(Circulation. 2001;103:836.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Dyslipidemia and an Unfavorable Fatty Acid Profile Predict Left Ventricular Hypertrophy 20 Years Later
From the Departments of Public Health and Caring Sciences (J.S., B.V., H.O.L.) and Medical Sciences (L.L., B.A.), Uppsala University, Sweden, and Department of Nutrition (A.A.), KTL (National Public Health Institute), Helsinki, Finland.
Correspondence to Johan Sundström, Department of Public Health and Caring Sciences/Geriatrics, PO Box 609, SE-75125 Uppsala, Sweden (Kålsängsgränd 10D, SE-75319 Uppsala, Sweden). E-mail johan.sundstrom{at}geriatrik.uu.se
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Abstract |
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Background—Left ventricular hypertrophy (LVH) is a common risk factor for cardiovascular mortality. Causes other than hypertension have not previously been investigated longitudinally. The aim of the present study was to determine hemodynamic, metabolic, and psychosocial predictors at 50 years of age for the prevalence of echocardiographic LVH and geometric subtypes at age 70 by use of a large sample of men from the general population followed up for 20 years.
Methods and Results—In 1970 to 1973, all men born from 1920 to 1924 and residing in Uppsala County, Sweden, were invited to participate in a health survey aimed at identifying risk factors for cardiovascular disease. At a reinvestigation 20 years later, echocardiographic left ventricular mass index was determined in 475 subjects. A 1-SD increase in body mass index, systolic or diastolic blood pressure, fasting LDL/HDL cholesterol, serum triglycerides, or the serum cholesterol ester proportion of several saturated fatty acids or oleic acid at age 50 significantly increased the odds of having LVH at age 70 by 27% to 41%, whereas an increase in linoleic acid proportion was protective. Almost all metabolic predictors were independent of ischemic heart disease, valvular disease, and use of antihypertensive medication at age 70.
Conclusions—Dyslipidemia and indices of a low dietary intake of linoleic acid and high intake of saturated and monounsaturated fats, as well as hypertension and obesity, at age 50 predicted the prevalence of LVH 20 years later in this prospective longitudinal cohort study, thereby suggesting that lipids may be important in the origin of LVH.
Key Words: hypertrophy • lipids • fatty acids • insulin • epidemiology
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Echocardiographically determined left ventricular hypertrophy (LVH) is an important risk factor for cardiovascular and all-cause mortality and morbidity,1 2 and an increased left ventricular relative wall thickness (RWT; wall thickness divided by ventricular diameter) also has an adverse prognosis.1 3
The cause of LVH is largely unknown. Cross-sectional studies4 5 6 have shown male sex, age, hypertension, obesity, certain valvular diseases, and previous myocardial infarction to be related to LVH or left ventricular mass index (LVMI). Heredity7 and alcohol use8 might also explain some of the variance in left ventricular mass. In a prospective study,9 average blood pressure over 30 years was associated with LVMI at follow-up. Hypertension is generally regarded as the worst culprit, as indicated by the large number of clinical trials on the subject.10 However, the variation in 24-hour blood pressure explains only 25% to 30% of the variation in left ventricular mass.11 Body size is a powerful determinant of left ventricular mass12 and may explain part of the sex difference in left ventricular mass.13 Weight reduction has been shown to decrease LVMI in overweight hypertensive patients even more than pharmacological antihypertensive treatment.14
Associations have recently been found15 16 17 between LVH and the insulin resistance syndrome.18 The left ventricular geometric correlates of insulin resistance are not clear; some studies16 17 19 20 have found insulin resistance or impaired glucose tolerance to be more closely related to thick left ventricular walls or increased RWT than to LVH.
The fatty acid composition of serum cholesterol esters (CEs) mainly reflects dietary fat quality over the previous 2 weeks21 and has been shown to predict myocardial infarction,22 but its relationship to LVH is not known. Furthermore, the relationships between smoking or other psychosocial factors and later LVH are not known.
Thus, there is a need for prospective studies of modifiable predictors of LVH. The aim of the present study was to determine hemodynamic, metabolic, dietary, and psychosocial predictors at age 50 years for the prevalence of echocardiographic LVH and left ventricular geometric subtypes at age 70 years by use of a large, regionally determined sample of men from the general population followed up for 20 years.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In 1970 to 1973, all men born from 1920 to 1924 and residing in Uppsala County were invited to participate in a health survey23 aimed at identifying risk factors for cardiovascular disease. Of the invited subjects, 2322 (82%) participated. At a reinvestigation of the cohort 20 years later, an echocardiographic examination was made in the first 583 consecutive subjects of 1221 available. The population of the present study consisted of 475 men in whom determination of left ventricular geometry was possible.24 All subjects gave informed consent, and the study was approved by the Ethics Committee of Uppsala University. Procedures followed were in accordance with department guidelines.
Investigations at Age 50
These investigations have been described
previously.23 Blood pressure
in the recumbent position was measured with a mercury manometer, and
radial pulse rate was counted. All blood samples were drawn in the
morning after an overnight fast. Blood glucose, serum insulin,
cholesterol, triglycerides, and HDL cholesterol were measured, and LDL
cholesterol was calculated with Friedewald’s formula. The CE
proportions of fatty acids (14:0 to 22:6 
3) were determined by gas
chromatography.22 No dietary
records were obtained, but in other population studies in middle-aged
men in the 1970s in Sweden, intake of fat corresponded to 
40%, of
carbohydrates to 45% to 50%, and of protein to 13% to 15% of energy
intake. The estimated intake of saturated fats corresponded to 17% to
18% of energy intake. At age 70, 7-day dietary records in 444 of the
475 subjects showed an intake of fat corresponding to 35%, of
carbohydrates to 48%, and of protein to 16% of energy intake, which
was comparable to other contemporary Swedish populations of the same
age.
A questionnaire covered level of physical activity (4 categories) and education (5 categories). Coding of smoking (smoker, nonsmoker, ex-smoker), civil status, and socioeconomic status (3 social classes, Central Bureau of Statistics) was based on interview reports.23
Investigations at Age 70
At age 70, 167 subjects were regularly using
antihypertensive medication, and 38 used lipid-lowering drugs, of whom
16 used statins, 15 fibrates, 6 resins, and 2 nicotinic acid, as
monotherapy or in combination. Fifty-four subjects had been
hospitalized owing to ischemic heart disease (ICD-9 codes 410 to 414)
between the investigations at 50 and 70 years of age. Seventeen
subjects had significant echocardiographic valvular disease (aortic or
mitral stenosis or regurgitation grades 3 or 4).
A comprehensive 2D and Doppler echocardiography examination
was performed as described
previously.24 Left
ventricular mass was divided by body surface area to obtain LVMI. LVH
was defined as an LVMI 
150 g/m2 according
to data from the Framingham Heart
Study,25 and a partition
value of 0.4426 was used for
RWT [(interventricular septum+posterior wall thickness)/left
ventricular end-diastolic diameter]. Thus, left ventricular geometry
was considered normal if RWT was <0.44 and LVMI was <150
g/m2. A normal LVMI with increased RWT was
denoted concentric
remodeling,26 and a
hypertrophic left ventricle was denoted eccentric if the RWT was normal
and concentric if the RWT was increased.
Statistical Analysis
Variables with a skewed distribution (fasting serum
insulin, triglycerides, LDL/HDL cholesterol, and CE proportion of
palmitoleic, stearic, 
-linolenic, 
-linolenic, eicosapentaenoic,
and docosahexaenoic acids) were logarithmically transformed to achieve
normal distribution, and these transformed variables were used in all
analyses. Logistic regression was used with LVH or increased RWT at age
70 as outcome variables and standardized continuous variables (mean=0,
SD=1) or indicator variables for multilevel nominal variables at age 50
as explanatory variables. Multiple logistic regression was used to
adjust for possible confounders, which were treated as dichotomous
variables. Squared terms and interaction terms were tested in all
regressions. ANOVA was used to calculate differences in means between
left ventricular geometric subgroups and factorial ANOVA to adjust for
possible confounders. Post hoc Bonferroni-adjusted comparisons were
only performed if overall ANOVA was significant. A
2 test was used to evaluate differences
in nominal variables between geometric subgroups. Two-tailed
significance values were given with
P<0.05 regarded as
significant. Stata 6.0 software was used (Stata
Corporation).
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Prediction of LVH
The prevalence of LVH at age 70 was 28% in the present cohort. Among the variables associated with the insulin resistance syndrome, a 1-SD increase in body mass index, systolic or diastolic blood pressure, fasting LDL/HDL cholesterol, or serum triglycerides at age 50 resulted in 27% to 41% increased odds of having LVH at age 70 (Table 1
). A 1-SD increase in the CE proportion of
any of myristic (14:0), palmitic (16:0), stearic (18:0), oleic (18:1),
or eicosapentaenoic acid (20:5 3) at age 50 increased the odds of
having LVH at age 70 by 29% to 37%, whereas a 1-SD increase in the
proportion of linoleic acid (18:2 6) at age 50 reduced the odds of
having LVH at age 70 by 24%
(Table 1). Levels of physical activity, education, smoking,
civil status, and socioeconomic status at age 50, crude or adjusted,
were not associated with later LVH (data not shown). With simultaneous
control for ischemic heart disease during follow-up, valvular disease,
and use of antihypertensive medication at age 70, the adjusted odds
ratios were similar to the crude odds ratios, but systolic and
diastolic blood pressure and palmitic acid were no longer significantly
associated with LVH
(Table 1). With control also for body mass index at age 50,
LDL/HDL cholesterol and proportions of stearic, oleic, linoleic, and
eicosapentaenoic acids remained significant predictors of
LVH.
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Prediction of Increased Left Ventricular
RWT
The prevalence of increased RWT at age 70 was 25% in
the present cohort. A 1-SD increase in CE proportion of oleic acid
(18:1), -linolenic acid (18:3 6), or dihomo--linolenic acid
(20:3 6) at age 50 increased the odds of having increased RWT at age
70 by 28% to 32%, whereas a 1-SD increase in the proportion of
linoleic acid (18:2 6) at age 50 reduced the odds of having
increased RWT at age 70 by 26%
(Table 2). The studied psychosocial issues were not
associated with increased RWT (data not shown). Controlling for
ischemic heart disease during follow-up, valvular disease, and use of
antihypertensive medication at age 70 gave results similar to the
unadjusted analysis
(Table 2). When body mass index at age 50 was also
controlled for, proportions of oleic and linoleic acid remained
significantly associated with increased RWT.
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We reperformed all the above analyses in a subsample of 421
subjects without ischemic heart disease during follow-up. In logistic
regression analysis with LVH at age 70 as the dependent variable,
adjusted for valvular disease and use of antihypertensive medication at
age 70, significant predictors were the same as when adjusted for
ischemic heart disease during follow-up in the total sample, with the
addition of total cholesterol and the exception of myristic acid
(14:0). When increased RWT was used as dependent variable, only
dihomo--linolenic acid (20:3 6) was significant in the ischemic
heart disease–free subsample.
In the total sample, when also adjusting for use of
lipid-lowering drugs at age 70 (adjusting for antihypertensive drugs,
lipid-lowering drugs, and valvular disease at age 70 and ischemic heart
disease during follow-up), the effect of triglycerides
(P=0.055) and LDL/HDL
cholesterol (P=0.063) on later
LVH became of borderline significance, but body mass index and CE
proportions of fatty acids 14:0, 18:0, 18:1, 18:2 6, and 20:5 3
remained significant, and the CE proportion of docosahexaenoic acid
(22:6 3) became significantly directly related to later LVH.
Regarding prediction of later increased RWT, the same adjustment made
oleic acid lose significance, but other predictors remained
significant.
Characteristics at Age 50 According to Left
Ventricular Geometric Patterns at Age 70
The levels of several variables associated with the
insulin resistance syndrome and CE proportions of several fatty acids
determined at age 50 varied significantly between the 4 left
ventricular geometry groups determined at age 70
(Table 3). In the concentric remodeling group, CE
proportions of oleic (18:1) and -linolenic acid (18:3 6) were
significantly higher and the proportion of linoleic acid (18:2 6)
was significantly lower than in the normal geometry group. In the
concentric LVH group, diastolic blood pressure and CE proportions of
myristic (14:0), palmitic (16:0), oleic (18:1), and eicosapentaenoic
acid (20:5 3) were significantly higher and linoleic acid (18:2
6) was significantly lower than in the normal geometry group. In the
eccentric LVH group, body mass index, systolic and diastolic blood
pressure, fasting serum triglycerides, and CE proportions of oleic
(18:1) and eicosapentaenoic acid (20:5 3) were significantly higher,
and linoleic acid (18:2 6) was significantly lower than in the
normal geometry group. The studied psychosocial factors did not vary
between the left ventricular geometry groups (data not shown). With
simultaneous control for ischemic heart disease during follow-up and
for valvular disease and use of antihypertensive medication at age 70,
differences between groups regarding proportions of oleic, linoleic,
-linolenic, and eicosapentaenoic acids were still significant,
whereas other differences lost significance. When body mass index at 50
was also controlled for, differences in oleic, linoleic, and
eicosapentaenoic acids remained
significant.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this 20-year follow-up of a large, regionally determined sample of men from the general population, dyslipidemia and a CE fatty acid composition indicating a high dietary intake of saturated and monounsaturated fats and low intake of linoleic acid at age 50 predicted the prevalence of LVH at age 70 to a similar degree as hypertension and obesity. The impact of obesity, dyslipidemia, and an unfavorable fatty acid profile on LVH was independent of history of ischemic heart disease, valvular disease, and use of antihypertensive medication at age 70. The relationships between dyslipidemia and an unfavorable fatty acid profile and later LVH were also independent of obesity at age 50. Previously, hypertension has been related to the development of LVH in a prospective study,9 but the predictive value of obesity, dyslipidemia, and indices of an unfavorable diet for LVH has never been shown.
Focus has recently turned to the association between LVH and the insulin resistance syndrome.15 16 17 19 20 Some cross-sectional population studies on the subject exist,15 19 20 but most studies have been made in small groups of hypertensive patients, which would not be ideal for the search for correlates to LVH other than hypertension. In the present study, lipid derangements, unfavorable fatty acid profile, and obesity seemed to be powerful longitudinal predictors of LVH development, in contrast to a cross-sectional analysis of the same cohort at age 70 in which several measures of glucose intolerance and insulin resistance were related to an increased RWT and concentric remodeling but less to LVH.20 The reason for these differences is not clear, but the metabolic associations may be affected by the normally observed age-related increase in RWT.27
The relationship between an unfavorable CE fatty acid
composition and later LVH is important, because the fatty acid
composition reflects dietary fat quality over the past couple of
weeks21 and thus is a
modifiable risk factor. Previous studies of the present cohort have
shown that a fatty acid profile indicating a high dietary intake of
saturated fats and low intake of linoleic acid is related to insulin
resistance28 and predicts
myocardial infarction over 19
years.22 Because the impact
of other traditional risk factors on myocardial
infarction22 was similar to
their impact on LVH in the present study, LVH might be regarded as an
intermediary risk factor on the pathway between the described risk
factor profile and myocardial infarction. The apparently reciprocal
effects of linoleic acid (which makes up >50% of all CE fatty acids)
and the saturated fatty acids may be due to passive redistribution of
the less abundant acids after changes in linoleic acid proportion occur
but may also reflect true pathophysiological effects of the saturated
fatty acids. In these men, the dietary source of oleic acid was not
olive oil (which was not used by middle-aged men in Sweden in the early
1970s) but food groups containing a high proportion of saturated fatty
acids, such as dairy products, solid margarines, and meat products. The
low impact of 3 polyunsaturated fatty acids, which are generally
regarded as favorable, and the initially surprising relationship
between eicosapentaenoic acid (20:5 3) levels and later LVH may be
because a high intake of linoleic acid–rich vegetable fats reduces
3-acid levels in serum21
by a decreased conversion of -linolenic acid (18:3 3) to
eicosapentaenoic acid (20:5 3) through competition for the same
enzyme systems. Other factors than dietary fat intake may affect CE
fatty acid profile, but the relationships between LDL/HDL cholesterol
and triglycerides and later LVH support the adverse role of a diet rich
in saturated fats.
No psychosocial variables were associated with development of LVH in the present study, in accordance with a cross-sectional population study15 in which exercise physical activity and smoking were not related to LVH. The present cohort has been closely monitored for 20 years and may therefore be healthier than average Swedish 70-year-old men. Thus, associations in the present study may be weaker than in the general population.
One limitation of the study is the lack of dietary records at baseline and the resulting lack of knowledge about any potential dietary certainties in the studied population, which might influence the generalizability of the findings of the present study. Other limitations of the study include absence of echocardiographic data at baseline, possible underestimation of the impact of variables with substantial measurement error or missing data, and bias due to loss to follow-up. Of course, confounding factors other than the ones for which we adjusted may also exist. Because many analyses were performed, some chance associations may have been found. This study has a limited generalizability to women and other age and ethnic groups, and further studies are needed for confirmation of these findings.
In conclusion, dyslipidemia and indices of a low dietary intake of linoleic acid and high intake of saturated and monounsaturated fats, as well as obesity and hypertension, at age 50 predicted the prevalence of LVH at age 70 in this 20-year follow-up of a large, regionally determined sample of men derived from the general population. The impact of obesity, dyslipidemia, and evidence of high dietary intake of saturated fats on LVH was independent of history of ischemic heart disease, valvular disease, and use of antihypertensive medication, indicating that lipids may be important in the origin of LVH.
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Acknowledgments |
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This study was supported by the Swedish Medical Research Council No. 5446, Trygg Hansa, Thuréus Foundation, Foundation for Geriatric Research (Stiftelsen för Geriatrisk Forskning), Geriatric Fund (Geriatriska Fonden), and Uppsala University.
Received July 20, 2000; revision received October 6, 2000; accepted October 10, 2000.
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