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Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-1554
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The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 2 673-677
Copyright © 2005 by The Endocrine Society

The Association of Thyroid Function with Cardiac Mass and Left Ventricular Hypertrophy

Marcus Dörr, Birger Wolff, Daniel M. Robinson, Ulrich John, Jan Lüdemann, Wieland Meng1, Stephan B. Felix and Henry Völzke

Department of Internal Medicine B (M.D., B.W., D.M.R., W.M., S.B.F.), Institute of Epidemiology and Social Medicine (U.J., H.V.), and Institute of Clinical Chemistry and Laboratory Medicine (J.L.), Ernst-Moritz-Arndt-University, D-17487 Greifswald, Germany

Address all correspondence and requests for reprints to: Marcus Dörr, M.D., Department of Internal Medicine B, Ernst Moritz Arndt University, Friedrich Loeffler Strasse 23a, D-17487 Greifswald, Germany. E-mail: mdoerr{at}uni-greifswald.de.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 Conclusions
 References
 
Decreased serum TSH levels predict cardiovascular mortality, which could be explained by left ventricular hypertrophy (LVH). The aim of this analysis was to investigate the association between thyroid function and LVH.

The population-based Study of Health in Pomerania was conducted in a previously iodine-deficient area. Data of 1510 individuals at least 45 yr of age with echocardiography and without thyroid disorders were analyzed. LVH was defined as a left ventricular mass index (LVMI) exceeding 150 g/m2 (men) or 120 g/m2 (women). Overt hyperthyroidism was associated with LVMI (P < 0.01), whereas euthyroid subjects and those with elevated TSH levels did not significantly differ with regard to LVMI. LVH was observed in three (15.0%) subjects with elevated serum TSH levels, in 127 (10.5%) euthyroid persons, in 24 (12.5%) individuals with decreased serum TSH levels, and in four (57.1%) subjects with hyperthyroidism (P < 0.01). Logistic regression analysis identified overt hyperthyroidism as an independent risk factor for LVH (odds ratio, 13.65; 95% confidence interval, 2.83–65.75; P < 0.01).

There is an association between thyroid function status, cardiac mass, and LVH. Hyperthyroidism is an independent risk factor for LVH.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 Conclusions
 References
 
THYROID DISORDERS ARE well known to influence the cardiovascular system. Thyroid hormones may cause hemodynamic changes, including an increase in myocardial contractility, a decrease in cardiovascular resistance, an elevation of cardiac output, and a widening of pulse pressure (1, 2, 3). Cardiac arrhythmias may also occur, such as sinus tachycardia, atrial and ventricular premature beats, and atrial fibrillation (1, 2).

Most of the cardiovascular effects of thyroid hormones are measurable mainly in patients with overt hyperthyroidism. In subclinical hyperthyroidism, some of these alterations have also been described, but the findings have not always been consistent and are still controversially discussed. Decreased serum TSH levels predict vascular and all-cause mortality (4). However, only the minority of persons with decreased serum TSH levels have overt hyperthyroidism (5). The association between decreased serum TSH levels and cardiovascular mortality cannot completely be explained by current knowledge.

Left ventricular hypertrophy (LVH) predicts cardiovascular mortality (6, 7). Experimental evidence and studies on small clinical-based samples suggest a relationship between overt hyperthyroidism and LVH (8, 9, 10, 11, 12, 13). Currently, it remains to be established whether decreased serum TSH levels may also be independently associated with LVH. Thus, the aim of the present study was to find potential predictors for LVH in addition to those already known and to elucidate the relationship of functional thyroid status and echocardiographically determined LVH in a population-based study.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 Conclusions
 References
 
The Study of Health in Pomerania (SHIP) is a cross-sectional epidemiological survey in West Pomerania, a region in the northeast of Germany including the three cities Greifswald, Stralsund, and Anklam and 29 surrounding communities (14). Like most parts in Germany, Western Pomerania is a region of former iodine deficiency (15). During the last decade, improved iodine supplementation has normalized this deficiency level. Currently, there is a median urine iodine excretion of 124 µg/liter in the SHIP population There were no significant changes of the urine iodine concentration over the 4 yr of the study (5). The total population comprised 212,157 inhabitants. A random sample aged 20–79 yr was drawn. The participants were selected using population registries in which every resident is listed. A total of 7008 subjects were sampled, with 292 persons of each sex in each of the twelve 5-yr age strata. The net sample (without migrated or deceased persons) comprised 6267 eligible subjects. The SHIP population finally comprised 4310 participants (corresponding to a final response rate of 68.8%) (14). Subjects with known thyroid disease or with uncertainty regarding a known thyroid disease (n = 369) as well as individuals with no blood drawn or missing data on serum thyroid function tests (n = 166) were excluded from further analysis. Among these individuals, only those aged 45 yr or older underwent echocardiographic investigation. After exclusion of indeterminate echocardiograms, a study population of 1510 participants was available for the present analysis. Data were collected between October 1997 and May 2001. All participants gave informed written consent. The study protocol complied with the Declaration of Helsinki and was approved by the institutional review committee of the University of Greifswald.

Sociodemographic characteristics and medical histories were assessed by computer-assisted personal interviews. Systolic and diastolic blood pressure were measured three times in seated subjects after a 5-min rest period, with each reading being followed by an additional rest period of 3 min. Mean blood pressure was calculated. Pulse pressure was defined as the difference between mean systolic and diastolic measurements. Hypertension was defined as a systolic blood pressure of 140 mm Hg or more, a diastolic blood pressure of 90 mm Hg or more, or self-reported use of antihypertensive drugs. As for smoking status, study participants were classified as nonsmokers or current smokers. Height and weight were measured for the calculation of body mass index: BMI = weight (kg)/height2 (m2). Present medication was recorded by a computer-aided method using the anatomic, therapeutic, and chemical code.

Blood samples were analyzed in a central laboratory. Serum TSH, free T4 (FT4), and free T3 (FT3) levels were analyzed by immunochemiluminescent procedures (FT3, LUMItest, Brahms, Berlin, Germany; TSH and FT4, LIA-mat, Byk Sangtec Diagnostica GmbH, Frankfurt, Germany). The functional sensitivity of the TSH assay was 0.03 mU/liter. The reference range was 0.3–3 mU/liter. Reference values for FT3 and FT4 were 2.2–4.6 ng/liter (3.4–7.1 pmol/liter) and 8–20 ng/liter (10–25 pmol/liter), respectively.

A thyroid function index was formed by dividing participants into four groups according to the serum TSH levels: 1) elevated serum TSH (serum TSH >3.0 mU/liter); 2) euthyroid (serum TSH within normal range); 3) decreased serum TSH (serum TSH <0.3 mU/liter); and 4) overt hyperthyroid (serum TSH <0.1 mU/liter with elevated serum FT3 and/or FT4 levels). Individuals who had serum TSH concentrations less than 0.1 mU/liter but no elevated serum FT3 and/or FT4 levels were assigned to group 3.

Two-dimensional and M-mode echocardiography was performed by certified physicians using a Vingmed CFM 800A system (GE Medical Systems, Waukesha, WI). All data and measurements were stored digitally. M-mode images of the left ventricle were recorded at papillary level. Left ventricular dimensions [interventricular septum thickness (IVS), posterior wall thickness (PW), and left ventricular end diastolic diameter (LVEDD)] were measured using the leading-edge convention, and left ventricular mass (LVM) was calculated according to the definition of the American Society of Echocardiography: LVM = 1.05x [(LVEDD + IVS + PW)3 -LVEDD3)] (16). All LVM measurements of intra-reader, intra-observer, inter-reader and inter-observer agreements revealed Spearman correlation coefficients of more than 0.85 and differences in mean (±2 SD) of less than 5% (<25%). Indices of echocardiographic parameters were calculated by dividing absolute values by body surface area (IVSI, PWI, LVEDDI, and LVMI). LVH was defined as a LVMI of more than 150 g/m2 in men and 120 g/m2 in women (16).

Statistics

Means ± SD are given for continuous data. Nominal data are expressed as absolute numbers or percentages as indicated. Comparisons between groups were made using linear ANOVA (continuous data) and {chi}2 test (nominal data). Multivariable analyses were performed using general linear model (LVMI) and logistic regression (LVH), respectively. Established risk factors for elevated LVMI such as demographic variables (age and sex) and clinical characteristics (pulse pressure, BMI, diabetes mellitus, and smoking status) as well as drugs influencing LVMI [ß-blockers, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II (AT-II) receptor inhibitors] were included in the analysis. Adjusted interval data are given as adjusted mean and SE. For nominal data, the adjusted odds ratio (OR) with its 95% confidence interval (CI) was calculated. A value of P < 0.05 was considered statistically significant. Analyses were performed with SPSS software version 11.0.1 (SPSS Inc., Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 Conclusions
 References
 
Among the study population of 1510 participants (684 women and 826 men), 23 had elevated serum TSH levels (1.5%) and 1279 were euthyroid (84.7%). In 201 individuals, decreased serum TSH levels were found (13.3%). Overt hyperthyroidism was observed in seven persons (0.5%).

Descriptive analyses revealed an association only between age and thyroid function. Subjects with elevated serum TSH levels were youngest, whereas hyperthyroid subjects were oldest. All other demographic and clinical characteristics did not differ between the thyroid function groups (Table 1Go).


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  		TABLE 1. Clinical characteristics with respect to thyroid function status

 
The thyroid function groups did not differ with respect to measurements of IVS, PW, LVEDD, and its standardized indices (Table 2Go). Only persons with hyperthyroidism tended to have a higher IVS than the other groups (Table 2Go). However, thyroid function was associated with LVM and LVMI, respectively (Table 2Go). Besides sex, age, BMI, pulse pressure, current smoking, and medication with ACE inhibitors or AT-II receptor inhibitors, overt hyperthyroidism was identified as an independent predictor for LVMI (Table 3Go). Considering correlates for LVM (age, sex, BMI, pulse pressure, diabetes mellitus, smoking status, and medication), adjusted means of LVM were 203.96 ± 11.07 for elevated serum TSH, 210.69 ± 4.03 for euthyroidism, 210.91 ± 5.16 for decreased serum TSH and 271.32 ± 17.90 for hyperthyroidism, respectively. Similar results were found for adjusted means of LVMI (Fig. 1Go).


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  		TABLE 2. Echocardiographic parameters with respect to thyroid function

 

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  		TABLE 3. Correlates to LVMI

 


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  		FIG. 1. LVMI with respect to functional thyroid status. Values are adjusted means ± SE Multivariate adjustments were made for sex, age, BMI, pulse pressure, smoking status, and antihypertensive medication (ß-blockers, ACE inhibitors, and AT-II receptor inhibitors). *, P < 0.05; {dagger}, P < 0.01 (ANOVA).

 
LVH was observed in three (15%) of the participants with elevated TSH levels, in 127 (10.5%) of the euthyroid persons, in 24 (12.5%) of the individuals with decreased TSH levels, and in four (57.1%) subjects with hyperthyroidism (Table 2Go). Compared with all other thyroid function groups, LVH was most frequent in the hyperthyroid group (P < 0.001) (Table 2Go). Logistic regression analysis identified overt hyperthyroidism as an independent risk factor for LVH (P = 0.001). The OR compared with euthyroidism was 13.65 (CI, 2.83–65.75) (Fig. 2Go). The risk for LVH was not elevated among subjects with decreased TSH levels (OR, 1.22; CI, 0.75–1.98) (Fig. 2Go). Furthermore, female sex, advanced age, increased BMI, and a widened pulse pressure were identified as independent risk factors for LVH (Table 4Go). Additionally, current medication with AT-II receptor inhibitors was associated with LVH (OR, 2.65; CI, 1.30–5.43), whereas the use of ß-blockers and ACE inhibitors was not (Table 4Go).



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  		FIG. 2. Association of functional thyroid status and LVH. OR ({blacksquare}) and 95% CI (horizontal lines) are shown. Multivariate adjustments were made for sex, age, BMI, pulse pressure, smoking status, and antihypertensive medication (ß-blockers, ACE inhibitors, and AT-II receptor inhibitors) and functional thyroid status. {dagger}, P < 0.01 (binary logistic regression analysis).

 

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  		TABLE 4. Association of LVH with selected risk factors

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
Conclusions
 References
 
The present study revealed an association between thyroid function status, cardiac mass, and LVH in a population-based sample of subjects aged 45–79 yr. Hyperthyroidism was independently associated with determinants of cardiac morphology such as LVM, LVMI, and LVH. In contrast, no association was found between decreased serum TSH levels and these parameters.

To the best of our knowledge, the present study is the first to analyze the association of thyroid status with LVH using population-based data. LVH predicts all-cause mortality, in particular of cardiovascular origin (6), and is an independent risk factor for atherosclerotic disease, stroke, cardiac failure, ventricular arrhythmias, and sudden cardiac death (6, 7). Our results suggest that LVH may indeed be an additional important determinant for increased cardiovascular mortality in overt hyperthyroidism. However, the results of the present study do not fully explain the association between decreased serum TSH levels and total mortality (4). In our study population, decreased serum TSH levels were not associated with an elevated risk of LVH. However, because of the cross-sectional design of the present study, it cannot be ruled out that persons with decreased serum TSH levels at baseline will become hyperthyroid during the following years and consequently develop LVH. This is of particular interest for populations living in iodine-deficient regions and also for those living in areas that have currently converted to a sufficient iodine supply. In these populations, subclinical hyperthyroidism is much commoner than in populations that have been living in iodine-replete areas for a long period of time (17, 18).

Among the study population, LVH was found in 10.5% of the euthyroid individuals. This is in agreement with data from the Framingham Study in which the prevalence rate was found to be similar (16). In contrast, LVH was found in 57.1% of the hyperthyroid individuals included in our analysis. Despite the relatively low number of subjects who were hyperthyroid, this association persisted after appropriate adjustment for potential confounding risk factors for LVH. Our findings are in agreement with the results of an echocardiographic study that examined persons who were not treated for thyroid disorders, including 30 persons with subclinical hyperthyroidism, 30 with overt hyperthyroidism, and 20 with euthyroidism. In this study, higher values of LVEDD and LVM were observed in hyperthyroid individuals compared with euthyroid controls, whereas there were no differences between euthyroid persons and those with subclinical hyperthyroidism (10). Previous experimental and clinical studies have revealed pathological cardiac hypertrophy as a possible complication of overt hyperthyroidism and thyroid hormone treatment (8, 19, 20) as well as an impairment in exercise capacity and cardiac function (3, 21).

However, an association of subclinical hyperthyroidism and changes in the cardiovascular system has not been consistently found and therefore is still undergoing controversial discussion (22). Some small clinical trials in endogenous and exogenous subclinical hyperthyroid individuals were reviewed (23). In two studies of endogenous disease (24, 25), an increase of LVM compared with euthyroidism was seen. In particular, Biondi et al. (24) demonstrated a marked increase in LVM in patients with endogenous subclinical hyperthyroidism. This seems to be in discordance with our results among participants with decreased TSH levels but might be explained by important differences in the population selection. First, Biondi et al. (24) analyzed data from patients, whereas our study was population based. Thus, our study was more likely to include (relatively) healthy persons. Among the patients who were enrolled in the other study (24), a higher prevalence of hypertension and, if present, a more severe disease might be expected. Thus, one may assume that LVH was much more pronounced among patients because of factors other than thyroid disorders. Second, Biondi et al. (24) included only patients with structural thyroid disorders, such as multinodular goiter or autonomously functioning thyroid nodule. All patients had known about their endogenous subclinical hyperthyroidism for a long time. In contrast, subjects with known thyroid disorders were excluded from our study. Probably, the subjects with decreased TSH levels from our study might represent an earlier stage of subclinical hyperthyroidism. Third, the study by Biondi et al. (24) included only 23 patients. In contrast, our study, to the best of our knowledge, is by far one of the largest dealing with this issue.

Besides overt hyperthyroidism, advanced age, increased BMI, and widened pulse pressure were also independently associated with LVH among our study population. This is in good agreement with previous investigations (6, 26, 27). According to other population-based studies, female sex was also identified as a risk factor. This finding, however, has not always been confirmed (26, 27, 28). Controversial results may be explained by the calculation method used for LVM and LVH, by the definition of cut-off points, and by the various population subgroups.


   Conclusions
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 Conclusions
References
 
We conclude that there is an association between thyroid function status, cardiac mass, and LVH in subjects aged 45–79 yr. Overt hyperthyroidism is an independent risk factor for LVH, whereas no such association was found for decreased serum TSH levels.


   Acknowledgments
 
The contributions to data collection made by field workers, study physicians, technicians, interviewers, and computer assistants are gratefully acknowledged.


   Footnotes
 
The population-based SHIP is part of the Community Medicine Research (CMR) Net of the University of Greifswald, Germany, which is funded by grants from the German Federal Ministry of Education and Research (Grant 01ZZ96030); the Ministry for Education, Research, and Cultural Affairs; and the Ministry for Social Affairs of the Federal State of Mecklenburg, West Pomerania. The CMR encompasses several research projects that share data from the population-based SHIP (http://www.medizin.uni-greifswald.de/cm).

First Published Online November 2, 2004

1 In memoriam Professor Wieland Meng, who died on May 30, 2004. Back

Abbreviations: ACE, Angiotensin-converting enzyme; AT-II, angiotensin II; BMI, body mass index; CI, confidence interval; IVS, interventricular septum thickness; LVEDD, left ventricular end diastolic diameter; LVEDDI, LVEDD index; LVH, left ventricular hypertrophy; LVM, left ventricular mass; OR, odds ratio; PW, posterior wall thickness; SHIP, Study of Health in Pomerania.

Received August 4, 2004.

Accepted October 25, 2004.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 Conclusions
 References
 

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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals