https://doi.org/10.1007/s00392-025-02625-4
1Universitäres Herz- und Gefäßzentrum Hamburg, Universitätsklinikum Hamburg-Eppendorf Klinik für Kardiologie Hamburg, Deutschland; 2Universitätsklinikum Hamburg-Eppendorf Klinik für Radiologie Hamburg, Deutschland; 3Universitätsklinikum Hamburg-Eppendorf III. Medizinische Klinik und Poliklinik Nephrologie/Rheumatologie Hamburg, Deutschland; 4Kardiologische Praxis Orchideenstieg Hamburg, Deutschland; 5Universitäres Herz- und Gefäßzentrum Hamburg Allgemeine und Interventionelle Kardiologie Hamburg, Deutschland
Thyroid dysfunction is associated with increased cardiovascular (CV) risk and mortality in later life. The underlying pathomechanisms for the development of CV disease in these individuals remain unclear. In this study, we aim to investigate the relationship between Thyroid-stimulating hormone (TSH) levels and cardiovascular risk profiles as well as (sub)clinical cardiovascular disease in a population setting. Furthermore, we investigate the potential correlation between TSH levels and evidence of myocardial fibrosis on cardiac magnetic resonance imaging (CMR).
Methods
The analysis was based on cross-sectional data from 10,000 participants from Hamburg, Germany, enrolled in the population-based, prospective Hamburg City Health Study (HCHS). We analyzed self-reported medical history, CV risk factors and general health status, as well as biomarkers, electrocardiogram, comprehensive echocardiography and cardiac MRI obtained at a single dedicated study center to identify cardiovascular phenotypes. Multivariable linear and logistic regression models adjusted for classic cardiovascular risk factors (age, sex, BMI, smoking status, diabetes, and hypertension) were calculated to determine associations.
Results
TSH levels were measured in 9612 individuals. Median TSH was 1.2 mU/L (reference range 0.8-1.6 mU/L). The median age was 63 years (IQR 55.0;70.0), 51% of the participants were women. In the study, 39% of participants had hypertension, 24% had dyslipidemia, and 8% had diabetes. In addition, 3% had a history of stroke, 5% had atrial fibrillation, and 4% had heart failure. In multivariable-adjusted models, we confirmed associations of higher TSH levels with the presence of modifiable cardiovascular risk factors such as higher diastolic blood pressure (beta 0.88 {CI 95% 0.07 – 1.70}, p=0.03), a history of hypertension (OR 0.76 (CI 95% 0.63– 0.91), p=0.003), total cholesterol (beta 5.53 {CI 95% 2.28 – 8.78}, p=0.001) and LDL cholesterol (beta 4.07 {CI 95% 1.09 – 7.06}, p=0.007). Moreover, we observed changes in ECG parameters such as slower heart rate (beta -2.25 (CI -3.24 - -1.26, p <0.001). Higher TSH levels were associated with a higher E/e’ ratio (beta 0.29 (CI 95% 0.10 – 0.49), p=0.03), but not with diastolic dysfunction or altered atrial strain. Furthermore, there was no association between TSH levels and markers of myocardial fibrosis on CMR (presence of LGE or elevated T1 levels; OR 0.91 (CI 95% 0.64 – 1.30), p=0.62), N=2366.
Conclusions
In this population-based sample, higher TSH levels are associated with the presence of modifiable cardiovascular risk factors (e.g., arterial hypertension, dyslipidemia) and subtle subclinical cardiovascular changes, but not strongly with manifest cardiovascular disease or evidence of myocardial fibrosis on CMR.