass/body surface area PV 116/104 were taller and thinner than those in the 2 concordant groups with or without LV hypertrophy by both criteria. By either criterion, there were no significant differences between different LV geometric patterns in clinical cardiovascular disease. Hypertensive patients with LV hypertrophy by ECG have a high prevalence of geometric abnormalities, especially eccentric hypertrophy, irrespective of method of indexation or PV. LV mass indexation by body surface area or height2.7 identifies lean and obese subjects, respectively. We found no difference in prevalent cardiovascular disease in subjects identified by either criterion, suggesting a similar high risk.


Key Words: echocardiography • electrocardiography • hypertrophy, left ventricular • hypertension, essential


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Left ventricular (LV) hypertrophy, as determined by echocardiography, has been shown to be a strong predictor of adverse prognosis independent of and, in most instances, stronger than conventional risk factors.1 2 3 On the basis of distributions of indexed echocardiographic LV mass in normal populations, LV hypertrophy has been identified by calculation of LV mass that has been indexed for body surface area (BSA)1 4 5 6 or for BSA1.5,7 height, height2.0,8 height2.13,9 height2.7,7 9 10 or height3.0.11 The combination of LV mass index (LVMI) and relative wall thickness (RWT) has been used to identify 3 different abnormal LV geometric patterns.2 12 RWT has been calculated either as the ratio of 2xposterior wall thickness/LV internal diameter13 or as the ratio of (interventricular septal+posterior wall thickness)/LV internal diameter.14

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
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Subjects
The present study evaluated 964 patients with stage I to III hypertension enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Study,20 21 constituting {approx}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 {approx}94% to 96% specificity and 45% to 50% sensitivity. Pilot data suggested that anatomic LV hypertrophy would be present in {approx}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 {approx}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 ({rho}=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 {chi}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
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
Patient Characteristics
Descriptive data of the whole LIFE population have been reported elsewhere.20 21 Of the 964 patients in the LIFE echocardiography study, 941 had the necessary LV measurements, and thus LV geometric pattern, to be included in the present study. Characteristics of the 941 subjects are reported in Table 1.


View this table:
[in this window]
[in a new window]
 
Table 1. Descriptive Data of the 941 LIFE Participants

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).


View this table:
[in this window]
[in a new window]
 
Table 2. Distribution of LV Geometric Patterns Using Different Modes of LVMI PVs With RWT Calculated as 2xPosterior Wall Thickness/LV Internal Dimensions (RWT1)


View this table:
[in this window]
[in a new window]
 
Table 3. Distribution of LV Geometric Patterns Using Different Modes of LVMI and PVs With RWT Calculated as (Interventricular Septum+Posterior Wall Thickness)/LV Internal Diameter (RWT2)

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.


View this table:
[in this window]
[in a new window]
 
Table 4. Distribution of LV Geometric Patterns by Percentage in Men and Women With Different Modes of LVMI and PVs

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.


View this table:
[in this window]
[in a new window]
 
Table 5. Selected Characteristics According to Presence or Absence of LVH Defined by LV Mass Indexed for BSA and Height2.7


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
Although several studies have proposed limits of LV mass and RWT based on confidence intervals derived from reference populations, to our knowledge, no study has evaluated the impact of using different PVs for both these variables on the prevalence of LV geometric patterns in hypertensive patients. Performance of the present analyses in the context of the LIFE trial provided a population in which, as predicted by calculation based on the known performance of the ECG criteria used to screen individuals for LIFE, {approx}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 {approx}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
 
This study was supported by grants from Merck & Co, Inc, The Else & Mogens Wedell-Wedellsborg Foundation, Copenhagen, Denmark, and National Heart. Lung, and Blood Institute grants HL-18323 and HL-30605. We would like to thank Mary Paranicas and Dawn Fishman for their valuable work in reading echocardiograms and managing the database and Anne-Grethe Thorn for her valuable help in preparing the manuscript. Furthermore, we would like to thank the following LIFE echocardiography study investigators: from Denmark, Jens Berning (Ålborg), Per Hildebrandt (Frederiksberg), John Larsen (Næstved), Ole Lederballe Pedersen (Viborg), Jens Rokkedal (Glostrup), and Kristian Wachtell (Glostrup); from Finland, Tapio Aalto (Helsinki), Erik Engblom (Turku), Markku S. Nieminen (Helsinki), and Antti Ylitalo (Oulu); from Iceland, Yfirlæknir Gudmundur Thorgeirsson (Reykjavik); from Norway, Vernon Bonarjee (Stavanger), Gisle Fröland (Tönsberg), Eva Gerdts (Haukeland), Agathe Nuland (Ullevål), Johannes Soma (Trondheim), Gunnar Smith (Ullevål), and Asbjørn Støylen (Trondheim); from Sweden, Kurt Boman (Skellefteå), Björn Dahlöf (Göteborg), Christer Höglund (Stockholm), and Leif Härdig (Göteborg); from the United Kingdom, Frank G. Dunn (Glasgow); and from the United States, Jerome Andersen (Oklahoma City, Okla), Gerard P. Aurigemma (Worcester, Mass), Martin Berk (Charlotte, NC), Maria Canossa-Terris (Miami Beach, Fla), Albert A. Carr (Augusta, Ga), Richard B. Devereux (New York, NY), Ted Feldmen (Coral Gables, Fla), Fetnat M. Fouad-Tarazi (Cleveland, Ohio), Anekwe Onwuayi (New York, NY), Thomas Giles (New Orleans, La), Mark C. Goldberg (Tucson, Ariz), Alan H. Gradman (Pittsburgh, Pa), William Graettinger (Reno, Nev), Charles J. Kaupke (Orange, Calif), Michael J. Koren (Jacksonville, Fla), Kenneth LaBresh (Pawtucket, RI), Phillip R. Liebson (Chicago, Ill), Shawna Nesbitt (Ann Arbor, Mich), Elizebeth O. Ofili (Atlanta, Ga), Vasilious Papademetriou (Washington, DC), Gilbert J. Perry (Birmingham, Ala), Robert A. Phillips (New York, NY), Otelio S. Randall (Washington, DC), Louis Salciccioli (Brooklyn, NY), Yaga Szalachic (Downey, Calif), Matthew Weir (Baltimore, Md), Jackson Wright (Cleveland, Ohio), and Miguel Zabalgoitia (San Antonio, Tex).

Received May 25, 1999; first decision July 20, 1999; accepted August 12, 1999.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. 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]

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;114:345–352.

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;273:1592–1597.[Abstract/Free Full Text]

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;105:173–178.

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;4:603S–607S.[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;117:831–836.

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;20:1251–1260.[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;76:952–956.[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;23:600–606.[Abstract/Free Full Text]

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;25:1056–1062.[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;76:699–701.[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;19:1550–1558.[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;103:202–209.[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;73:247–252.[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;25:871–878.[Abstract]

16. Krumholz HM, Larson M, Levy D. Prognosis of left ventricular geometric patterns in the Framingham Heart Study. J Am Coll Cardiol. 1995;25:879–884.[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;78:197–202.[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;31:1635–1640.[Abstract/Free Full Text]

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;153:154–183.[Abstract/Free Full Text]

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;10:705–713.[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;32:989–997.[Abstract/Free Full Text]

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;20:1180–1186.[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;25:417–423.[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;27:124–131.[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; 1995:1969–1985.

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;78:61–65.[Medline] [Order article via Infotrieve]

28. Devereux RB, Roman MJ, de Simone G, O’Grady 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;96:1416–1423.[Abstract/Free Full Text]

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;58:1072–1083.[Abstract/Free Full Text]

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;2:358–367.[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;57:450–458.[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;34:1625–1632.[Abstract/Free Full Text]

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;7:639–650.[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;59:956–960.[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;17:863–871.

36. National Institutes of Health Consensus Development Conference. Health implications of obesity. Ann Intern Med. 1985;103(pt 2):977–1077.

37. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Association of carotid atherosclerosis and left ventricular hypertrophy. J Am Coll Cardiol. 1995;25:83–90.[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;45:6–14.[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;64:1066–1068.[Medline] [Order article via Infotrieve]

40. Gardin JM, Siscovick D, Anton Culver H, Lynch JC, Smith VE, Klopfenstein HS, Bommer WJ, Fried L, O’Leary 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;91:1739–1748.[Abstract/Free Full Text]

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;69:205–211.[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;4:1222–1230.[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-26–I-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;12:996–1004.[Abstract]

45. Jones EC, Devereux RB, O’Grady MJ, Schwartz JE, Liu JE, Pickering TG, Roman MJ. Relation of hemodynamic volume load to arterial and cardiac size. J Am Coll Cardiol. 1997;29:1303–1310.[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;29:641–647.[Abstract]




This article has been cited by other articles:


Home page
HypertensionHome page
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]


Home page
ANGIOLOGYHome page
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]


Home page
HypertensionHome page
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]


Home page
HypertensionHome page
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]


Home page
J Am Coll CardiolHome page
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]


Home page
CirculationHome page
R. S. Vasan
Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations
Circulation, May 16, 2006; 113(19): 2335 - 2362.
[Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
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]


Home page
J Am Coll CardiolHome page
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]


Home page
J Am Coll CardiolHome page
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]


Home page
HypertensionHome page
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]


Home page
J Am Coll CardiolHome page
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]


Home page
Eur Heart JHome page
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]


Home page
HeartHome page
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]


Home page
HypertensionHome page
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]


Home page
HypertensionHome page
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]


Home page
JAMAHome page
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]


Home page
ANGIOLOGYHome page
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]


Home page
ANGIOLOGYHome page
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]


Home page
CirculationHome page
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]


Home page
CirculationHome page
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]


Home page
HypertensionHome page
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]


Home page
CirculationHome page
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]


Home page
J Am Coll CardiolHome page
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]


Home page
CirculationHome page
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]


Home page
HypertensionHome page
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]


Home page
J. Am. Soc. Nephrol.Home page
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]


Home page
HypertensionHome page
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]


Home page
CirculationHome page
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]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wachtell, K.
Right arrow Articles by Devereux, R. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wachtell, K.
Right arrow Articles by Devereux, R. B.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*High Blood Pressure
Related Collections
Right arrow Hypertrophy