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Madalena von Hafe Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal

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João Sergio Neves Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar São João, Porto, Portugal

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Catarina Vale Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal

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Marta Borges-Canha Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar São João, Porto, Portugal

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Adelino Leite-Moreira Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal

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Thyroid hormones have a central role in cardiovascular homeostasis. In myocardium, these hormones stimulate both diastolic myocardial relaxation and systolic myocardial contraction, have a pro-angiogenic effect and an important role in extracellular matrix maintenance. Thyroid hormones modulate cardiac mitochondrial function. Dysfunction of thyroid axis impairs myocardial bioenergetic status. Both overt and subclinical hypothyroidism are associated with a higher incidence of coronary events and an increased risk of heart failure progression. Endothelial function is also impaired in hypothyroid state, with decreased nitric oxide-mediated vascular relaxation. In heart disease, particularly in ischemic heart disease, abnormalities in thyroid hormone levels are common and are an important factor to be considered. In fact, low thyroid hormone levels should be interpreted as a cardiovascular risk factor. Regarding ischemic heart disease, during the late post-myocardial infarction period, thyroid hormones modulate left ventricular structure, function and geometry. Dysfunction of thyroid axis might even be more prevalent in the referred condition since there is an upregulation of type 3 deiodinase in myocardium, producing a state of local cardiac hypothyroidism. In this focused review, we summarize the central pathophysiological and clinical links between altered thyroid function and ischemic heart disease. Finally, we highlight the potential benefits of thyroid hormone supplementation as a therapeutic target in ischemic heart disease.

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Tsuneo Ogawa Cardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, Canada K1Y 4W7

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Adolfo J de Bold Cardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, Canada K1Y 4W7

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The concept of the heart as an endocrine organ arises from the observation that the atrial cardiomyocytes in the mammalian heart display a phenotype that is partly that of endocrine cells. Investigations carried out between 1971 and 1983 characterised, by virtue of its natriuretic properties, a polypeptide referred to atrial natriuretic factor (ANF). Another polypeptide isolated from brain in 1988, brain natriuretic peptide (BNP), was subsequently characterised as a second hormone produced by the mammalian heart atria. These peptides were associated with the maintenance of extracellular fluid volume and blood pressure. Later work demonstrated a plethora of other properties for ANF and BNP, now designated cardiac natriuretic peptides (cNPs). In addition to the cNPs, other polypeptide hormones are expressed in the heart that likely act upon the myocardium in a paracrine or autocrine fashion. These include the C-type natriuretic peptide, adrenomedullin, proadrenomedullin N-terminal peptide and endothelin-1. Expression and secretion of ANF and BNP are increased in various cardiovascular pathologies and their levels in blood are used in the diagnosis and prognosis of cardiovascular disease. In addition, therapeutic uses for these peptides or related substances have been found. In all, the discovery of the endocrine heart provided a shift from the classical functional paradigm of the heart that regarded this organ solely as a blood pump to one that regards this organ as self-regulating its workload humorally and that also influences the function of several other organs that control cardiovascular function.

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Hugo R Ramos Department of Internal Medicine, Section of Metabolic Vascular Medicine, Division of Diabetes and Nutritional Sciences, Cardiovascular Endocrinology Laboratory, Faculty of Medicine, Hospital de Urgencias, National University of Córdoba, X5000 Córdoba, Argentina

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Andreas L Birkenfeld Department of Internal Medicine, Section of Metabolic Vascular Medicine, Division of Diabetes and Nutritional Sciences, Cardiovascular Endocrinology Laboratory, Faculty of Medicine, Hospital de Urgencias, National University of Córdoba, X5000 Córdoba, Argentina
Department of Internal Medicine, Section of Metabolic Vascular Medicine, Division of Diabetes and Nutritional Sciences, Cardiovascular Endocrinology Laboratory, Faculty of Medicine, Hospital de Urgencias, National University of Córdoba, X5000 Córdoba, Argentina

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Adolfo J de Bold Department of Internal Medicine, Section of Metabolic Vascular Medicine, Division of Diabetes and Nutritional Sciences, Cardiovascular Endocrinology Laboratory, Faculty of Medicine, Hospital de Urgencias, National University of Córdoba, X5000 Córdoba, Argentina

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Since their discovery in 1981, the cardiac natriuretic peptides (cNP) atrial natriuretic peptide (also referred to as atrial natriuretic factor) and brain natriuretic peptide have been well characterised in terms of their renal and cardiovascular actions. In addition, it has been shown that cNP plasma levels are strong predictors of cardiovascular events and mortality in populations with no apparent heart disease as well as in patients with established cardiac pathology. cNP secretion from the heart is increased by humoral and mechanical stimuli. The clinical significance of cNP plasma levels has been shown to differ in obese and non-obese subjects. Recent lines of evidence suggest important metabolic effects of the cNP system, which has been shown to activate lipolysis, enhance lipid oxidation and mitochondrial respiration. Clinically, these properties lead to browning of white adipose tissue and to increased muscular oxidative capacity. In human association studies in patients without heart disease higher cNP concentrations were observed in lean, insulin-sensitive subjects. Highly elevated cNP levels are generally observed in patients with systolic heart failure or high blood pressure, while obese and type-2 diabetics display reduced cNP levels. Together, these observations suggest that the cNP system plays a role in the pathophysiology of metabolic vascular disease. Understanding this role should help define novel principles in the treatment of cardiometabolic disease.

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Sigrid Bjerge Gribsholt Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark

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Morten Schmidt Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark

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Eskild Bendix Kristiansen Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark

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Bjørn Richelsen Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

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Henrik Toft Sørensen Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

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Objective

The aim was to examine the association between hospital-diagnosed overweight/obesity and incident CVD according to the time period of the overweight/obesity diagnosis.

Design

This is a cohort study.

Methods

From Danish national health registries, we identified all residents with a first-time hospital-based overweight/obesity diagnosis code, 1977–2018 (n = 195,221), and an age and sex-matched general population comparison cohort (n = 1,952,210). We computed adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) using Cox regression. We adjusted for comorbidities and educational level and applied 10 years of follow-up.

Results

The overall incidence rate was 10.1 (95% CI 10.0–10.1) per 1000 person-years for the comparison cohort and 25.1 (95% CI 24.8–25.4) per 1000 person-years for the overweight/obesity cohort, corresponding to an aHR of 2.5 (95% CI 2.4–2.5). The aHR was elevated for all subtypes of CVD: heart failure: 3.9 (95% CI 3.7–4.1), bradyarrhythmia: 2.9 (95% CI 2.7–3.1), angina pectoris: 2.7 (95% CI 2.7–2.8), atrial fibrillation or flutter: 2.6 (95% CI 2.5–2.6), acute myocardial infarction: 2.4 (95% CI 2.3–2.4), revascularization procedure: 2.4 (95% CI 2.2–2.5), valvular heart disease: 1.7 (95% CI 1.6–1.8), ischemic stroke: 1.6 (95% CI 1.4–1.7), transient ischemic attack: 1.6 (95% CI 1.5–1.7), and cardiovascular death: 1.6 (95% CI 1.5–1.6). The 1–10-year aHR of any CVD associated with an overweight/obesity diagnosis decreased from 2.8 (95% CI 2.7–2.9) in 1977–1987 to 1.8 (95% CI 1.8–1.9) in 2008–2018.

Conclusion

Patients with hospital-diagnosed overweight/obesity had high rates of ischemic heart disease, heart failure, structural heart disease, arrhythmia, stroke, and death, although the strength of the association decreased in recent years.

Significance statement

Obesity is linked to metabolic abnormalities that predispose individuals to an increased risk of subtypes of CVD. In this population-based nationwide 40-year cohort study, we found that of 195,221 patients with an overweight/obesity diagnosis, more than 31,000 (15.9%) were admitted to hospital within 10 years because of CVD; corresponding to a 2.5-fold greater relative risk of any CVD associated with overweight/obesity than in the general population. We observed an increased risk for most CVD subtypes, including ischemic heart disease, heart failure, structural heart disease, arrhythmia, stroke, and cardiovascular death, although the strength of the association decreased in recent years. Our study emphasizes the importance of improved clinical handling of obesity and underscores the need to prevent associated complications to alleviate the burden of obesity.

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Peter Wolf Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria

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Yvonne Winhofer Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria

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Martin Krššák Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
High Field MR Centre, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Vienna, Austria

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Michael Krebs Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria

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Cardiovascular disease is the leading cause of death in general population. Besides well-known risk factors such as hypertension, impaired glucose tolerance and dyslipidemia, growing evidence suggests that hormonal changes in various endocrine diseases also impact the cardiac morphology and function. Recent studies highlight the importance of ectopic intracellular myocardial and pericardial lipid deposition, since even slight changes of these fat depots are associated with alterations in cardiac performance. In this review, we overview the effects of hormones, including insulin, thyroid hormones, growth hormone and cortisol, on heart function, focusing on their impact on myocardial lipid metabolism, cardiac substrate utilization and ectopic lipid deposition, in order to highlight the important role of even subtle hormonal changes for heart function in various endocrine and metabolic diseases.

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Thera P Links Division of Endocrinology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands

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Trynke van der Boom Division of Endocrinology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands

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Wouter T Zandee Division of Endocrinology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands

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Joop D Lefrandt Division of Vascular Medicine, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands

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Thyroid hormone stimulates cardiac inotropy and chronotropy via direct genomic and non-genomic mechanisms. Hyperthyroidism magnifies these effects, resulting in an increase in heart rate, ejection fraction and blood volume. Hyperthyroidism also affects thrombogenesis and this may be linked to a probable tendency toward thrombosis in patients with hyperthyroidism. Patients with hyperthyroidism are therefore at higher risk for atrial fibrillation, heart failure and cardiovascular mortality. Similarly, TSH suppressive therapy for differentiated thyroid cancer is associated with increased cardiovascular risk. In this review, we present the latest insights on the cardiac effects of thyroid suppression therapy for the treatment of thyroid cancer. Finally, we will show new clinical data on how to implement this knowledge into the clinical practice of preventive medicine.

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Alexander V Amram Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Stephen Cutie Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Guo N Huang Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Research conducted across phylogeny on cardiac regenerative responses following heart injury implicates endocrine signaling as a pivotal regulator of both cardiomyocyte proliferation and heart regeneration. Three prominently studied endocrine factors are thyroid hormone, vitamin D, and glucocorticoids, which canonically regulate gene expression through their respective nuclear receptors thyroid hormone receptor, vitamin D receptor, and glucocorticoid receptor. The main animal model systems of interest include humans, mice, and zebrafish, which vary in cardiac regenerative responses possibly due to the differential onsets and intensities of endocrine signaling levels throughout their embryonic to postnatal organismal development. Zebrafish and lower vertebrates tend to retain robust cardiac regenerative capacity into adulthood while mice and other higher vertebrates experience greatly diminished cardiac regenerative potential in their initial postnatal period that is sustained throughout adulthood. Here, we review recent progress in understanding how these three endocrine signaling pathways regulate cardiomyocyte proliferation and heart regeneration with a particular focus on the controversial findings that may arise from different assays, cellular-context, age, and species. Further investigating the role of each endocrine nuclear receptor in cardiac regeneration from an evolutionary perspective enables comparative studies between species in hopes of extrapolating the findings to novel therapies for human cardiovascular disease.

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M L M Barreto-Chaves Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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N Senger Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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M R Fevereiro Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A C Parletta Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A P C Takano Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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The cardiac growth process (hypertrophy) is a crucial phenomenon conserved across a wide array of species and is critically involved in the maintenance of cardiac homeostasis. This process enables an organism to adapt to changes in systemic demand and occurs due to a plethora of responses, depending on the type of signal or stimuli received. The growth of cardiac muscle cells in response to environmental conditions depends on the type, strength and duration of stimuli, and results in adaptive physiological responses or non-adaptive pathological responses. Thyroid hormones (TH) have a direct effect on the heart and induce a cardiac hypertrophy phenotype, which may evolve to heart failure. In this review, we summarize the literature on TH function in the heart by presenting results from experimental studies. We discuss the mechanistic aspects of TH associated with cardiac myocyte hypertrophy, increased cardiac myocyte contractility and electrical remodeling, as well as the associated signaling pathways. In addition to classical crosstalk with the sympathetic nervous system (SNS), emerging work pointing to the new endocrine interaction between TH and the renin-angiotensin system (RAS) is also explored. Given the inflammatory potential of the angiotensin II peptide, this new interaction may open the door for new therapeutic approaches which target the key mechanisms responsible for TH-induced cardiac hypertrophy.

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Chaiho Jeong Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Bongseong Kim Department of Medical Statistics, Soongsil University of Korea, Seoul, Republic of Korea

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Jinyoung Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Hansang Baek Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Mee Kyoung Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Tae-Seo Sohn Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Ki-Hyun Baek Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Ki-Ho Song Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Hyun-Shik Son Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Kyungdo Han Department of Medical Statistics, Soongsil University of Korea, Seoul, Republic of Korea

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Hyuk-Sang Kwon Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

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Objective

Real-world-based population data about the optimal low-density lipoprotein cholesterol (LDL-C) level for preventing cardiovascular disease in very high-risk populations is scarce.

Methods

From 2009 to 2012, 26,922 people aged ≥ 40 years with type 2 diabetes mellitus (T2DM) who had a history of percutaneous coronary intervention (PCI) were analyzed. Data from the Korean National Health Insurance System were used. They were followed up to the date of a cardiovascular event or the time to death, or until December 31, 2018. Endpoints were recurrent PCI, newly stroke or heart failure, cardiovascular death, and all-cause death. Participants were divided into the following categories according to LDL-C level: <55 mg/dL, 55–69 mg/dL, 70–99 mg/dL, 100–129 mg/dL, 130–159 mg/dL, and ≥ 160 mg/dL.

Results

Compared to LDL-C < 55 mg/dL, the hazard ratios (HR) for re-PCI and stroke increased linearly with increasing LDL-C level in the population < 65 years. However, in ≥ 65 years old, HRs for re-PCI and stroke in LDL-C = 55–69 mg/dL were 0.97 (95% CI: 0.85–1.11) and 0.96 (95% CI: 0.79–2.23), respectively. The optimal range with the lowest HR for heart failure and all-cause mortality were LDL-C = 70–99 mg/dL and LDL-C = 55–69 mg/dL, respectively, in all age groups (HR: 0.99, 95% CI: 0.91–1.08 and HR: 0.91, 95% CI: 0.81–1.01).

Conclusion

LDL-C level below 55 mg/dL appears to be optimal in T2DM patients with established cardiovascular disease aged < 65 years, while an LDL-C level of 55–69 mg/dL may be optimal for preventing recurrent PCI and stroke in patients over 65 years old.

Open access
Peter D Mark Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Mikkel Andreassen Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Claus L Petersen Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Andreas Kjaer Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Jens Faber Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Purpose

The aim of this study was to investigate structure and function of the heart in subclinical hyperthyroidism (SH) before and after obtaining euthyroidism by radioactive iodine treatment, using high precision and observer-independent magnetic resonance imaging (MRI) technology.

Methods

Cardiac MRI was performed before and after euthyroidism was obtained by radioactive iodine treatment in 12 otherwise healthy patients (11 women and one man, mean age 59 years, range 44–71 years) with a nodular goiter and SH, and compared with eight healthy controls investigated at baseline. Cardiac data were expressed as an index, as per body surface area, except for heart rate (HR) and ejection fraction.

Results

Post-treatment cardiac MRI was performed in median 139 days after a normalized serum TSH value had been recorded. During treatment, serum TSH increased from (median (range)) 0.01 (0.01–0.09) to 0.88 (0.27–3.99) mU/l. Patients with untreated SH had increased resting HR (P<0.01) as well as cardiac index (cardiac output as per body surface area) (P<0.01) compared with controls. Obtaining euthyroidism resulted in a significant decrease in left ventricular mass index (LVMI) of 2.7 g/m2 (P=0.034), in HR of 8 bpm (P=0.001), and in cardiac index of 0.24 l/min per m2 (P=0.017).

Conclusions

Normalization of thyroid function by radioactive iodine treatment of SH resulted in significant reductions in clinically important heart parameters such as LVMI, HR, and cardiac index. SH should be regarded as a condition in which aggressive treatment should be considered to protect cardiac function.

Open access