(Circulation. 2001;103:2346.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Echocardiographic and Electrocardiographic Diagnoses of Left Ventricular Hypertrophy Predict Mortality Independently of Each Other in a Population of Elderly Men
From the Departments of Public Health and Caring Sciences (J.S., J.Ä., B.Z., H.O.L.) and Medical Sciences (L.L., B.A.), Uppsala University, Uppsala, Sweden.
Correspondence to Johan Sundström, MD, PhD, Department of Public Health and Caring Sciences/Geriatrics, PO Box 609, SE-75125 Uppsala, Sweden. E-mail johan.sundstrom{at}geriatrik.uu.se
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Abstract |
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Background—The increased risk associated with left ventricular hypertrophy (LVH) diagnosed echocardiographically (Echo-LVH) or electrocardiographically (ECG-LVH) is well known, but the clinically relevant question of how much additional prognostic information would be provided by echocardiographically assessing LVH if a subject’s ECG-LVH and hypertension status are known has not been addressed.
Methods and Results—We investigated whether Echo-LVH and ECG-LVH predicted total and cardiovascular mortality and morbidity independently of each other and of other cardiovascular risk factors by using a population-based sample of 475 men investigated at age 70 with a median follow-up time of 5.2 years. Echocardiographic left ventricular mass index (LVMI) predicted total mortality (hazards ratio [HR] 1.44, 95% CI 1.09 to 1.92, for a 1-SD increase in LVMI) and cardiovascular mortality (HR 2.38, 95% CI 1.52 to 3.73) independently of ECG-LVH and other cardiovascular risk factors. ECG-LVH, defined as Cornell product >244 µV · s, predicted total mortality (HR 2.89, 95% CI 1.41 to 5.96) independently of LVMI and other cardiovascular risk factors. Thus, Echo-LVH and ECG-LVH provided complementary prognostic information, especially in hypertensive subjects.
Conclusions—Echo-LVH and ECG-LVH predict mortality independently of each other and of other cardiovascular risk factors, implying that Echo-LVH and ECG-LVH in part carry different prognostic information. Therefore, to fully assess the increased risk associated with these conditions, both ECG and echocardiography should be performed.
Key Words: hypertrophy • diagnosis • mortality • insulin • risk factors
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Left ventricular hypertrophy (LVH) imposes a great cardiovascular risk whether it is diagnosed by ECG1 2 3 4 or by echocardiography.5 6 7 However, both these methods for detecting LVH have setbacks. The ECG is rather insensitive in detecting anatomic LVH, but the increased risk associated with electrocardiographically diagnosed LVH (ECG-LVH) has nevertheless been thought to reflect an increased left ventricular mass. Echocardiography is a more expensive and less available method, and it is also sometimes difficult to distinguish physiological from pathological LVH and thereby to grade cardiovascular risk. To our knowledge, no attempt has previously been made to investigate whether subjects with echocardiographically diagnosed LVH (Echo-LVH) who later suffer morbid events or die also have ECG-LVH, or vice versa, or whether the methods provide complementary prognostic information.
Echo-LVH and an increased left ventricular relative wall thickness are related to the insulin resistance syndrome of potent cardiovascular risk factors, including hypertension.8 9 10 It is not fully known whether the increased cardiovascular risk associated with Echo-LVH or ECG-LVH is independent of the associated metabolic disturbances and hypertension.
The aim of the present study was to investigate, by use of a large cohort of elderly men from the general population, whether Echo-LVH and ECG-LVH predict total and cardiovascular mortality and morbidity independently of each other and of the insulin resistance syndrome. We also investigated how much additional prognostic information was provided by an echocardiographic examination if the subject’s ECG-LVH and hypertension status were known.
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Methods |
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Subjects
From 1970 to 1973, all men born from 1920 to 1924 and residing in the county of Uppsala were invited to a health survey aimed at identifying risk factors for cardiovascular disease. The cohort was reinvestigated 20 years later, at 70 years of age (the baseline of the present study, Table 1
), which has been extensively described
previously.8 The population
of the present study consisted of 475 of the first 583 consecutive
men in the latter investigation who had technically satisfactory
echocardiographic examinations. Fifty-four subjects had
been hospitalized because of ischemic heart disease
(International Classification of Diseases [ICD]-9 codes 410 to 414)
before the baseline investigation. Two hundred twelve subjects (45%)
were hypertensive (systolic blood pressure 
160 mm Hg or
diastolic blood pressure 95 mm Hg at a single
office visit or regular use of antihypertensive medication). All
subjects gave written informed consent, and the study was approved by
the Ethics Committee of Uppsala University. Procedures followed
were in accordance with departmental guidelines.
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Follow-Up
The subjects had a median follow-up time of 5.2 years
(range 0.7 to 6.4 years), contributing to 2415.6 person-years. End
points were defined by using the Swedish national cause-of-death and
hospital discharge registers. During follow-up, 44 subjects died (rate
1.82/100 person-years at risk [PYAR]); 18 deaths were from
cardiovascular disease (ICD codes 390 to 459, rate
0.75/100 PYAR), with 7 deaths from acute myocardial infarction and 4
deaths from stroke. Morbidity was defined as first hospitalization or
death from cardiovascular disease or any cause and was
evaluated only for subjects who had not previously been hospitalized
for cardiovascular disease or any cause, respectively.
During follow-up, 48 (39%) of 122 subjects (rate 9.50/100 PYAR) had a
morbid event of any cause, and 64 (19%) of 338 subjects (rate 4.09/100
PYAR) had a cardiovascular morbid
event.
Electrocardiography
A standard 12-lead ECG was recorded at 50
mm/s and 10 mm/mV. Because different LVH criteria measure
different cardiac
properties,11 we
analyzed several criteria: Sokolow-Lyon voltage, Cornell
voltage, and left ventricular strain, which have previously
been validated in prospective
studies,1 2 12
and the Cornell product, which has not been previously validated in
a prospective study but has been used as inclusion criterion in the
Losartan Intervention for Endpoint Reduction in Hypertension
(LIFE) study.13 LVH was
defined as a Sokolow-Lyon voltage amplitude of
(SV1+RV5 or
RV6) 3.5 mV, a Cornell voltage of
(SV3+RaVL) >2.8 mV, or a Cornell product of
[(SV3+RaVL)xQRS duration] >244 µV · s.
Left ventricular strain was defined as a downsloping
ST-segment depression >0.1 mV with T-wave flattening or inversion in
leads V4 to V5.
Sensitivities/specificities (%) for detection of
echocardiographic LVH were 27/88 for Sokolow-Lyon
voltage 3.5 mV, 17/91 for Cornell voltage >2.8 mV, 28/88 for Cornell
product >244 µV · s, and 21/92 for left
ventricular strain, in the present
population.
Echocardiography
Comprehensive 2D and Doppler
echocardiography was performed as described
previously.14 Left
ventricular dimensions (interventricular septal
thickness [IVS], posterior wall thickness [PW], and left
ventricular end-diastolic diameter [LVEDD])
were measured at end of diastole with M-mode by using the
leading-edge–to–leading-edge convention. Left ventricular
mass was determined by using the Troy formula according to the
recommendations of the American Society of
Echocardiography
(ASE)15 : left
ventricular mass (g)=1.05[(LVEDD+
IVS+PW)3 -LVEDD3 ].
Left ventricular mass was divided with body surface area to
obtain the left ventricular mass index (LVMI). LVH was
defined as LVMI 150 g/m2, according to
data from the Framingham Heart
Study.15 Examinations and
readings of the images were performed by one experienced physician
(B.A.) who was unaware of the other data of the subjects. A
reproducibility study was made in 22 subjects 
1 month after the
original investigations. The intraindividual coefficients of variation
were 8.8% for IVS, 6.7% for PW, 3.5% for LVEDD, and 12.5% for
LVMI.
Other Cardiovascular Risk
Factors
These analyses have been described in detail
previously.8 Insulin
sensitivity was determined with the hyperinsulinemic
euglycemic clamp technique, performed according to the
method of DeFronzo et al16
with a slight modification: insulin was infused at a constant rate of
56 mU/(min · m2). The insulin sensitivity
index was calculated by dividing glucose disposal, calculated as
milligrams glucose infused/(min · kg body wt), by the mean plasma
insulin concentrationx100 (mU/L) during the last 60 minutes of the
2-hour clamp. Blood samples for fasting concentrations were drawn in
the morning after an overnight fast. Proinsulin concentrations were
measured with a specific 2-site immunoradiometric assay
technique.17
Cholesterol and triglyceride concentrations in
serum and HDL were assayed by enzymatic techniques, and LDL
cholesterol was calculated by using Friedewald’s
formula. The coding of smoking was based on interview reports. Supine
systolic and diastolic blood pressures were
measured twice in the right arm after 10 minutes of rest, and the means
were calculated.
Statistical Analysis
Variables with a skewed distribution
(triglycerides and proinsulin) were logarithmically
transformed to achieve normal distribution, and these transformed
variables were used in all analyses. Two-tailed 95% CIs
and significance values were given, with a value of
P<0.05 regarded as
significant. The prognostic value of transfer from one level of a
dichotomous variable to another, or a 1-SD increase in a continuous
variable, was investigated with Cox proportional hazards ratios
(HRs). The proportionality of hazards was confirmed with Kaplan-Meier
plots. Adjustments were made for either LVMI, previous ischemic
heart disease, or 9 cardiovascular risk factors (clamp
insulin sensitivity index, proinsulin, LDL and HDL
cholesterol, triglycerides, waist
circumference, smoking, hypertension, and previous ischemic
heart disease) in multiple Cox proportional hazards analyses.
There was no adjustment for age because all subjects were of the same
age at baseline, with a narrow age span. Cutoff levels for LVMI
other than 150 g/m2 were sought by using
histograms of quartiles of LVMI for cardiovascular and
total mortality and by performing logistic regression and receiver
operating characteristic (ROC) curves. Stata 6.0 software (Stata Corp)
was used.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Predictive Value of Echo-LVH
Echo-LVH (as a dichotomous variable) was a significant (HR 1.91 and 3.97) predictor of cardiovascular morbidity and mortality (see Table 2
for details). Also, LVMI as a continuous
variable was a significant predictor of morbidity and mortality
from cardiovascular disease and total mortality (HR
1.51 to 2.37 for a 1-SD increase,
Table 2). Because these results indicated that some
predictive information was lost when dichotomizing LVMI, cutoff levels
other than the proposed 150 g/m2
level15 were sought by using
quartiles of LVMI and logistic regressions and ROC curves, with total
and cardiovascular mortality as dependent
variables. Total mortality seemed to increase rather linearly with
increasing LVMI
(Figure 1), and no obvious cutoff level for prediction of
total mortality was found. In contrast, the risk for
cardiovascular mortality was markedly increased in only
the fourth quartile of LVMI (LVMI 154 to 250
g/m2,
Figure 1). This information combined with the ROC curve for
LVMI regarding cardiovascular mortality
(Figure 2) indicated that 150 g/m2
was the cutoff level that provided a reasonable combination of
sensitivity and specificity for detection of this increased
risk.
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Nine cardiovascular risk factors were also evaluated as risk factors for mortality and morbidity. Smoking (HR 3.38, 95% CI 1.33 to 8.59) or a 1-SD increase in proinsulin (HR 1.94, 95% CI 1.36 to 2.77) increased the risk, and a 1-SD increase in HDL cholesterol (HR 0.48, 95% CI 0.26 to 0.88) decreased the risk of mortality from cardiovascular disease. Smoking predicted total morbidity (HR 2.00, 95% CI 1.09 to 3.66).
When adjusting for these 9 cardiovascular
risk factors, the predictive value of LVMI as a continuous variable
for total and cardiovascular mortality remained
significant, whereas the impact of dichotomized Echo-LVH on later
cardiovascular mortality decreased in significance
(Table 2
).
Predictive Value of
Electrocardiographic-LVH
LVH that was defined as Sokolow-Lyon voltage 3.5 mV
was a significant predictor of total mortality (HR 2.00; see
Table 2 for details). LVH that was defined as Cornell voltage >2.8 mV was a
significant predictor of total mortality (HR 2.89), even after
adjustment for LVMI. LVH that was defined as Cornell product >244
µV · s was a strong (HR 3.56 and 3.82) predictor of both
cardiovascular and total mortality, even after
adjustment for 9 other cardiovascular risk factors.
Adjustment for LVMI made the prediction of
cardiovascular mortality, but not total mortality,
decrease in significance. The left ventricular strain
pattern predicted morbidity only from cardiovascular
disease (HR 2.39).
Comparison Between the Predictive Capacities of
Echo-LVH and ECG-LVH
In multivariate Cox proportional
hazards analyses with LVMI, Cornell product >244 µV ·
s, Sokolow-Lyon voltage 3.5 mV, and 9 other
cardiovascular risk factors as independent
variables
(Table 3), LVMI and Cornell product >244 µV · s
were significant predictors of total mortality. LVMI, previous
ischemic heart disease, HDL cholesterol, smoking,
and proinsulin were significant predictors of
cardiovascular mortality. No interaction terms between
LVMI and the ECG-LVH criteria were significant predictors in the
analyses.
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By assessing Echo-LVH if ECG Cornell product 
244
µV · s, another 7 (16%) of the 44 total deaths (rate 1.39/100
PYAR) (another 6 [33%] of the 18 cardiovascular
deaths [rate 1.19/100 PYAR]) could be predicted
(Figure 3). By assessing the ECG Cornell product if
echocardiography showed no LVH, another 8 (18%) of
the 44 total deaths (rate 4.03/100 PYAR) (another 2 [11%] of the 18
cardiovascular deaths [rate 1.01/100 PYAR]) could be
predicted
(Figure 3).
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We also stratified for hypertension. In 263 normotensive
subjects, no more total or cardiovascular deaths could
be predicted by assessing Echo-LVH if ECG Cornell product 244
µV · s. In 212 hypertensive subjects, another 7 of the 19 total
deaths (another 6 of the 12 cardiovascular deaths)
could be predicted by assessing Echo-LVH if ECG Cornell product
244 µV · s.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, echocardiographic LVMI and the ECG-LVH criterion (Cornell product >244 µV · s) predicted mortality independently of each other and of other cardiovascular risk factors, which indicates that Echo-LVH and ECG-LVH were not identical conditions. It was also shown that many but not all of the subjects whose deaths were predicted by ECG-LVH were also identified by echocardiography, and vice versa.
The main new finding of the present study is that the
previously known prognostic value of ECG-LVH to some extent is
independent of echocardiographic LVMI, and vice versa.
Therefore, we have assessed the clinically relevant question of how
much additional prognostic information would be gained by referring a
subject to an echocardiographic examination if the
subject’s ECG-LVH and hypertension status are known. Our conclusion is
that the additional prognostic value of an Echo-LVH assessment if ECG
Cornell product 244 µV · s was low in normotensive subjects,
whereas in hypertensive subjects or the population as a whole,
echocardiography and ECG provided complementary
prognostic information. Today, ECG is generally regarded as merely a
less sensitive method than echocardiography for
detecting anatomic LVH, but in view of the findings of the present
study, the LVH information obtained with ECG should rather be regarded
as of equal prognostic importance as Echo-LVH information. The
implication for the clinician assessing the risk associated with LVH is
that the decision of which patient to refer to
echocardiography should be based on knowledge of
ECG-LVH and hypertension status. A normotensive patient without ECG-LVH
may well have Echo-LVH, but the latter information is of low prognostic
importance and hardly motivates an echocardiographic
examination.
Echo-LVH appeared to be slightly more associated with the
prevalence of concomitant cardiovascular risk factors
than ECG-LVH defined as Cornell product >244 µV · s
(Table 1). This was also reflected in the observation that
adjusting for cardiovascular risk factors made the
impact of Echo-LVH, but not Cornell product >244 µV · s, on
later cardiovascular mortality decrease in significance
(Table 2). The relationships between left
ventricular geometry and cardiovascular
risk factors in this population have been investigated
previously.8
Total mortality seemed to increase linearly with increasing
LVMI, but the risk of cardiovascular mortality was
markedly increased only in the fourth quartile of LVMI. This finding
may be due to the limited number of cardiovascular
deaths but may also reflect true relationships. In 2 previous
studies,5 7 the
relationships between LVMI and coronary or
cardiovascular morbidity were linear, but in 1 larger
study,6
cardiovascular disease and all-cause mortality rates
seemed substantially increased in the highest quartile of LVMI only.
Defining LVH as LVMI 150 g/m2 (a cutoff
level originally derived from a healthy, middle-aged sample of men
living in Framingham15 )
seems to limit the information carried in the continuous-variable
LVMI regarding prediction of all-cause mortality but was relevant for
the prediction of cardiovascular mortality and
morbidity in the present population. Altogether, a cutoff level of
150 g/m2 seems appropriate for LVMI measured
with the leading-edge–to–leading-edge convention and the Troy
formula, corresponding to 131 g/m2 measured
with the Penn convention and the modified cube
formula.15 Left
ventricular mass by both conventions correlates well with
left ventricular mass determined at
necropsy18 but slightly
overestimates it (6% by the Penn convention and 25% by the ASE
convention). Thus, LVMI measured with the
leading-edge–to–leading-edge convention and the Troy formula can
easily be transformed to reflect anatomic
measurements18 : left
ventricular mass=0.80(ASE mass)+0.6 g.
One of the strengths of the present study is that all subjects were the same age at baseline, which overcomes the problem of age differences between quantiles of LVMI found in other studies.5 6 7 The subjects are also of the same sex and ethnicity, which eliminates the need for adjustment for the influence of these important determinants of LVMI and other cardiovascular risk factors but limits the generalizability of the study to women and other ethnic and age groups. Other limitations of the present study include possible misclassification of end points, although the accuracy of the Swedish hospital discharge and cause-of-death registers has been shown to be high.19 Confounding factors other than the ones adjusted for in the present study may, of course, exist. However, we could show that echocardiographic LVMI was a powerful predictor of mortality independent of components of the insulin resistance syndrome (a condition recently found to be related to LVH and increased left ventricular relative wall thickness8 9 10 ), smoking, previous ischemic heart disease, and the novel risk factor proinsulin (which was an independent predictor of cardiovascular mortality in a 27-year follow-up study from age 50 in this cohort [B. Zethelius, unpublished data, 2000]).
In conclusion, total and cardiovascular mortality risk increases with increasing echocardiographic LVMI, independent of other cardiovascular risk factors, and cardiovascular risk was fairly well assessed by dichotomized Echo-LVH. ECG-LVH also predicted total and cardiovascular mortality, especially the Cornell product criterion, which predicted total mortality independent of LVMI and other risk factors. Thus, Echo-LVH and ECG-LVH are not identical conditions, and to fully assess the considerable risk associated with either condition, both an ECG and an echocardiogram should be performed, especially in hypertensive subjects.
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Acknowledgments |
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This study was supported by the Swedish Medical Research Council (grant 5446), Trygg Hansa, Thuréus Foundation, Foundation for Geriatric Research (Stiftelsen för Geriatrisk Forskning), Geriatric Fund (Geriatriska Fonden), and Uppsala University.
Received November 15, 2000; revision received February 8, 2001; accepted March 1, 2001.
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J. A. Laukkanen, S. Kurl, J. Eranen, M. Huttunen, and J. T. Salonen Left Atrium Size and the Risk of Cardiovascular Death in Middle-aged Men Arch Intern Med, August 8, 2005; 165(15): 1788 - 1793. [Abstract] [Full Text] [PDF]
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E. Nunez, D. K. Arnett, E. J. Benjamin, P. R. Liebson, T. N. Skelton, H. Taylor, and M. Andrew Optimal Threshold Value for Left Ventricular Hypertrophy in Blacks: The Atherosclerosis Risk in Communities Study Hypertension, January 1, 2005; 45(1): 58 - 63. [Abstract] [Full Text] [PDF]
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R. H. Fagard, J. A. Staessen, L. Thijs, H. Celis, W. H. Birkenhager, C. J. Bulpitt, P. W. de Leeuw, G. Leonetti, C. Sarti, J. Tuomilehto, et al. Prognostic Significance of Electrocardiographic Voltages and Their Serial Changes in Elderly With Systolic Hypertension Hypertension, October 1, 2004; 44(4): 459 - 464. [Abstract] [Full Text] [PDF]
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P. M. Okin, R. B. Devereux, M. S. Nieminen, S. Jern, L. Oikarinen, M. Viitasalo, L. Toivonen, S. E. Kjeldsen, S. Julius, S. Snapinn, et al. Electrocardiographic Strain Pattern and Prediction of Cardiovascular Morbidity and Mortality in Hypertensive Patients Hypertension, July 1, 2004; 44(1): 48 - 54. [Abstract] [Full Text] [PDF]
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M. P. Schneider, A. U. Klingbeil, C. Delles, M. Ludwig, R. E. Kolloch, M. Krekler, K. O. Stumpe, and R. E. Schmieder Effect of Irbesartan Versus Atenolol on Left Ventricular Mass and Voltage: Results of the CardioVascular Irbesartan Project Hypertension, July 1, 2004; 44(1): 61 - 66. [Abstract] [Full Text] [PDF]
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E. Lonn, R. Shaikholeslami, Q. Yi, J. Bosch, B. Sullivan, P. Tanser, A. Magi, and S. Yusuf Effects of ramipril on left ventricular mass and function in cardiovascular patients with controlled blood pressure and with preserved left ventricular ejection fraction: A substudy of the Heart Outcomes Prevention Evaluation (HOPE) trial J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2200 - 2206. [Abstract] [Full Text] [PDF]
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P. M. Okin, M. J. Roman, E. T. Lee, J. M. Galloway, B. V. Howard, and R. B. Devereux Combined Echocardiographic Left Ventricular Hypertrophy and Electrocardiographic ST Depression Improve Prediction of Mortality in American Indians: The Strong Heart Study Hypertension, April 1, 2004; 43(4): 769 - 774. [Abstract] [Full Text] [PDF]
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P. E. Gates, H. Tanaka, J. Graves, and D. R. Seals Left ventricular structure and diastolic function with human ageing: Relation to habitual exercise and arterial stiffness Eur. Heart J., December 2, 2003; 24(24): 2213 - 2220. [Abstract] [Full Text] [PDF]
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B. M. Mayosi, B. Keavney, A. Kardos, C. H. Davies, P. J. Ratcliffe, M. Farrall, and H. Watkins Electrocardiographic measures of left ventricular hypertrophy show greater heritability than echocardiographic left ventricular mass Eur. Heart J., December 2, 2002; 23(24): 1963 - 1971. [Abstract] [PDF]
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