(Circulation. 1997;96:1416-1423.)
© 1997 American Heart Association, Inc.
Articles |
Relations of Left Ventricular Mass to Demographic and Hemodynamic Variables in American Indians
The Strong Heart Study
From the Department of Medicine, The New York (NY) Hospital–Cornell Medical Center (R.B.D., M.J.R., G. de S., M.J.O., M.P.); the Medlantic Research Institute, Washington, DC (B.V.H.); the University of Oklahoma School of Public Health Sciences, Oklahoma City (J.Y.); and the Division of Epidemiology and Disease Control, NHLBI, Bethesda, Md (R.R.F.).
Correspondence to Richard B. Devereux, MD, Division of Cardiology, Box 222, The New York Hospital–Cornell Medical Center, 525 E 68th St, New York, NY 10021. E-mail rbdevere{at}mail.med.cornell.edu
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Abstract |
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Background Previous studies have identified associations of left ventricular (LV) mass with demographic (body habitus and sex) and hemodynamic variables (blood pressure, stroke volume [SV], and myocardial contractility), but the relative strength and independence of these associations remain unknown.
Methods and Results We examined the relations of echocardiographically determined LV mass to demographic variables, blood pressure, Doppler SV, and measures of contractility (end-systolic stress [ESS]/end-systolic volume index and midwall fractional shortening [MFS] as a percentage of predicted for circumferential end-systolic stress [stress-independent shortening]) in 1935 American Indian participants in the Strong Heart Study phase 2 examination without mitral regurgitation or segmental wall motion abnormalities. Weak positive relations of LV mass with systolic and diastolic pressures (r=.22 and r=.20) were exceeded by positive relations with height (r=.30), weight (r=.47), body mass index (r=.31), body surface area (r=.49), and Doppler SV (r=.50) and negative relations with ESS/volume index ratios (r=-.33 and -.29) and stress-independent MFS (r=-.26, all P<.0001). In multivariate analyses that included blood pressure, SV, and a different contractility measure in each model, systolic pressure, stroke volume, and the contractility measure were independent correlates of LV mass (multiple R=.60 to .66, all P<.0001). When demographic variables were added, LV mass was more strongly predicted by higher SV and lower afterload-independent MFS than by greater systolic pressure, height, and body mass index (each P<.00001, multiple R=.71).
Conclusions Additional characterization of volume load and contractile efficiency improves hemodynamic prediction of LV mass (R2=.30 to .44) over the use of systolic blood pressure alone (R2=.05), with a further increase in R2 to .51 when demographic variables are also considered. However, nearly half of the ventricular mass variability remains unexplained.
Key Words: blood pressure • contractility • ventricles • echocardiography
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Introduction |
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Left ventricular hypertrophy strongly predicts morbidity and mortality in individuals with or without known cardiovascular disease,1 2 3 but factors associated with the wide variability of LV mass in the general population remain incompletely characterized. One line of investigation has identified independent relations of body build, sex, age, and arterial pressures to LV mass in population samples.4 5 6 7 Other studies have identified additional hemodynamic associations with LV mass—beyond the well-known association of blood pressure—of the level of hemodynamic volume load and myocardial contractile efficiency.8 9 10 11 However, the latter data are limited by small sizes of study populations,8 the use of potentially limited measures of SV and LV contractility,8 and reliance on experimental models such as Goldblatt hypertension or exaggerated salt intake that may not be directly applicable to most humans.8 9 10 11 It also is not known whether the associations of SV and myocardial performance with LV mass are independent of relevant demographic variables.
Accordingly, the present study was undertaken to examine the relations of echocardiographic LV mass to body size, sex, age, resting blood pressure, Doppler-derived SV, and indexes of myocardial performance in a large population of middle-aged to older adults with a wide range of body habitus and blood pressure.
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Methods |
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Subjects
Study subjects are participants in the SHS, a population-based survey of cardiovascular risk factors and prevalent and incident cardiovascular disease in American Indian communities in Arizona, Oklahoma, and South and North Dakota. As described previously,12 13 14 members 45 to 82 years of age of the (1) Gila River and Salt River Pima, Maricopa, and Akchin/Papago communities in Arizona; (2) the Seven Tribes of Southwestern Oklahoma (Apache, Caddo, Comanche, Delaware, Fort Sill Apache, Kiowa, and Wichita); and (3) Oglala and Cheyenne River Sioux and the Spirit Lake Community in South and North Dakota were recruited from all eligible individuals (overall participation rate, 62%) for an initial examination (phase 1) between July 1989 and January 1992. Extensive characterization of subjects included standardized measurement of seated brachial blood pressure; aspects of body habitus, including body mass index, waist-to-hip ratio, and percent body fat by bioelectric impedance; fasting glucose, insulin, lipid, and lipoprotein concentrations; and 2-hour glucose tolerance test and glycosylated hemoglobin levels. The SHS phase 2 examination began in August 1993 to assess change over time of most baseline measures and to add echocardiography. For the present analysis, to fulfill the assumption of symmetric LV shape underlying LV mass determination by M-mode echocardiography, participants with segmental LV dysfunction were excluded. Similarly, to assess LV volume load by Doppler echocardiographic transaortic SV, individuals with more than trivial mitral regurgitation detected by color-flow mapping were excluded.
Echocardiographic Methods
To standardize echocardiogram performance in variably
remote sites, sonographers for each center underwent local pretraining
with written materials, including a procedure manual, followed by a 1-
to 2-week training course at the Echocardiography
Reading Center in New York that incorporated hands-on studies of
patients by the SHS protocol; imaging and Doppler
parameters were measured by clinical center sonographers in
each study using a standardized worksheet. These worksheets and
telephone calls were used to communicate from the Reading Center to
examining sonographers.
Echocardiographic Performance Protocol
Studies were performed by use of commercially available
phased-array echocardiographs with M-mode, two-dimensional
and pulsed, continuous-wave and color-flow Doppler capabilities.
Specialized vans were constructed with examining tables with special
cutouts to facilitate apical imaging for use in Arizona and Oklahoma,
and similar arrangements were made in fixed Indian Health Service
facilities in the Dakotas. Subjects were examined with the head of the
examining table elevated 
30° in a partial decubitus position.
Recordings were made by a standardized protocol under which the
parasternal acoustic window was used to record at least 10
consecutive beats of two-dimensional and M-mode recordings of
the LV internal diameter and wall thicknesses at or just below the tips
of the anterior mitral leaflets in both long- and short-axis views,
long-axis views of the mitral valve and color-flow recordings
to search for mitral and aortic regurgitation, and
M-mode and two-dimensional short- and long-axis views of the aortic
root and left atrium. The apical acoustic window was used to record
at least 10 cycles of two- and four-chamber images and color
Doppler recordings to assess LV wall motion and to identify
mitral and aortic regurgitation. Pulsed Doppler
sample volumes were placed at the center of the mitral annulus in the
four-chamber view and at the aortic annulus in the apical long-axis or
"five-chamber" view to record diastolic
transmitral and systolic transaortic blood flow.
Echocardiographic Measurements
Correct orientation of planes for imaging and Doppler
recordings was verified by use of previously described
procedures.15 Measurements were made with a computerized
review station equipped with digitizing tablet and monitor screen
overlay. LV internal dimension and wall thicknesses were measured at
end diastole and end systole according to American Society
of Echocardiography recommendations16
on up to three cardiac cycles. Left atrial dimension was measured from
the trailing edge of the posterior aortic-anterior left atrial complex
to avoid including the connective tissue–filled space between these
structures erroneously in atrial size.17 When optimal
orientation of imaging views could not be obtained, as is common in
subjects who are overweight and/or >60 years of age, correctly
oriented linear dimension measurements were made with two-dimensional
imaging by the leading-edge American Society of
Echocardiography convention.18 The
diameters of the aortic annulus and aortic root at the sinuses of
Valsalva were measured in the long-axis view that maximized these
dimensions.19 Aortic annular diameter was measured from
trailing edge to leading edge at the hinging points of the aortic cusps
to the annulus; aortic root dimensions were measured by use of the
leading-edge convention.19
Doppler transaortic flow was assessed in the projection in which peak flow velocity was maximal by tracing, after calibration for velocity and time, the black-white interface of the Doppler flow envelope.20 Heart rate was measured simultaneously. Doppler color-flow maps were used to exclude mitral and aortic regurgitation or, when present, to grade their severity on a 1 to 4+ scale according to standard criteria.
Calculation of Derived Variables
End-diastolic LV dimensions were used to calculate
LV mass by an anatomically validated formula,21 relative
wall thickness as posterior wall thickness/LV radius, and
systolic fractional shortening in percent of the LV internal
dimension by standard methods.15 Aortic annular
cross-sectional area (in square centimeters) was calculated from the
measured aortic annulus and multiplied by the aortic time-velocity
integral in centimeters to yield Doppler SV.20
Measures of Myocardial Performance
The primary approach used to assess myocardial contractile
efficiency was examination of LV systolic shortening in
relation to ESS.22 Because the traditional practice of
relating endocardial shortening to mean ESS across the LV wall may
yield misleading results in individuals with concentric
hypertrophy or remodeling22 or with LV
dilatation,23 primary reliance was placed on the relation
of MWS to midwall circumferential ESS measured at the level of the LV
minor axis.22 24 25 MWS was calculated by taking into
account the epicardial migration of the midwall during systole. Similar
to the ellipsoidal model used by Shimuzu et al25 to
determine the physiological position of the
end-diastolic midwall during systole, constant volumes of
the total LV wall and its inner and outer halves during the cardiac
cycle were assumed. The formulas used to calculate MWS, midwall
circumferential ESS, and mean meridional ESS have been previously
reported.22 24 26 To evaluate LV performance
taking ESS into account, observed shortening was expressed as a
percentage of the value predicted from meridional and circumferential
ESS with equations derived from previously studied normal
subjects.22 These variables are called
stress-independent MWS and endocardial fractional shortening.
To permit comparison with previous studies, several secondary measures of LV performance were also examined. ESS/end-systolic volume index ratios, which have proved useful in previous studies,8 27 were calculated by dividing both meridional and midwall ESS by LV end-systolic volume calculated from end-systolic LV dimension by the method of Teichholz et al.28
Statistical Analyses
Data are expressed as mean±SD. Relations between variables
were assessed by Pearson or Spearman correlation coefficients, and
multivariate analyses were performed by forward
stepwise linear regression analysis with a probability value to
enter and remove of P<.05 and assessment of collinearity
diagnostics. The strength of correlations of different
variables to the same reference standard was compared by use of
Fisher's z statistic. Because of differences between SHS
participants in different regions for several of the evaluated clinical
variables (data not shown), a dummy variable
representing these regions was entered as a covariate.
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Results |
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Subject Characteristics
Of the first 3123 participants in SHS phase 2 who underwent echocardiography, 2212 were free of both segmental LV wall motion abnormalities and mitral regurgitation. Of these subjects, 1986 (90%) had LV measurements suitable for mass measurement, 2116 (96%) had recordings of transaortic flow and aortic annular diameter adequate to calculate Doppler SV, and 1935 (87%) had both. These subjects ranged widely in age (47 to 82 years), height (132 to 196 cm), weight (34 to 181 kg), BSA (1.22 to 2.89 m2), and body mass index (14.00 to 78.6 kg/m2); 1260 (65%) were women. A total of 54 subjects (2.8%) had at least mild LV systolic dysfunction without segmental wall motion abnormalities, and 115 (8.5%) had at least mild aortic regurgitation. Blood pressure was 129±20/75±10 mm Hg on SHS examination 2 and 132±20/77±11 mm Hg on SHS examination 1. Doppler SV ranged from 24 to 172 mL, and LV mass ranged from 64 to 388 g.
Relation of LV Geometry to Clinical Variables
Age was not statistically related to LV mass because of opposing
weak positive relations between age and LV wall thicknesses and
negative relations with LV chamber size (Table 1
). The significant relations of LV mass
to male sex, height, body mass index, and most strongly weight and BSA
were due to positive relations of LV wall thicknesses and even more so
of LV chamber size to these variables. Indexation of LV mass for
BSA eliminated statistical relations between LV mass and measures of
body size, whereas indexation of LV mass for height2.7
strengthened its correlation with body mass index.
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Relations of LV Geometry to Resting Blood Pressure
The data in Table 2 reveal that LV
mass and its index were significantly but weakly related to
arterial pressure at the time of
echocardiography and at the first SHS examination
nearly 4 years earlier. These relations were generally stronger for
systolic than diastolic pressure and were at most
slightly strengthened when the two sets of pressure measurements were
averaged. Each pressure measurement was significantly related to all
measures of LV wall thicknesses but was at most marginally related to
end-diastolic chamber dimension.
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Relation of LV Geometry to SV and LV Contractile
Efficiency
As Table 3 shows, LV mass and
chamber size exhibited strong positive relations to Doppler SV; SV
was more weakly related to ventricular wall thicknesses and
actually showed a weak inverse relation to LV relative wall thickness.
Stress-independent MWS had a moderate inverse relation to LV mass
because of strong inverse relations of this
contractility measure with LV wall thicknesses and a
weak positive relation between it and chamber size. LV MWS unadjusted
for ESS exhibited a similar pattern of inverse relations with LV mass
and mass/BSA (both r=-.40), interventricular
septal and posterior wall thicknesses (r=-.50 and -.48),
and relative wall thickness (r=-.36) but was statistically
unrelated to LV chamber size. Equally strong inverse relations were
observed between all measures of LV mass and chamber size and the
ratios of either meridional or circumferential ESS/end-systolic
LV volume index. These contractility indexes were
statistically unrelated to LV wall thicknesses but exhibited positive
relationships with LV relative wall thicknesses.
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Multivariate Analyses
An initial multivariate analysis
considered clinically available variables (age, sex, height, body
mass index, and systolic blood pressure) as potential
correlates of LV geometric variables. As Table 4
shows, LV mass and larger LV chamber size
were predicted moderately well (r=.50) by models with the
strongest contribution from larger body mass index followed by greater
height and male sex, with an additional contribution from age only for
LV mass. Relative wall thickness was predicted most weakly
(r=.19) by lesser height and older age.
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In multivariate models that considered
hemodynamic variables (systolic and
diastolic blood pressures, Doppler SV, and an index of
contractile efficiency), systolic (but not
diastolic) blood pressure, SV, and the
contractility measure consistently remained
independent predictors of LV mass and LV mass index (r=.60
to .66). When systolic pressure, SV, and stress-adjusted MWS
were considered, each contributed strongly (P<.00001) to
the resultant model (Table 5). Indexation
of LV mass and SV for BSA did not affect the strong independent
contribution of the three predictors to the resultant model.
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Alternative use of the circumferential ESS/end-systolic volume
ratio, systolic pressure, Doppler SV yielded the
multivariate model shown in Table 6
(top). Of note, the multiple R
value (r=.64) slightly exceeded that obtained with
stress-adjusted MWS as the contractility index (Table 5
), and systolic pressure made a greater relative contribution
to the model. Indexation of LV mass, SV, and end-systolic
volume for BSA raised the multiple R value minimally to .66
and resulted in a model (Table 6, bottom) in which systolic
pressure had more than twice as high a ß coefficient as Doppler
SV in the statistical model for prediction of LV mass. Substitution of
the meridional ESS/end-systolic volume ratio as a measure of LV
contractility had virtually no effect on the
results.
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A final multivariate analysis considered the
demographic (height, body mass index, sex, and age) and hemodynamic
(systolic blood pressure, Doppler SV, and
afterload-independent MWS) variables that had been independent
correlates of LV mass in previous analyses. As Table 7
shows, SV and afterload-independent MWS
were the strongest contributors to the resultant model, with smaller
and approximately equal contributions from systolic pressure
and body mass index and lesser contributions from height and male sex;
age did not bear a significant relation to LV mass. The independent
contributions of the several demographic and
hemodynamic variables to the prediction of LV mass
and the large proportion of LV mass variability that remained
unexplained by this analysis (49%) are displayed visually in
the Figure.
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Discussion |
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The present study examines for the first time in a large population sample the relative strengths of association of readily accessible subject characteristics (age, sex, body build, and blood pressure) and additional components of hemodynamic load on the heart—SV and contractile efficiency of the myocardium—with LV muscle mass. The main result of the study is that Doppler-derived SV and measures of myocardial performance based on LV stress-shortening relations and ESS/volume ratios are more closely associated with LV mass than resting blood pressure and remain independent correlates of LV mass when sex, body build, and age are taken into account. This finding both helps explain the recognized weak relation between blood pressure and LV mass and suggests that increased attention to factors causing variations in SV and myocardial contractile efficiency may be of value in future epidemiological and clinical studies.
Relation of Demographic Variables to LV Mass and
Geometry
Both univariate and multivariate
analyses (Tables 4 and 7) confirm the strong relations of body
mass index and male sex to LV mass, wall thicknesses, and chamber size.
After these variables were taken into account, body height and age
had less consistent associations with LV geometric
variables, similar to previous findings in other
populations.4 5
Relation of Concurrent and Multiple Blood Pressures to LV
Geometry
The relations observed in the present study between blood
pressure and LV dimensions are statistically highly significant but
have r2 values that suggest that pressure levels
predict at most 10% of variability of LV size. The correlations
between systolic and diastolic pressures at either
the current examination or the phase 1 examination 4 years earlier and
LV mass or mass index (r
.26) fall at the lower end of the
range seen in clinical studies4 29 30 but closely resemble
those seen in the predominantly white population of the Framingham
Heart Study.5 31 The tendency toward weaker relations in
population samples than in clinical populations probably reflects the
greater representation of individuals with severe abnormalities
in the latter setting. Similar to most previous studies,
systolic pressure was a stronger predictor of LV mass than
diastolic pressure. Correlations of LV mass with some but
not all measures of arterial pressure were slightly
increased by averaging two separate measures of blood pressure.
Somewhat greater increases in the strength of these relations were
accomplished when larger numbers of pressure measurements on multiple
examinations were used in the Framingham study31 and on
multiple outpatient visits over months to years by clinical
investigators.32 33
Relation of Volume Load to LV Geometry
SV measured by Doppler echocardiography
bore a considerably stronger relationship to LV mass (r=.50)
than did the most predictive measure of blood pressure. The respective
coefficients of determination (r2) of .25 and
.07 suggested that SV was >21/2 times as strong a predictor of
LV mass in the present population as systolic pressure.
Although few comparable data have been published, Ganau et
al8 reported a higher r2 compared
with LV mass for two-dimensional echocardiographic SV
(r2=.36) than systolic pressure
(r2=.20). Of note, the measurements used to
calculate Doppler SV are completely separate from the LV dimensions
used to calculate LV mass.
The ability to measure LV SV provides a readily accessible index of circulatory volume load. In the absence of mitral regurgitation or intracardiac shunts, LV SV reflects the LV filling volume in diastole. Increased LV filling volumes contribute to elevation of end-diastolic stress, providing a well-documented stimulus to LV hypertrophy.9 In a cross-sectional study, however, it is not possible to exclude the converse possibility that greater LV mass could have contributed in some subjects to generating a higher SV.
Relation of Contractility Measures to LV
Geometry
The inverse relations that we observed between several indirect
indexes of LV contractility and LV mass or mass index
had correlation coefficients of .26 to .45 that were intermediate
between those for systolic pressure and SV. Again, the
present results parallel those reported by Ganau et
al.8 The weakest of these relations in the present
study, with stress-adjusted LV MWS, was with the
contractility measure that was least related to LV
chamber volume. In fact, stress-adjusted MWS fell steeply with
increasing LV wall thicknesses but rose slightly with greater chamber
size, whereas stress/volume ratio measures of
contractility had strong inverse relations to LV
chamber size but weak positive relations to wall thicknesses (Table 2).
Multivariate Prediction of LV Mass
Extensive multivariate analyses
demonstrated the consistent statistical independence of
arterial pressure at the time of
echocardiography, SV, and a measure of LV
contractility for prediction of LV mass. This result
was unaffected in additional analyses (not shown) in which the
average of all available blood pressures was substituted as the measure
of pressure load. When stress-independent MWS, which was recently shown
to predict an adverse prognosis in asymptomatic
hypertensive patients,34 was used as the
contractility measure, both it and Doppler SV were
stronger predictors than arterial pressure of LV mass
(Table 5). Substitution of ESS/volume ratios as the
contractility indexes (Table 6) had little effect on
the overall multiple R values but increased the
proportionate contribution of arterial pressure and the
contractility index to the model. The reductions of the
predictive importance of SV, albeit still highly significant, probably
reflected the strong relation between the ESS/volume ratios and LV
chamber size seen in Table 2. Of note, the highest multiple
R values for prediction of LV mass were obtained by use of
the sets of predictor variables (ESS/volume ratios, Doppler SV,
and systolic blood pressure) that did not incorporate any of
the end-diastolic LV measurements used to calculate LV
mass.
When both demographic and hemodynamic variables
were considered together, the strongest correlates of LV mass were
Doppler SV (positive) and stress-independent MWS (negative). The
contribution of body mass index to the predictive model for LV mass was
less (ß=0.23 versus 0.38) than when only demographic variables
were considered (Table 4) and approximately equaled that of
systolic pressure. Male sex added weakly to the
multivariate model but age did not when age-related
increases in systolic pressure (r=.23) were taken
into account. However, after the additive association of demographic
and hemodynamic variables was considered, nearly
half the variability of LV mass remained unexplained. Possible
contributors to this include both genetic factors and the levels of
arterial pressure and SV during usual activities.
Study Limitations
The present study determined SV and assessed myocardial
performance by methods less precise than invasive measurements
involving the Fick principle or using solid-state manometry and
angiography to assess LV pressure and volume responses to load
manipulation. Nevertheless, when meticulously applied with reference to
invasive reference standards, the Doppler
echocardiographic method we used measures SV and
cardiac output accurately.20 35 The measures of
contractile efficiency we used are—like other noninvasive indexes that
can be applied in diverse, unselected populations—limited by inability
to measure LV filling pressures (and hence myocardial preload) and to
manipulate LV load sufficiently to generate ESS-dimension or
stress-volume relations. However, the ability of the stress shortening
and stress volume measures that we used to provide approximate
estimates of myocardial contractile efficiency is supported by both
methodological comparison studies and studies in which these
variables have been shown to predict an adverse prognosis. Thus,
Reichek et al26 showed a close correlation of ESS measured
by cuff blood pressures and echocardiographic LV
measurements with ESS derived with solid-state pressure transducers in
the LV cavity. Equivalent results concerning midwall stress-shortening
relations in pressure-overload hypertrophy have been
obtained using invasive and noninvasive
measurements.24 25 36 37 In addition, the stress
shortening and stress/volume indexes we used predicted adverse outcomes
in patients with hyper-tension,34 valvular
heart disease,37 and dilated
cardiomyopathy.38
Another potential limitation of the present study—its performance in an American Indian population—may instead, we believe, constitute a strength. The ability to assess biologically fundamental relations among cardiac load, function, and structure in a segment of the population that has hitherto been largely excluded from systematic pathophysiological research because of its geographical remoteness from biomedical research centers illustrates the portability and robustness of imaging and Doppler echocardiography. Nevertheless, it must be pointed out that the present results depended on extensive preparation and training and by intensive efforts by the involved personnel. Further research is needed to determine the applicability of the present findings in other populations with different ethnic composition and lower prevalences of obesity, as are studies in which longitudinal changes in blood pressure, SV, and contractility indexes could be related to changes in LV mass.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by cooperative agreement grants U01-HL-41642, U01-HL-41652, and U01-HL-41654 from the NHLBI and M10RR0047-34 (GCRC) from the NIH, Bethesda, Md. We would like to thank the Indian Health Service facilities, the SHS participants, and the participating tribal communities for the extraordinary cooperation and involvement that made this study possible; Betty Jarvis, RN, Martha Stoddart, and Beverly Blake, RN, for their coordination of the three study centers; Drs Antonello Ganau, Frans Leenen, and Gerald Aurigemma for their critical reading of the manuscript; Elizabeth A. Wood for the design and maintenance of the computer databases; and Virginia Burns for her invaluable assistance in the preparation of the manuscript. We also thank Taqueer Ali, MD; Helen Beaty, RDMS; Joanne Carter, RDMS; Michael Cyl, RDMS; and Neil Sykes, RDMS, for their technical assistance. The views expressed in this paper are those of the authors and do not necessarily reflect those of the Indian Health Service.
Received November 25, 1996; revision received March 20, 1997; accepted March 26, 1997.
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