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A. Sato, L. Tarnow, F.S. Nielsen, E. Knudsen, H.-H. Parving, Left ventricular hypertrophy in normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment, QJM: An International Journal of Medicine, Volume 98, Issue 12, December 2005, Pages 879–884, https://doi.org/10.1093/qjmed/hci137
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Abstract
Background: Left ventricular hypertrophy (LVH) is an independent risk factor for myocardial ischaemia, cardiac arrhythmia, sudden death, and heart failure, all common findings in patients with type 2 diabetes.
Aim: To determine the prevalence of, and risk factors for, LVH in normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment.
Design: Cross-sectional study.
Methods: From 1994 to 1998, M-mode echocardiography was performed by one experienced examiner in 262 consecutive, normoalbuminuric Caucasian type 2 diabetic patients, all with blood pressure <160/95 mmHg and not taking antihypertensive medication. Mean ± SD age was 54 ± 10 years, 109 were women, and median known duration of diabetes was 4 (range 1–28) years. Body mass index (BMI) was 28 ± 5 kg/m2, and blood pressure 134 ± 13/79 ± 8 mmHg, all means ± SD. Median urinary albumin excretion rate was 9 (range 2–30) mg/24 h.
Results: The prevalence of LVH indexed to height2.7 was 43% (95%CI 38–50%), and was similar in men and women. BMI, HbA1c and log urinary albumin excretion were significantly associated with left ventricular hypertrophy in a logistic regression model, whereas sex, age, known duration of diabetes and blood pressure were not. Similar results were obtained for left ventricular mass index.
Discussion: LVH was frequent in our normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment. Several potentially modifiable risk factors, such as raised BMI, poor glycaemic control and elevated urinary albumin excretion rate, were associated with LVH.
Introduction
Type 2 diabetic patients have raised morbidity and mortality from cardiovascular disease, compared with the non-diabetic background population.1 Abnormalities in well-established cardiovascular risk factors (arterial hypertension, dyslipidaemia, smoking, glycaemic control, elevated urinary albumin excretion, body mass index) cannot fully account for these findings.1,2 Recently, data from the Third National Health and Nutrition Examination Survey (NHANES III) demonstrated that a combination of diabetes and risk factors in the NCEP (National Cholesterol Education Program) metabolic syndrome accounts for 54.7% of the attributable risk for coronary heart disease in a US population aged 50 years.3
Starting as an adaptation, left ventricular hypertrophy can itself contribute to increased rates of cardiovascular events, through its effects on ventricular function, coronary circulation, and arrhythmogenesis. Available data provide substantial evidence of a consistent and strong relationship between the presence of LVH, either detected by an echocardiogram or an electrocardiogram (ECG), and subsequent cardiovascular morbidity (mean weighted relative risk 2.3), as well as all-cause mortality (relative risk 2.5).4 These results have been consistent in various clinical and population samples.4 Conversely, a reduction in LVH predicts a lesser risk for subsequent morbid events.5
The aim of our cross-sectional study was to evaluate the prevalence of left ventricular hypertrophy, and risk factors for its development, in normoalbuminuric type 2 diabetic patients without antihypertensive medication.
Methods
Study population
Between 1994 and 1998, all Caucasian type 2 diabetic patients without known cardiac disease and antihypertensive medication and with urinary albumin excretion rate <30 mg/day, referred to the Steno Diabetes Center (n = 426), were invited to participate in the study and have echocardiography performed. In total, 359 (84%) were recruited. At the time of investigation, 43 had an arterial blood pressure >160/95 mmHg (WHO criteria 1993) and were therefore not included. In addition, 13 were excluded because they had echocardiographic signs of valvular or myocardial disease. Furthermore, in 41 the study quality of echocardiography was too poor for quantitative measurements. Thus 262 normoalbuminuric type 2 diabetic patients without antihypertensive medication were evaluated in this study.
Type 2 diabetic patients were diagnosed according to WHO criteria as patients with relative insulin deficiency.6 In clinical practice, patients were considered to have type 2 diabetes mellitus if they were treated with diet alone or in combination with oral hypoglycaemic agents, or if they were treated with insulin and had an onset of diabetes after age of 40 years and a body mass index >25 kg/m2 at the time of diagnosis.7 In Denmark, 40% of men and 27% of women are overweight.8 The study was approved by the local ethical committee, and all patients gave fully informed consent.
Echocardiography
M-mode and pulsed Doppler echocardiography were performed according to the recommendations of the American Society of Echocardiography9 using a VingmedCFM725 equipped with a 3.25 MHz transducer. In the parasternal long-axis view, a two-dimensional image was used to guide proper recording of M-mode parameters used for quantification of left ventricular mass.
The following M-mode parameters were measured: left ventricular end-diastolic diameter (LVDD) and end-systolic diameter (LVDS), ventricular septum thickness (STD) and posterior wall thickness in diastole (PWTD). Left ventricular mass (LVM) was calculated according to the Penn formula: 1.04 × ((STD + LVDD + PWTD)3 − (LVDD)3) − 13.6.10 Left ventricular mass index (LVMI) was calculated by dividing LVM by height2.7 and left ventricular hypertrophy was considered present if LVMI was ⩾46.7 g/m2.7 in women and ⩾49.2 g/m2.7 for men.11 Data on LVH indexed to height2.7 are presented. For comparison, LVM indexed to body surface area was calculated.12 Relative posterior wall thickness was calculated according to the formula: 2×PWT/LVDD.13 Elevated relative posterior wall thickness with increased LVMI identified the presence of concentric (as opposed to eccentric) hypertrophy, and in the presence of normal LVMI identified concentric left ventricular remodelling. A partition value of 0.44 for relative wall thickness was used for both men and women.14 Systolic function was assessed by fractional shortening (FS) of the left ventricle calculated using the following equation: (LVDD–LVDS)/LVDD. Left ventricular wall motion was inspected in each of the 16 segments defined by the American Society of Echocardiography.9 All measurements were averaged over five cycles. Echocardiography was performed by one experienced investigator (AS) masked to the clinical data. Intra-observer error was <2% on LVDD, 3% on LVDS, and 4% on STD and PWTD, based on separate examinations of 15 healthy subjects performed on two consecutive days. Furthermore, in a comparison (10 diabetic patients and 10 healthy controls) with another skilled echocardiographer (S. Ali), no systematic deviations were revealed, and the inter-observer variability on LVM was <10%.
Clinical and laboratory measurements
Arterial blood pressure was measured in the sitting position after 10 min rest, using a standard sphygmomanometer and appropriate-sized cuff. Measurements were performed in duplicate and averaged. Diastolic blood pressure was recorded at the disappearance of the fifth phase of the Korotkoff sounds. Mean of two office recordings at the time was used. Retinopathy was assessed by fundus photography after pupillary dilatation and graded: nil, simplex or proliferative diabetic retinopathy.
Urinary albumin concentration was measured using an enzyme immunoassay method1524-h urine collections. Normoalbuminuria was defined as persistent urinary albumin excretion rate <30 mg/24 h in two out of three 24-h urine collections. Urinary concentration of creatinine was used as a measure of compliance with 24-h urine collections.
Haemoglobin A1c was measured by HPLC (Bio Rad DIAMAT) (normal range 4.1–6.4%).
Statistical analysis
Normally distributed variables are quoted as means (SD). Urinary albumin excretion rate was log-transformed before statistical analysis because of the skewed distribution and is given as median (range). Comparisons between groups were performed by an unpaired Student's t-test or analysis of variance (ANOVA). Frequencies are given as percentages with 95%CIs, and non-continuous variables were compared using the χ2 test. Multiple logistic regression analyses with stepwise backwards selection were used to calculate the relative contributions of sex, age, known duration of diabetes, BMI, HbA1c, mean arterial blood pressure, and log UAE to the presence/absence of LVH (kg/m2.7). For LVMI as outcome, a multiple linear regression analysis was applied with the same independent covariates.
A p value (two-tailed) ⩽0.05 was considered significant. All calculations were made with commercially available programs (Statgraphics and SPSS).
Results
Clinical and laboratory data in type 2 diabetic patients with and without LVH are shown in Table 1. Patients with LVH had higher BMI (p < 0.001), poorer glycaemic control (p = 0.02), and although within the normoalbuminuric range, slightly elevated urinary albumin excretion rate (p = 0.002), compared to patients with normal LVMI. There was no significant difference between patients with and without LVH regarding sex, age, systolic or diastolic blood pressure, known duration of diabetes or presence of retinopathy.
Characteristic . | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
Sex (M/F) | 67/47 | 86/62 | NS |
Age (years) | 54.2 (10.0) | 54.6 (10.3) | NS |
Known duration of diabetes (years) | 3 (1–29) | 4 (1–28) | NS |
BMI (kg/m2) | 30.2 (5.4) | 25.6 (3.8) | <0.001 |
HbA1c (%) | 8.8 (1.6) | 8.4 (1.6) | 0.02 |
Systolic blood pressure (mmHg) | 133 (12) | 135 (14) | NS |
Diastolic blood pressure (mmHg) | 79 (7) | 79 (8) | NS |
Urinary albumin excretion rate (mg/24 h) | 10 (3–30) | 8 (2–30) | 0.002 |
Retinopathy (nil/simplex/proliferative) | 77%/22%/1% | 78%/21%/1% | NS |
Hypoglycaemic agents (diet alone/OHA/insulin) | 24%/50%/26% | 33%/47%/20% | NS |
Aspirin (%) | 4% | 3% | NS |
Statins (%) | 0 | 1% | NS |
Characteristic . | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
Sex (M/F) | 67/47 | 86/62 | NS |
Age (years) | 54.2 (10.0) | 54.6 (10.3) | NS |
Known duration of diabetes (years) | 3 (1–29) | 4 (1–28) | NS |
BMI (kg/m2) | 30.2 (5.4) | 25.6 (3.8) | <0.001 |
HbA1c (%) | 8.8 (1.6) | 8.4 (1.6) | 0.02 |
Systolic blood pressure (mmHg) | 133 (12) | 135 (14) | NS |
Diastolic blood pressure (mmHg) | 79 (7) | 79 (8) | NS |
Urinary albumin excretion rate (mg/24 h) | 10 (3–30) | 8 (2–30) | 0.002 |
Retinopathy (nil/simplex/proliferative) | 77%/22%/1% | 78%/21%/1% | NS |
Hypoglycaemic agents (diet alone/OHA/insulin) | 24%/50%/26% | 33%/47%/20% | NS |
Aspirin (%) | 4% | 3% | NS |
Statins (%) | 0 | 1% | NS |
Data are numbers (%), means (SD), or medians (range).
Characteristic . | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
Sex (M/F) | 67/47 | 86/62 | NS |
Age (years) | 54.2 (10.0) | 54.6 (10.3) | NS |
Known duration of diabetes (years) | 3 (1–29) | 4 (1–28) | NS |
BMI (kg/m2) | 30.2 (5.4) | 25.6 (3.8) | <0.001 |
HbA1c (%) | 8.8 (1.6) | 8.4 (1.6) | 0.02 |
Systolic blood pressure (mmHg) | 133 (12) | 135 (14) | NS |
Diastolic blood pressure (mmHg) | 79 (7) | 79 (8) | NS |
Urinary albumin excretion rate (mg/24 h) | 10 (3–30) | 8 (2–30) | 0.002 |
Retinopathy (nil/simplex/proliferative) | 77%/22%/1% | 78%/21%/1% | NS |
Hypoglycaemic agents (diet alone/OHA/insulin) | 24%/50%/26% | 33%/47%/20% | NS |
Aspirin (%) | 4% | 3% | NS |
Statins (%) | 0 | 1% | NS |
Characteristic . | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
Sex (M/F) | 67/47 | 86/62 | NS |
Age (years) | 54.2 (10.0) | 54.6 (10.3) | NS |
Known duration of diabetes (years) | 3 (1–29) | 4 (1–28) | NS |
BMI (kg/m2) | 30.2 (5.4) | 25.6 (3.8) | <0.001 |
HbA1c (%) | 8.8 (1.6) | 8.4 (1.6) | 0.02 |
Systolic blood pressure (mmHg) | 133 (12) | 135 (14) | NS |
Diastolic blood pressure (mmHg) | 79 (7) | 79 (8) | NS |
Urinary albumin excretion rate (mg/24 h) | 10 (3–30) | 8 (2–30) | 0.002 |
Retinopathy (nil/simplex/proliferative) | 77%/22%/1% | 78%/21%/1% | NS |
Hypoglycaemic agents (diet alone/OHA/insulin) | 24%/50%/26% | 33%/47%/20% | NS |
Aspirin (%) | 4% | 3% | NS |
Statins (%) | 0 | 1% | NS |
Data are numbers (%), means (SD), or medians (range).
The prevalence of LVH indexed by height2.7 was 43% (38–50%), and was similar in men and women. The corresponding prevalence of LVH indexed for body surface area was 32% (26–37%) for women and 25% (20–30%) for men (p = 0.19). All structural measurements of the left ventricle: LVDD, STD, and PWT were increased in patients with LVH, and thus contributed to the increase in LVMI (Table 2). Concentric hypertrophy was present in six women (13%), whereas 41 women had eccentric hypertrophy. For males, the corresponding figures were 15 (22%) and 52 men, respectively (p = 0.19 comparing men and women). BMI, HbA1c, and blood pressure were similar in men and women. No correlation between relative posterior wall thickness and urinary albumin excretion was found. All included patients had a symmetrically contracting left ventricle, and showed no signs of focal hypokinetic segments. Fractional shortening as a measure of systolic function was normal and similar in the two groups (Table 2).
. | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
LVDD (mm) | 53.8 (4.5) | 48.7 (4.4) | <0.001 |
STD (mm) | 10.3 (1.8) | 8.6 (1.4) | <0.001 |
PWTD (mm) | 10.4 (1.5) | 8.7 (1.3) | <0.001 |
LVM (g) | 258 (76) | 167 (38) | <0.001 |
LVMI (g/m2.7) | 59.8 (12.4) | 38.0 (6.5) | <0.001 |
LVMI (g/m2) | 128 (30) | 87 (15) | <0.001 |
Fractional shortening (mm) | 40.0 (5.5) | 40.5 (5.1) | NS |
. | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
LVDD (mm) | 53.8 (4.5) | 48.7 (4.4) | <0.001 |
STD (mm) | 10.3 (1.8) | 8.6 (1.4) | <0.001 |
PWTD (mm) | 10.4 (1.5) | 8.7 (1.3) | <0.001 |
LVM (g) | 258 (76) | 167 (38) | <0.001 |
LVMI (g/m2.7) | 59.8 (12.4) | 38.0 (6.5) | <0.001 |
LVMI (g/m2) | 128 (30) | 87 (15) | <0.001 |
Fractional shortening (mm) | 40.0 (5.5) | 40.5 (5.1) | NS |
Data are means (SD). LVDD, left ventricular end-diastolic diameter; STD, ventricular septum thickness; PWTD, posterior wall thickness in diastole; LVM, left ventricular mass; LVMI, left ventricular mass index.
. | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
LVDD (mm) | 53.8 (4.5) | 48.7 (4.4) | <0.001 |
STD (mm) | 10.3 (1.8) | 8.6 (1.4) | <0.001 |
PWTD (mm) | 10.4 (1.5) | 8.7 (1.3) | <0.001 |
LVM (g) | 258 (76) | 167 (38) | <0.001 |
LVMI (g/m2.7) | 59.8 (12.4) | 38.0 (6.5) | <0.001 |
LVMI (g/m2) | 128 (30) | 87 (15) | <0.001 |
Fractional shortening (mm) | 40.0 (5.5) | 40.5 (5.1) | NS |
. | With LVH (n = 114) . | Without LVH (n = 148) . | p . |
---|---|---|---|
LVDD (mm) | 53.8 (4.5) | 48.7 (4.4) | <0.001 |
STD (mm) | 10.3 (1.8) | 8.6 (1.4) | <0.001 |
PWTD (mm) | 10.4 (1.5) | 8.7 (1.3) | <0.001 |
LVM (g) | 258 (76) | 167 (38) | <0.001 |
LVMI (g/m2.7) | 59.8 (12.4) | 38.0 (6.5) | <0.001 |
LVMI (g/m2) | 128 (30) | 87 (15) | <0.001 |
Fractional shortening (mm) | 40.0 (5.5) | 40.5 (5.1) | NS |
Data are means (SD). LVDD, left ventricular end-diastolic diameter; STD, ventricular septum thickness; PWTD, posterior wall thickness in diastole; LVM, left ventricular mass; LVMI, left ventricular mass index.
If stricter blood pressure criteria of ⩾140/90 mmHg were applied for the definition of hypertension (n = 182, 69%) the prevalence of LVH was only slightly changed at 46% (38–53).
None of the patients fulfilled the classical Sokolow-Lyon electrocardiogram criteria for LVH.
BMI, HbA1c and log urinary albumin excretion were significantly associated with left ventricular hypertrophy in a logistic regression model, whereas sex, age, known duration of diabetes and blood pressure were not (Table 3). Furthermore, BMI, HbA1c, log urinary albumin excretion rate, and sex were independently associated with higher LVMI (data not shown).
. | Odds ratio (95%CI) . | p . |
---|---|---|
BMI (per 1 kg/m2 increase) | 1.26 (1.17–1.35) | <0.001 |
HbA1c (per 1% increase) | 1.25 (1.04–1.49) | 0.02 |
Log urinary albumin excretion rate (per 10-fold increase) | 2.96 (1.00–8.88) | 0.05 |
. | Odds ratio (95%CI) . | p . |
---|---|---|
BMI (per 1 kg/m2 increase) | 1.26 (1.17–1.35) | <0.001 |
HbA1c (per 1% increase) | 1.25 (1.04–1.49) | 0.02 |
Log urinary albumin excretion rate (per 10-fold increase) | 2.96 (1.00–8.88) | 0.05 |
Not included in the final model were sex, age, duration of diabetes, and blood pressure.
. | Odds ratio (95%CI) . | p . |
---|---|---|
BMI (per 1 kg/m2 increase) | 1.26 (1.17–1.35) | <0.001 |
HbA1c (per 1% increase) | 1.25 (1.04–1.49) | 0.02 |
Log urinary albumin excretion rate (per 10-fold increase) | 2.96 (1.00–8.88) | 0.05 |
. | Odds ratio (95%CI) . | p . |
---|---|---|
BMI (per 1 kg/m2 increase) | 1.26 (1.17–1.35) | <0.001 |
HbA1c (per 1% increase) | 1.25 (1.04–1.49) | 0.02 |
Log urinary albumin excretion rate (per 10-fold increase) | 2.96 (1.00–8.88) | 0.05 |
Not included in the final model were sex, age, duration of diabetes, and blood pressure.
Discussion
Our cross-sectional study demonstrated LVH to be a common condition in normoalbuminuric Caucasian type 2 diabetic patients predominantly without micro- or macrovascular complications and hypertension. None of the patients were receiving antihypertensive medication. Increased thickness of the ventricular walls, in combination with dilatation of the left ventricle, both contribute to the observed increase in left ventricular mass. Potentially modifiable risk factors such as obesity, glycaemic control, and urinary albumin excretion rate were associated with left ventricular hypertrophy.
The prevalence of LVH in the predominately non-diabetic (>95%) population in the Framingham Heart Study assessed by echocardiography was reported to be 16% in men and 21% in women.16 In that study, 42 women had diabetes and were characterized by an increased left ventricular wall thickness and a 22% greater left ventricular mass than their non-diabetic peers.17 No association of diabetes with left ventricular mass was found in men.17 Struthers and Morris18 reported that in a local survey, left ventricular hypertrophy was present in 32% (57/173) of patients with type 2 diabetes, independent of blood pressure or use of angiotensin-converting-enzyme (ACE) inhibitors. Similar observations have been reported from an American Indian population.19
In contrast to the present study, data in the three above mentioned studies were generated from type 2 diabetic patients with and without arterial hypertension, and with and without antihypertensive treatment. Although generalization of findings from this study is limited by the selection criteria applied, our data are in good accordance with observations from other studies16–19reporting elevated left ventricular mass in type 2 diabetes.
None of our patients fulfilled the classical Sokolow-Lyon electrocardiogram criteria for LVH. This agrees with the Framingham Heart Study,16 which demonstrated on ECG a LVH prevalence of 0.5%, applying the same method. In contrast, a recent Italian study reported a prevalence of ECG-LVH of 17% in type 2 diabetic patients.20 These patients were, however, characterized by old age, long known duration of diabetes, arterial hypertension, and micro- or macroalbuminuria in nearly half of the population.
The prevalence of LVH increases with severity of hypertension, ranging from 38% to 72% in hypertensive diabetic populations.21,22 In a previous study, we found the prevalence of LVH to be 51% in 53 type 2 diabetic patients with normoalbuminuria. In the present study, >40% of patients had LVH, even though none of the included type 2 diabetic patients was receiving or had prior treatment with antihypertensive medications, and all had an arterial blood pressure below the recommended (at the time) cut-off of 160/95 mmHg.23 The majority of patients had an arterial blood pressure below the more strict criteria for hypertension of ⩾140/90 mmHg.24 In this subset, the prevalence of LVH was similar: 46% (39–53%). Whereas other studies have found a relationship between arterial blood pressure and left ventricular mass20 in diabetic patients with and without hypertension, this was not the case in the present study, where blood pressure levels were lower.
That urinary albumin excretion rate is strongly associated with the degree of left ventricular mass hypertrophy has been demonstrated in the present and several previous studies of non-diabetic,25 type 126 and type 2 diabetic patients with micro- and macroalbuminuria.20,27,28 Furthermore, in hypertensive diabetic and non-diabetic patients with LVH, increased urinary albumin excretion rate resulted in increased risk for cardiovascular morbidity and mortality.29 The prognostic implication of LVH in normoalbuminuric type 2 diabetic patients without hypertension remains to be elucidated.
In addition to blood pressure, urinary albumin excretion rate, BMI30 and blood glucose,31 it has also been suggested that coronary microvascular dysfunction,32 endothelial dysfunction and chronic inflammation,33 and abnormalities in the tissue renin-angiotensin-aldosterone-bradykinin system or the encoding genes34 might play a role in the pathogenesis of left ventricular hypertrophy. The observation that some type 2 diabetic patients have asymmetrical and some concentric hypertrophy, might suggest that the underlying pathology is not homogenous, but rather reflects the interaction of several of the above mentioned risk factors.
In conclusion, our cross-sectional study demonstrated LVH to be a common condition in type 2 diabetic patients without albuminuria and antihypertensive medication. The prognostic importance and effectiveness of intervention against left ventricular hypertrophy in normotensive type 2 diabetes patients remains to be elucidated.
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Author notes
From the Steno Diabetes Center, Gentofte and 1Faculty of Health Science, University of Aarhus, Aarhus, Denmark