Relations of Left Ventricular Mass to Demographic and Hemodynamic Variables in American Indians
The Strong Heart Study
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.
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.
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.
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.
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
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.
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.
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.
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.
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.
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.
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 β 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.
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⇓.
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 (β=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.
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.
Selected Abbreviations and Acronyms
|BSA||=||body surface area|
|LV||=||left ventricular/left ventricle|
|MWS||=||midwall fractional shortening|
|SHS||=||Strong Heart Study|
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.
- Copyright © 1997 by American Heart Association
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