(Circulation. 2001;103:820.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Relations of Stroke Volume and Cardiac Output to Body Composition
The Strong Heart Study
From Cornell Medical Center, New York, NY (T.C., R.B.D., M.J.R., G.d.S.); University of Oklahoma Health Sciences Center, Oklahoma City (J.-L.Y.); MedStar Research Institute, Washington, DC (B.V.H.); National Heart, Lung, and Blood Institute, Bethesda, Md (R.R.F.); and Aberdeen Area Tribal Chairmen’s Health Board, Rapid City, SD (T.K.W.).
Correspondence to Richard B. Devereux, MD, Division of Cardiology, Box 222, Cornell Medical Center, 525 E 68th St, New York, NY 10021. E-mail rbdevere{at}med.cornell.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Although cardiac output (CO) plays the vital role of delivering nutrients to body tissues, few data are available concerning the relations of stroke volume (SV) and CO to body composition in large population samples.
Methods and
Results—Doppler and 2D echocardiography and
bioelectric impedance in 2744 Strong Heart Study participants were used
to calculate SV and CO and to relate them to fat-free body mass (FFM),
adipose mass, and demographic variables. Both SV and CO were higher in
men than women and in overweight than normal-weight individuals, but
these differences were diminished or even reversed by normalization for
FFM or body surface area. In both sexes, SV and CO were more strongly
related to FFM than adipose mass, other body habitus measures, arterial
pressure, diabetes, or age. In multivariate analyses using the average
of Doppler and left ventricular SV to minimize measurement variability,
FFM was the strongest correlate of SV and CO; other independent
correlates were adipose mass, systolic pressure, diabetes, age, and use
of digoxin and calcium channel and
-blockers.
Conclusions—In a population-based sample, SV and CO are more strongly related to FFM than other variables; increased FFM may be the primary determinant of increased SV and CO in obesity.
Key Words: American Indians • diabetes mellitus • echocardiography • ventricles
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The association between obesity and cardiac output (CO) has been observed since the 1950s, when Alexander et al1 characterized obesity as a state in which elevated blood volume, enlarged vascular tree, and increased CO were all thought necessary to sustain the metabolic demands of an expanded adipose tissue mass. Messerli et al2 later confirmed increases in intravascular volume in obese subjects and demonstrated that this elevation of CO was related primarily to increases in stroke volume (SV) rather than in heart rate. The observed changes in total blood volume and CO were again assumed to be secondary to metabolic demands of excess adipose tissue.2 3
Overweight, however, is also associated with increased fat-free mass (FFM),4 and the relative contributions of adipose body mass and FFM as determinants of CO have not been studied to date. Because FFM represents metabolically active tissue and because the increased weight in obese individuals is in part due to increased FFM, the present study was undertaken to test the hypothesis that FFM is a stronger determinant of SV and CO than adipose mass or other clinical characteristics. An additional goal was to determine whether differences in FFM between overweight and normal-weight adults might account for the increased CO in the former group.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The Strong Heart Study (SHS) is 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 previously described,5 6 7 members of 3 tribal communities in Arizona, 7 in Oklahoma, and 3 in South/North Dakota, 45 to 74 years old, were recruited from tribal members living on reservations or (in Oklahoma) in a defined geographic area (overall participation rate 62%) for an initial examination in 1989 to 1992.
The second SHS examination was conducted in 1993 to 1995 to assess change in body habitus, blood pressure, and other baseline measures and to add echocardiography among surviving participants.7 Standardized measurements of seated brachial blood pressure; anthropometric measures, including height, weight, body mass index (BMI), waist/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 were obtained. Diabetes was diagnosed by World Health Organization criteria.8
FFM and adipose body mass were estimated by use of an RJL impedance meter5 (model B1410) and equations based on total body water:
Watermales
(L)=e{1.1782xlog
[height
(cm)]-0.5968xlog
[resistance
(
)]+0.3226xlog
[weight
(kg)]}.
Waterfemales
(L)=e{1.2004xlog
[height
(cm)]-0.5529xlog
[resistance
()]+
0.2164xlog [weight (kg)]}.
FFM=water (L)/0.732.
Adipose body mass=weight-FFM.
Assessment of FFM by bioelectric impedance has been validated in American Indians by comparison with FFM determined by underwater weighing alone or in combination with dual-energy x-ray absorptiometry (r=0.86 to 0.97).9 10 To calculate waist/hip ratio, waist circumference was measured in the supine position with an anthropometric tape; hip circumference was measured at the maximum protrusion of the gluteal muscles in the standing position. Overweight was recognized by BMI>27.3 kg/m2 in men and 27.8 kg/m2 in women.
For the present study, participants were included if they
had technically satisfactory Doppler echocardiographic measurements of
SV, CO, and bioelectric impedance measurements and no hemodynamically
significant (
2+) aortic or mitral regurgitation by color Doppler
echocardiography.
Echocardiographic Methods
Studies were performed by a protocol previously
described in
detail11 12 using
phased-array echocardiographs with M-mode, 2D, and pulsed and
color-flow Doppler capabilities. Subjects were examined with the head
of the examining table elevated 
30° in the partial decubitus
position. Pulsed Doppler sample volumes were placed at the center
of the aortic annulus in the apical long-axis or
"five-chamber" view to record systolic transaortic blood
flow.
Echocardiographic Measurements
Correct orientation of planes for imaging and Doppler
recordings was verified as previously
described.13 Measurements
were made with computerized review stations equipped with digitizing
tablet and monitor screen overlay for calibration and measurement. Left
ventricular (LV) internal dimension and septal and posterior wall
thicknesses were measured at end diastole and end systole by American
Society of Echocardiography (ASE) M-mode
recommendations14 on up to 3
cardiac cycles. When optimal orientation of the LV cursor could not be
obtained, correctly oriented linear dimension measurements were made by
the ASE 2D leading-edge
convention.15 The diameter
of the aortic annulus was measured in the long-axis view that maximized
it from trailing edge to leading edge at the hinging points of the
aortic cusps to the annulus, with color Doppler used to clarify
tissue-blood interfaces if
necessary.16 Doppler
transaortic flow was assessed in the projection in which peak flow
velocity was maximal by tracing the black-white interface outlining the
Doppler flow envelope, as previously shown to yield accurate estimates
of invasively measured SV.17
Heart rate was measured simultaneously. Doppler color-flow maps and,
when applicable, pulsed-wave recordings were used to grade mitral and
aortic regurgitation on a scale of 0 to 4+ by standard
criteria.18 19
Calculation of Derived Variables
Doppler SV was calculated as aortic annular
cross-sectional area (in square centimeters) times the aortic
time-velocity integral in centimeters. CO was derived as SV times heart
rate. SV was also measured from LV end-diastolic and end-systolic
volumes calculated from LV internal dimensions by a method validated in
individuals with normal-sized to dilated
LVs.20 To assess whether
reducing the variability of SV and CO by averaging results of 2
measurements would strengthen their relations to body habitus and other
variables, "average" SV and CO were calculated as the mean of
Doppler and LV measurements.
Data Handling and Statistical Analyses
Data are presented as mean±SD for continuous
variables and proportions for categorical variables. Because of the
known impact of sex on body composition, analyses were performed
separately in men and women. Partial correlations between independent
variables and SV and CO were adjusted for possible center effects by
use of 2 dummy variables. Multiple linear regression analysis using an
enter procedure with assessment of collinearity diagnostics was used to
determine the independence of correlates of SV and CO. Measures of body
composition considered in these analyses were FFM and adipose mass,
height to the power of its allometric relations with SV and CO
(height2.04 and
height1.83,
respectively21 ), BMI, and
waist/hip ratio. Partial correlation coefficients were used to estimate
the proportion of variance of dependent variables explained by each
independent variable. The strength of correlations of different
variables to the same reference standard was compared by use of
Fisher’s z statistic.
Two-tailed P<0.05 indicated
statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Technically satisfactory Doppler echocardiograms, body composition measurements, and other needed clinical data for the present study were obtained in 2744 participants in the second SHS examination without
2+ aortic or mitral regurgitation or segmental LV
wall motion abnormalities
(Table 1
). Ages of men and women ranged from 48 to 81
and 46 to 80 years, respectively. All measures of body size, including
FFM, were higher in men, whereas body adiposity was greater in women.
SV and CO were higher by 10% in men; mean differences were similar
for average SV and CO, with smaller SDs.
|
Overweight individuals were younger, heavier, and had higher
adipose mass, percent body fat, and waist/hip ratio than normal-weight
participants. FFM was higher, by a mean of 14%, and SV and CO were
9% higher in overweight individuals. Use of average values of SV
and CO resulted in nearly identical mean differences between groups
with smaller SDs.
Correlates of SV
In men, SV correlated better with FFM than with adipose
mass, BMI, waist/hip ratio, height, or
height2.04
(Table 2). SV had a weak positive relation with systolic
pressure and a weak negative one with age. Body weight was as strong a
correlate of SV as FFM. Average SV had a similar pattern of
relationships, with generally slightly higher correlation
coefficients.
|
In women, SV was moderately and equivalently correlated with FFM, adipose mass, body weight, and BMI. Weaker, but still significant, positive relations were observed between SV and waist/hip ratio, height and height2.04, and systolic pressure but not age. Average SV had a minimally stronger set of relations with body habitus variables and SV. SV (as well as CO) was higher (P<0.001) in diabetic women.
Correlates of CO
In men, CO was more closely correlated with FFM than
adipose mass, waist/hip ratio, height, or
height1.83
(Table 3). Relations of CO with body weight and BMI,
however, were similar to that with FFM. CO also had a weak positive
relation with systolic pressure and a weak negative one with age.
Average CO was correlated slightly more closely with most measures of
body size and systolic pressure. CO was higher in diabetic than
nondiabetic men (mean, 5.3 versus 5.0 L/min,
P<0.001) because of higher
heart rate.
|
Among women, CO had similar moderate, positive relations with FFM and body weight and slightly weaker ones with adipose mass and BMI. Positive, but more weakly positive, relations were observed between CO and waist/hip ratio, height, height1.83, and systolic pressure but not age. Use of average CO slightly strengthened most relations, except those with height.
Multivariate Analyses
SV had the strongest independent positive correlation
with FFM, followed by adipose mass, in both sexes
(Table 4). Diabetes had an independent negative relation
with SV in men, with a parallel trend in women; systolic pressure had a
weak positive relation to SV in women, with a parallel trend in men;
age did not enter the model in either sex. When women and men were
considered together, with an indicator variable for sex, larger SV was
independently related to higher FFM (=0.333), adipose mass
(=0.181), absence of diabetes (=-0.081), and higher systolic
pressure (=0.061, all
P<0.001) but not age or
sex.
|
Alternative analyses used average SV as the dependent
variable. In men, the multiple
R increased from 0.31 to 0.39
because of stronger associations with FFM (=0.286), adipose mass
(=0.148), and absence of diabetes (=-0.138) (all
P<0.001) but not age or
systolic pressure. In women, the multiple
R also increased (0.44 versus
0.41), principally because of stronger association with FFM
(=0.285), with smaller increases in associations with adipose mass
(=0.198), systolic pressure (=0.092), and absence of diabetes
(=-0.073) but not age. When women and men were considered
together, the multiple R
increased slightly (from 0.39 and 0.44 in the 2 sexes to 0.48), with
average SV most strongly associated with higher FFM (=0.416),
followed by higher adipose mass (=0.181) and systolic pressure
(=0.083) and absence of diabetes (=-0.107) (all
P<0.001). In further analysis
considering major cardioactive medications, SV was independently
related (R=0.51) to FFM
(=0.419), adipose mass (=0.219), absence of diabetes (=0.094),
higher systolic pressure (=0.087) (all
P<0.001), and use of digoxin
(=0.061, P=0.002) and
calcium blockers (=0.060,
P=0.003) but not sex, age, or
use of diuretics, ACE inhibitors, or -blockers.
Sex-specific regression analyses to identify independent
correlates of CO are summarized in
Table 5. In both sexes, FFM was the strongest correlate of
CO. Adipose mass was the second strongest correlate of CO in women but
was not independently associated with it among men. In both sexes,
systolic pressure was positively associated with CO, whereas age and
diabetes were not. When the sexes were combined, CO was most strongly
(R=0.39) associated with FFM
(=0.304), followed by adipose mass (=0.159) and systolic pressure
(=0.092, all P<0.001) but
not age, diabetes, or sex.
|
Alternative regression analyses used average CO as the
dependent variable. The multiple R increased slightly in women
(R=0.42 versus 0.39),
principally because of the stronger association with FFM (=0.292,
P<0.001), with minimal changes
in associations with adipose mass (=0.137,
P<0.001) and systolic pressure
(=0.087). In men, multiple R increased modestly (0.39 versus 0.34)
because of stronger positive associations of CO with FFM (=0.257)
and systolic pressure (=0.124, both
P<0.001) and stronger negative
association with age (=-0.098,
P=0.004), with unchanged
positive association with adipose mass (=0.096,
P=0.021). When the sexes were
combined, CO had positive relations to FFM (=0.372), adipose mass
(=0.145), and systolic pressure (=0.105; all
P<0.0001) and a negative one
with age (=-0.054,
P=0.004) but not diabetes or
sex (R=0.43). In further
analysis that also considered cardioactive medications, CO was
independently related (R=0.46)
to FFM (=0.368), adipose mass (=0.171), systolic pressure
(=0.102) (all P<0.001),
calcium blocker use (=0.072) and absence of -blocker use
(=-0.071) (both P=0.001),
younger age (=0.050,
P=0.024), and digoxin use
(=0.044) but not sex, diabetes, or diuretic or ACE inhibitor
use.
Associations of Sex and Obesity With Different
Normalizations of SV and CO
Absolute SV and CO were higher in men than women,
whereas normalization for body surface area eliminated the sex
difference in SV and resulted in marginally higher cardiac index in
women
(Table 6). SV and CO normalized for FFM were considerably
smaller in men than women. Average SV and CO had virtually identical
mean sex differences, with smaller within-group SDs.
|
Overweight participants had higher absolute SV and CO than nonoverweight participants, whereas these differences were eliminated by normalization for body surface area and reversed by indexation by FFM. These findings were confirmed in analyses using averaged Doppler and LV determinations of SV and CO.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
To the best of our knowledge, this is the first study to examine the relations of SV and CO to FFM and adipose mass in a large population sample. The principal finding of the study is that both SV and CO are more strongly related to FFM than to adipose mass, other anthropometric measures, sex, age, blood pressure, diabetes, or effects of cardioactive medications.
These results, although new, are not surprising in view of studies demonstrating increased FFM in obese individuals in a variety of populations and age groups: FFM accounts for 20% to 40% (average, 29%) of the weight difference between lean and overweight groups.4 Consistent with these observations, FFM accounted for 6.8 kg, or 30%, of the 22.5 kg greater body weight in overweight than normal-weight SHS participants.
Results of Multivariate Analyses
When both sexes were combined, with addition of an
indicator variable for sex, Doppler SV was most strongly related to
FFM, with associations, as judged by standardized regression
coefficients (), 67% as strong with adipose body mass and 25%
as strong with systolic pressure and absence of diabetes. Neither sex
nor age was independently associated with Doppler SV in this
model.
In a similar analysis, CO was most strongly related to FFM,
with additional associations 50% as strong with adipose mass and
25% as strong with systolic blood pressure and absence of diabetes
but not sex or age. These observations are in accord with previous
evidence that different normal limits for indexed SV or CO are not
needed in relation to either sex or age among
adults.21
Impact of Using Average of Doppler and LV
Measurements
One problem in assessing the determinants of many
physiological measurements, exemplified by arterial pressure, is
considerable between-measurement variability. Although use of many
measurements is optimal,22
up to a 30% reduction in variability can be obtained by using one
additional measurement. In the present study, we took advantage of the
fact that our protocol provides separate measurements of SV by
validated Doppler and LV
methods11 17 to
calculate average SV and, consequently, average CO. As expected,
average SV and CO showed lower within-group variability and had
somewhat stronger relations than primary Doppler measurements with body
habitus variables. Of greatest biological importance, use of averaged
measures of cardiac pump function increased the disparity between FFM
and adipose mass as independent determinants thereof. Additional
consideration of medication usage confirmed these results and revealed
independent associations between digoxin or calcium blockers and SV
(with mean increments of +5.9 and +2.2 mL) and between
digitalis, calcium blockers, and -blockers and cardiac index (by
+357, +234, and -356
mL · min-1 · m-2
on average).
Physiological Mechanisms
FFM (comprising organ cell mass and nonfatty tissues,
including tendons, ligaments, and
bone)23 represents
metabolically active tissue; up to 99% of body metabolism takes place
in the body cell mass.24
Given that CO is known to be intimately related to the level of
metabolism, through tissue demands for
oxygen,25 it is tempting to
ascribe the importance of FFM as a correlate of CO in both lean and
obese subjects to the "metabolic load" accompanying FFM and to
attribute part of the increased CO of obesity to increased FFM
associated with obesity.
In addition to associations between FFM and SV and CO, the present study has also shown the latter variables to be more weakly associated with adipose mass. These associations may reflect blood flow needed to support the energy expenditure, albeit small, of adipose tissue as well as possible shunt flow through this tissue and increased cutaneous blood flow to dissipate body heat in overweight individuals. In addition, despite reasonable accuracy of bioelectric impedance FFM measurements, residual errors may have attributed some FFM to adipose mass, thereby overestimating the associations of adipose mass with CO.
One important result of the present study is that only a small portion of variability of SV and CO is associated with and thus potentially explained by body composition and demographic characteristics that were considered, with R2 values ranging from 0.10 to 0.26 in multivariate analyses. Because the factor associated with resting CO that is most strongly physiologically regulated is matching oxygen delivery to tissue needs, the CO needed for a given level of tissue metabolism will be inversely related to blood hemoglobin concentration. It is attractive to speculate that higher SV and CO indexed for FFM in women than men may have been a compensation for lower hemoglobin concentration in women.26 Unfortunately, hemoglobin was not measured in the present study.
|
Acknowledgments |
|---|
This study was supported in part by grants U01-HL-41642, U01-HL-41652, and U01-HL-41654 from the National Heart, Lung, and Blood Institute and M10-RR-0047-34 (GCRC) from the National Institutes of Health, Bethesda, Md. We would like to thank Indian Health Service facilities, SHS participants, and participating tribal communities for the extraordinary cooperation and involvement that made this study possible; Betty Jarvis, RN, Tauqeer Ali, MD, and Alan Crawford for study center coordination; Tauqeer Ali, MD, Helen Beaty, Joan Carter, Michael Cyl, and Neil Sikes for expert performance of echocardiograms; and Virginia Burns for invaluable assistance in manuscript preparation.
|
Footnotes |
|---|
The views expressed in this article are those of the authors and do not necessarily reflect those of the Indian Health Service.
Received June 1, 2000; revision received September 27, 2000; accepted October 4, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Alexander SK, Dennis EW, Smith WG, et al. Blood volume, cardiac output, and distribution of systemic blood flow in extreme obesity. Cardiovasc Res Cent Bull. 1953;1:39–44.
2.
Messerli FH,
Ventura HO, Reisin E, et al. Borderline hypertension and obesity: two
prehypertensive states with elevated cardiac output.
Circulation. 1982;66:55–60.
3. Messerli FH, Sundgaard-Riise K, Reisin ED, et al. Dimorphic cardiac adaptation to obesity and arterial hypertension. Ann Intern Med. 1983;99:757–761.
4. Forbes GB, Welles SL. Lean body mass in obesity. Int J Obes. 1983;7:99–107.[Medline] [Order article via Infotrieve]
5.
Lee ET, Welty TK,
Fabsitz R, et al. The Strong Heart Study: a study of cardiovascular
disease in American Indians: design and methods.
Am J Epidemiol. 1990;132:1141–1155.
6. Howard BV, Welty TK, Fabsitz RR, et al. Risk factors for coronary heart disease in diabetic and non-diabetic Native Americans. Diabetes. 1992;41(suppl 2):4–11.
7.
Welty TK, Lee ET,
Yeh JL, et al. Cardiovascular disease risk factors among American
Indians: the Strong Heart Study. Am J
Epidemiol. 1995;142:269–287.
8. WHO Expert Committee on Diabetes Mellitus. Second report. Geneva, Switzerland: World Health Organization; 1980 (Technical Report Series 646).
9.
Stolarczyk LM,
Heyward VH, Hicks VL, et al. Predictive accuracy of bioelectric
impedance in estimating body composition of Native American women.
Am J Clin Nutr. 1994;59:964–970.
10.
Rising R,
Swinburn B, Larson K, et al. Body composition in American Indians:
validation of bioelectric resistance.
Am J Clin Nutr. 1991;53:594–598.
11. Devereux RB, Roman MJ, Paranicas M, et al. Relations of Doppler stroke volume and its components to left ventricular stroke volume in normotensive and hypertensive American Indians: the Strong Heart Study. Am J Hypertens. 1997;10:619–628.[Medline] [Order article via Infotrieve]
12.
Devereux RB,
Roman MJ, de Simone G, et al. Relations of left ventricular mass to
demographic and hemodynamic variables in American Indians: the Strong
Heart Study. Circulation. 1997;96:1416–1423.
13. Devereux RB, Roman MJ. Evaluation of cardiac and vascular structure by echocardiography and other noninvasive techniques. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, Treatment. 2nd ed. New York, NY: Raven Press; 1995:1969–1985.
14.
Sahn DJ, De Maria
A, Kisslo J, et al. Recommendations regarding quantitation in M-mode
echocardiography: results of a survey of echocardiographic
measurements. Circulation. 1978;58:1072–1083.
15. Schiller NB, Shah PM, Crawford M, et al, American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–367.[Medline] [Order article via Infotrieve]
16. Roman MJ, Devereux RB, Kramer-Fox R, et al. Two-dimensional echocardiographic aortic root dimensions in children and adults: biologic determinants and normal limits. Am J Cardiol. 1989;64:507–512.[Medline] [Order article via Infotrieve]
17. Dubin J, Wallerson DC, Cody RJ, et al. Comparative accuracy of Doppler echocardiographic methods for clinical stroke volume determinations. Am Heart J. 1990;120:116–123.[Medline] [Order article via Infotrieve]
18.
Helmcke F, Nanda
NC, Hsiung MC, et al. Color Doppler assessment of mitral regurgitation
with orthogonal planes.
Circulation. 1987;75:175–183.
19.
Lebowitz NE,
Bella JN, Roman MJ, et al. Prevalence and correlates of aortic
regurgitation in American Indians: the Strong Heart Study.
J Am Coll Cardiol. 2000;36:461–467.
20. de Simone G, Devereux RB, Ganau A, et al. Estimation of left ventricular chamber and stroke volume by limited M-mode echocardiography and validation by two-dimensional and Doppler echocardiography. Am J Cardiol. 1996;78:801–807.[Medline] [Order article via Infotrieve]
21.
de Simone G,
Devereux RB, Daniels SR, et al. Stroke volume and cardiac output in
normotensive children and adults: assessment of relations with body
size and impact of overweight.
Circulation. 1997;95:1837–1843.
22. Fagard R, Staessen J, Thijs L, et al. Multiple standardized clinic blood pressures may predict left ventricular mass as well as ambulatory monitoring: a metaanalysis of comparative studies. Am J Hypertens. 1995;8:533–540.[Medline] [Order article via Infotrieve]
23. Roubenoff R, Kehayias JJ. The meaning and measurement of lean body mass. Nutr Rev. 1991;46:163–175.
24.
Moore FD. Energy
and the maintenance of body cell mass. J
Parenter Enteral Nutr. 1980;4:228–260.
25. Guyton AC, Jones CE, Coleman TG. Circulatory Physiology: Cardiac Output and Its Regulation. Philadelphia, Pa: WB Saunders; 1973:323–353.
26. de Simone G, Devereux RB. Hemorheologic abnormalities in obesity: hemodynamic and prognostic implications. Nutr Metab Cardiovasc Dis. 1992;2:185–190.
This article has been cited by other articles:
 |
|
 |
|
  V. Palmieri, C. Russo, E. A. Palmieri, S. Pezzullo, and A. Celentano Changes in components of left ventricular mechanics under selective beta-1 blockade: insight from traditional and new technologies in echocardiography Eur J Echocardiogr, May 22, 2009; (2009) jep055v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. C.Y. Poon, N. A. Kametas, N. Maiz, R. Akolekar, and K. H. Nicolaides First-Trimester Prediction of Hypertensive Disorders in Pregnancy Hypertension, May 1, 2009; 53(5): 812 - 818. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Mohty, J. G. Dumesnil, N. Echahidi, P. Mathieu, F. Dagenais, P. Voisine, and P. Pibarot Impact of prosthesis-patient mismatch on long-term survival after aortic valve replacement: influence of age, obesity, and left ventricular dysfunction. J. Am. Coll. Cardiol., January 6, 2009; 53(1): 39 - 47. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. J. M. Lemmens, L. J. Saidman, E. I. Eger II, and M. J. Laster Obesity Modestly Affects Inhaled Anesthetic Kinetics in Humans Anesth. Analg., December 1, 2008; 107(6): 1864 - 1870. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Mathew, L. Francis, A. Kayalar, and J. Cone Obesity: Effects on Cardiovascular Disease and its Diagnosis J Am Board Fam Med, November 1, 2008; 21(6): 562 - 568. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kozakova, C. Palombo, M. Paterni, C.-H. Anderwald, T. Konrad, M.-P. Colgan, A. Flyvbjerg, J. Dekker, and on behalf of the Relationship between Insulin Sens Body Composition and Common Carotid Artery Remodeling in a Healthy Population J. Clin. Endocrinol. Metab., September 1, 2008; 93(9): 3325 - 3332. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. W. Chance, C. Rhee, C. Yilmaz, D. M. Dane, M. L. Pruneda, P. Raskin, and C. C.W. Hsia Diminished Alveolar Microvascular Reserves in Type 2 Diabetes Reflect Systemic Microangiopathy Diabetes Care, August 1, 2008; 31(8): 1596 - 1601. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Eilat-Adar, J. Xu, C. Loria, C. Mattil, U. Goldbourt, B. V. Howard, and H. E. Resnick Dietary Calcium Is Associated with Body Mass Index and Body Fat in American Indians J. Nutr., August 1, 2007; 137(8): 1955 - 1960. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Poirier, T. D. Giles, G. A. Bray, Y. Hong, J. S. Stern, F. X. Pi-Sunyer, and R. H. Eckel Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss. Arterioscler. Thromb. Vasc. Biol., May 1, 2006; 26(5): 968 - 976. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Poirier, T. D. Giles, G. A. Bray, Y. Hong, J. S. Stern, F. X. Pi-Sunyer, and R. H. Eckel Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss: An Update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease From the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism Circulation, February 14, 2006; 113(6): 898 - 918. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. X. Whalen, O. Gajic, G. B. Thompson, M. L. Kendrick, F. L. Que, B. A. Williams, M. J. Joyner, R. D. Hubmayr, D. O. Warner, and J. Sprung The Effects of the Alveolar Recruitment Maneuver and Positive End-Expiratory Pressure on Arterial Oxygenation During Laparoscopic Bariatric Surgery Anesth. Analg., January 1, 2006; 102(1): 298 - 305. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. D. Chantler, R. E. Clements, L. Sharp, K. P. George, L.-B. Tan, and D. F. Goldspink The influence of body size on measurements of overall cardiac function Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H2059 - H2065. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. de Simone, K. Wachtell, V. Palmieri, D. A. Hille, G. Beevers, B. Dahlof, U. de Faire, F. Fyhrquist, H. Ibsen, S. Julius, et al. Body Build and Risk of Cardiovascular Events in Hypertension and Left Ventricular Hypertrophy: The LIFE (Losartan Intervention For Endpoint reduction in hypertension) Study Circulation, April 19, 2005; 111(15): 1924 - 1931. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. de Simone, R. B Devereux, J. R Kizer, M. Chinali, J. N Bella, A. Oberman, D. W Kitzman, P. N Hopkins, D. Rao, and D. K Arnett Body composition and fat distribution influence systemic hemodynamics in the absence of obesity: the HyperGEN Study Am. J. Clinical Nutrition, April 1, 2005; 81(4): 757 - 761. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. A. Whalley and R. N. Doughty Definition of physiological hypertrophy in ultramarathon athletes J. Am. Coll. Cardiol., July 21, 2004; 44(2): 469 - 469. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||