(Circulation. 1995;92:805-810.)
© 1995 American Heart Association, Inc.
Articles |
Left Ventricular Hypertrophy Has a Greater Impact on Survival in Women Than in Men
From the Department of Preventive Medicine and Epidemiology (Y.L., R.S.C., D.L.M.), Loyola University Medical Center, Maywood, Ill, and the Division of Cardiology (G.A.M.), Vanderbilt University School of Medicine, Nashville, Tenn.
Correspondence to Dr Youlian Liao, Loyola University Medical Center, 2160 S First Ave, Maywood, IL 60153. E-mail YLIAO@LUCCPUA.IT.LUC.EDU.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Echocardiographically determined left ventricular hypertrophy (LVH) has a well-demonstrated association with cardiovascular morbidity and mortality. However, whether or not there is a sex differential in the impact of LVH on mortality has never been systematically explored.
Methods and Results This study enrolled 436 consecutive black
patients (163 men and 273 women) free of angiographic coronary
artery disease from a hospital registry. LVH (left
ventricular [LV] mass/body surface area 
117
g/m2 in men and 104 g/m2 in women) was
present in 84 men (52%) and 119 women (44%). During a mean of 5
years' follow-up (range, 0 to 9), 49 patients (26 men and 23 women)
died. The mortality rate was 5.40 per 100 patient-years in men with LVH
and 2.58 in men without LVH (crude relative risk [RR]=2.09)
and 3.21
and 0.66, respectively, in women (RR=4.87). In Cox regression
analysis, adjusting for age, hypertension, and ejection
fraction, the RR of total death for LVH versus non-LVH was 2.0 (95%
confidence interval [CI], 0.8 to 5.0) in men and 4.3 (95% CI, 1.6 to
11.7) in women. For cardiac death, RR was 1.3 (95% CI, 0.4 to 3.7) and
7.5 (95% CI, 1.6 to 33.8) in men and women, respectively.
Analyses using LV mass indexed by height or
height2.7 with the use of different LVH cut points,
comparing patients in the highest sex-specific tertile of mass index to
those in the lower two tertiles, and the use of LV mass indexes as
continuous variables similarly demonstrated a greater increase in
risk of either fatal end point among women than men.
Conclusions These findings indicate a sex difference in the contribution of LV mass and hypertrophy to mortality in the absence of coronary artery disease.
Key Words: hypertrophy • risk factors • coronary disease
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Echocardiographically determined left ventricular hypertrophy is a powerful, independent predictor of cardiovascular morbidity and mortality in patients with uncomplicated essential hypertension1 2 3 as well as the general population.4 5 An association of increased left ventricular mass with adverse outcomes has been consistently reported in men and women3 4 5 6 ; however, the question of whether or not the relative risk is similar in the two sexes has never been systematically explored. This study examines the impact of left ventricular mass and hypertrophy on mortality in men and women without previous angiographically diagnosed coronary artery disease in a hospital-based patient series.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Study Patients
Between January 1983 and June 1991, 2445 consecutive black patients underwent cardiac catheterization for the diagnostic evaluation of presumed coronary artery disease in Cook County Hospital, a public general hospital in Chicago, Ill, primarily serving a minority population. Among these patients, 1174 (48%) patients were free of significant coronary artery disease angiographically, and satisfactory echocardiography was obtained in 534 patients (Table 1
). This analysis excluded 85 patients
with missing data on ejection fraction and 13 patients with missing
data on body surface area. The final analytic cohort for this study
consisted of a total of 436 patients (163 men and 273 women). Patients
with coronary artery disease were not included to reduce gender
interactions with that condition.
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Patients who reported a diagnosis of diabetes or who currently were taking insulin or oral hypoglycemic agents were defined as diabetic cases. Obesity was defined according to the National Institutes of Health Consensus Panel7 as body mass index (weight in kilograms per square meter of height) greater than 27.8 in men and 27.3 in women.
Measurements
Coronary cineangiograms were obtained in
multiple projections, including angulated views in the sagittal
plane. Low ejection fraction was defined as <45%. Significant
coronary artery disease was defined as a 50% reduction in
the cross-sectional area of any major coronary artery.
Two-dimensionally guided M-mode echocardiography
was studied according to the recommendations of the American Society of
Echocardiography (ASE) using a leading
edge–to–leading edge convention.8 Left
ventricular posterior wall thickness,
ventricular septum thickness, and left
ventricular internal dimension were measured at end
diastole as defined by the onset of the QRS complex. Left
ventricular mass was calculated using the formula of Troy
and colleagues9 : ASE-Cube left ventricular
mass=1.05 ([left ventricular internal diameter+left
ventricular septal thickness+posterior wall
thickness]3-[left ventricular internal
diameter]3). Because this calculation results in an
overestimation of left ventricular mass by about 20%, the
equation developed by Devereux et al10 was used to
recalculate left ventricular mass: 0.80 (ASE-Cube left
ventricular mass)+0.6. Left ventricular mass
indexes were calculated by dividing left ventricular mass
by height, height2.7, and body surface area. The
criteria to define the presence of left ventricular
hypertrophy were adapted from studies that used different
methods to create a left ventricular mass index. Using mass
indexed by height, the Framingham Heart Study suggested cutoff values
for hypertrophy of 143 g/m and 102 g/m for men and women,
respectively.11 When left ventricular mass was
normalized for height2.7, the upper limits of 50
g/m2.7 and 47 g/m2.7 were defined by the study
from the Cornell Medical Center.12 13 By using mass
indexed by body surface area, the partition values of 131
g/m2 and 100 g/m2 for men and women,
respectively, were chosen in the Framingham Heart Study,11
whereas 117 g/m2 and 104 g/m2 were selected in
the study of the Cornell Medical Center.12 13
Additional
analyses using cutoff values of 125 g/m2 for men
and women were also performed.3 The success rate of
echocardiography examination was 85% to 90% in
this hospital.
Follow-up
An attempt was made to contact all patients either
during an
outpatient visit, by telephone, or by review of medical records of
clinic attendance. In addition, the database provided by the National
Death Index, which contains a standard set of identifying data for each
decedent of the nation, was searched annually until December 31, 1991,
for all members of the original cohort.14 Death
certificates of the decedents were obtained from the departments of
public health in the states where the patients died. Patients who were
not contacted and thus not confirmed to be alive and who were not
matched to a death certificate were considered alive as of the last
date included in the National Death Index File.
Statistical Analysis
Comparisons of baseline characteristics
between patients with
left ventricular hypertrophy and those without
hypertrophy were made by sex using the
2 test and a two-tailed Student t test
where appropriate. Mortality rate was expressed as per 100
patient-years. The crude relative risk was the ratio of the two
mortality rates (exposed versus nonexposed). A Cox proportional hazards
model was used to examine the risk of death independently associated
with left ventricular hypertrophy or increase
in left ventricular mass index for men and women separately
in the following manner. First, relative risks and their 95%
confidence intervals were calculated for patients with left
ventricular hypertrophy using various mass
indexation and defining criteria for the two death end points. Risks
then were estimated for patients in the highest sex-specific tertile of
mass versus those in the lower two tertiles. Finally, left
ventricular mass index values were entered into the Cox
regression model as continuous measures, and risks were calculated for
each 50-g/m increment in mass indexed by height, 20-g/m2.7
increment in mass indexed by height2.7, and
45-g/m2 increment in mass indexed by body surface area. The
units of increment were arbitrarily chosen and were approximately equal
to 1 SD of the relevant index. To further evaluate the sex difference
with respect to the prognostic significance of left
ventricular hypertrophy to mortality, the
interaction term between sex and left ventricular
hypertrophy or between sex and ventricular mass
index was tested in the Cox regression model with men and women
combined. All the analyses were done with adjustment for
baseline age, hypertension, and ejection fraction. Additional
adjustment for diabetes and obesity yielded similar results; hence,
they were not included in the final regression models.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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The prevalence rates of left ventricular hypertrophy varied from 36% to 53% in men and from 44% to 63% in women, depending on the criteria used for hypertrophy (Table 1
). The baseline characteristics for men
and women with and without hypertrophy are
presented in Table 2, in which left
ventricular mass indexed by body surface area and the
cutoffs developed in the Cornell Medical Center12 13
were
used to define the presence of left ventricular
hypertrophy. For both men and women, patients with
hypertrophy were older and had higher rates of
hypertension. The differences were not statistically significant,
however. Diabetes was more common in women with
hypertrophy. Mean body mass index and percent obesity were
not higher in patients with hypertrophy than in those
without, since body surface area had been used to adjust for body size.
When mass was indexed by height2.7,
ventricular hypertrophy was associated with
significantly greater mean body mass index (32.5 kg/m2
versus 29.6 kg/m2) and prevalence of obesity (43% versus
26%) as well as diabetes (27% versus 17%) in women. Compared with
patients without ventricular hypertrophy,
patients with hypertrophy had a lower mean ejection
fraction and a higher rate of impairment in ventricular
function (ejection fraction <45%) in men and women. By definition,
patients with hypertrophy had greater left
ventricular mass index.
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During a mean follow-up of 5 years (range, 0 to 9), 49 patients died
(26 men and 23 women), among whom 32 died from cardiac causes (18 men
and 14 women). Table 3 shows the sex-specific crude
mortality rate (per 100 patient-years) from all causes and cardiac
diseases by various definitions of left ventricular
hypertrophy. Patients with hypertrophy had a
greater mortality rate than those without both for men and women and
for both end points. The crude relative risk associated with
hypertrophy was greater in women than in men. In general,
women live longer than men. However, varied with the criteria
used to define hypertrophy and the study end points, women
with left ventricular hypertrophy had similar
or greater mortality than men without hypertrophy.
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Mortality rate for noncardiac causes was 2.10 per 100 patient-years in
men with left ventricular hypertrophy
(mass/body surface area 117 g/m2 in men and 104
g/m2 in women) versus 0.32 in those without (relative
risk=6.51, P<.05). For women, it was 1.07 per 100
patient-years and 0.40, respectively (relative risk=2.70, NS). No death
was attributed to stroke, but there was a tendency toward more renal or
other organ failure in patients with hypertrophy. The small
numbers in each specific death category prohibited further detailed
analysis.
The multivariate-adjusted relative risks and 95%
confidence intervals of death from all causes and cardiac diseases for
left ventricular hypertrophy are
presented in Table 4. Left
ventricular hypertrophy conferred a small to
moderate risk of death, with 95% confidence intervals including 1 in
men. In contrast, a significantly increased risk for both death end
points was observed in women. For all causes of death, the risks were
20% to 115% higher in women than in men. For cardiac death, the risks
were 3 to 5 times higher in women compared with men. Among four pairs
of sex-hypertrophy interactions, statistical significance
was found in two (P<.05) and was borderline in the other
two (P=.070 and .072).
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Risk of death for patients in the highest sex-specific tertile of mass
index was compared with those in the lower two tertiles (Table
5). A greater increase in risk of either end point was
found for women and was more prominent for cardiac death. All
sex-hypertrophy interaction terms were statistically
significant (P<.05) except for those based on mass indexed
by body surface area with all causes of death as the end point
(P=.085). The median values of the highest tertile for the
three mass indexes in Table 5 were 185 g/m, 71
g/m2.7, and 169 g/m2,
respectively, in men and 153 g/m, 67 g/m2.7, and 134
g/m2, respectively, in women. For the lower two
tertiles, the corresponding values were 110 g/m, 44
g/m2.7, and 99 g/m2 in men and 99 g/m,
43 g/m2.7, and 86 g/m2 in women. Thus,
differences in relative risk by tertile were not an artifact of the
distribution (ie, greater interquartile distance).
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Using left ventricular mass indexes as continuous
variables in the Cox regression analyses (Table 6), the
adjusted relative risk of death for each 50-g/m
increment in left ventricular mass was 1.4 in men and 1.7
in women (P=.339 for sex-mass index interaction). The
corresponding values for death from cardiac diseases were 1.2 in men
and 2.1 in women (P=.074 for sex-mass index interaction).
The risk with increasing mass indexed by height2.7 and mass
indexed by body surface area in men and women followed similar
patterns, with women having a higher risk, especially for cardiac
death. The differences were not statistically significant, however.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Evidence presented here suggests a larger relative risk associated with left ventricular hypertrophy in women than in men. Although not previously discussed in the literature, published data are consistent with the inference that left ventricular mass is a stronger risk factor in women than in men (Table 7
). Koren et al6 found that the
relative risk of 10-year cardiovascular morbid events
associated with left ventricular mass greater than 125
g/m2 was increased among hypertensive women compared with
hypertensive men. This finding held for all
cardiovascular events.3 Fatal cardiac
events and all-cause mortality were not reported by sex, however. In
the Framingham Heart Study,5 the risk factor–adjusted
relative risk of death from all causes was likewise higher in women
than men. In an elderly cohort (aged 59 years and older), the risk for
4-year incidence of coronary heart disease was similar between
men and women.4 None of these studies formally examined
the sex difference in the relative risk associated with left
ventricular hypertrophy, but the greater
adverse effect of left ventricular mass in women seems
apparent.
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Different indexes of left ventricular mass have been
proposed for normalization of mass for body
size.11 12 13 15 16 17 18 19
The optimal index, if a generalizable one
exists, is still undefined, and the use of differing indexes in the
literature can cause confusion. Additionally, for each of the current
indexes, left ventricular hypertrophy has been
defined as mass index above some arbitrary cutoff points, leading to
widely varying reports of the prevalence of left
ventricular hypertrophy (Table 1). The cut
points advocated, though often sex-specific, were developed in
cross-sectional studies of predominantly white participants. Their
appropriateness beyond these populations is not known. Risk of
cardiovascular morbidity and mortality might be
stratified more effectively in epidemiological studies by using left
ventricular mass index as a continuous variable rather
than simply using an arbitrary cut point.20
If there is a sex differential in the impact of left ventricular hypertrophy on mortality, the underlying mechanism is unclear. One possibility would be a higher prevalence of the concentric geometric abnormality in women than men. However, both in our data and in a previously published study by de Simone et al,13 concentric hypertrophy was actually higher in men. Among our patients with left ventricular hypertrophy, 65% of men and 54% of women were classified as having concentric hypertrophy when mass to height2.7 indexation was used.
A major limitation of our study is its small sample size, both in terms of the number of patients and events. We have previously demonstrated the prognostic role of left ventricular hypertrophy in predominantly black patients with both sexes combined.21 The current report examined this question by sex with extended follow-up and with more patients enrolled. The power of our study to discern an interaction is small unless it is reasonably strong.22 Thus, it is perhaps surprising that we were able to demonstrate an interaction that was reasonably consistent.
All of our inferences were based on standard statistical procedures and probability assumptions that require large sample sizes for validity. The conclusion of a study with small sample size may sometimes result from a few outliners. We therefore also conducted the "approximate permutation tests"23 based on a large number of random permutations of the data. We randomly assigned 163 patients as men and 273 as women repeatedly for 1000 times. A sex-hypertrophy interaction was found less than 5% of the time. Thus, it is unlikely that any significant interaction found in our standard test is due to chance.
At all ages, women in the United States experience lower mortality than men. In the presence of certain disease states, however, relative survival differences between men and women may either disappear or reverse; two of these conditions are coronary artery disease24 25 and diabetes.26 27 28 29 In this study, we demonstrated that women with left ventricular hypertrophy tend to lose their underlying survival advantage and their mortality risk becomes greater than, or at least similar to, men without hypertrophy. The beneficial effect of therapy for regression of left ventricular hypertrophy, in terms of morbidity and mortality, has not been well defined. However, screening and the institution of the specific choice of treatment for established hypertrophy assumes added importance, particularly in women, where both the relative and absolute increase in mortality is considerable.
Summary
Our findings indicate a sex difference in the
contribution of left
ventricular mass and hypertrophy to mortality
in patients without angiographically confirmed coronary artery
disease. This suggestion was strengthened by evidence that regardless
of the various mass indexations and criteria used to define left
ventricular hypertrophy, and no matter whether
the mass index was used as a categorical or continuous variable,
excess risk of mortality associated with increasing left
ventricular mass was more prominent in women than in men.
This outcome was consistent with other published data, even
though the relevant reports did not draw such a conclusion.
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Acknowledgments |
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This research was supported by a grant from the National Institutes of Health (RO1-HL-38557).
Received December 1, 1994; revision received February 2, 1995; accepted February 12, 1995.
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References |
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G. Schillaci, P. Verdecchia, C. Porcellati, O. Cuccurullo, C. Cosco, and F. Perticone Continuous Relation Between Left Ventricular Mass and Cardiovascular Risk in Essential Hypertension Hypertension, February 1, 2000; 35(2): 580 - 586. [Abstract] [Full Text] [PDF]
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G. Olivetti, E. Cigola, R. Maestri, C. Lagrasta, D. Corradi, and F. Quaini Recent advances in cardiac hypertrophy Cardiovasc Res, January 1, 2000; 45(1): 68 - 75. [Full Text] [PDF]
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E. O. Weinberg, C. D. Thienelt, S. E. Katz, J. Bartunek, M. Tajima, S. Rohrbach, P. S. Douglas, and B. H. Lorell Gender differences in molecular remodeling in pressure overload hypertrophy J. Am. Coll. Cardiol., July 1, 1999; 34(1): 264 - 273. [Abstract] [Full Text] [PDF]
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H.-W. Hense, B. Gneiting, M. Muscholl, U. Broeckel, B. Kuch, A. Doering, G.u. A. J. Riegger, and H. Schunkert The associations of body size and body composition with left ventricular mass: impacts for indexation in adults J. Am. Coll. Cardiol., August 1, 1998; 32(2): 451 - 457. [Abstract] [Full Text] [PDF]
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P. M. Okin, M. J. Roman, J. E. Schwartz, T. G. Pickering, and R. B. Devereux Relation of Exercise-Induced Myocardial Ischemia to Cardiac and Carotid Structure Hypertension, December 1, 1997; 30(6): 1382 - 1388. [Abstract] [Full Text]
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P. M. Okin, M. J. Roman, R. B. Devereux, and P. Kligfield Association of Carotid Atherosclerosis With Electrocardiographic Myocardial Ischemia and Left Ventricular Hypertrophy Hypertension, July 1, 1996; 28(1): 3 - 7. [Abstract] [Full Text]
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