Subclinical thyroid dysfunction is a marker for atrial fibrillation (AF) and stroke risk.

This study explored the effects of AF screening according to thyroid-stimulating hormone (TSH) levels.

An AF screening trial (the LOOP study) was analyzed post hoc according to baseline TSH. The primary outcome was stroke or systemic embolism (SE). Secondary outcomes included major bleeding, all-cause death, and the combination of stroke, SE, and cardiovascular death.

TSH measurements were available in 6003 of 6004 trial participants, 1500 randomized to implantable loop recorder (ILR) screening for AF and anticoagulation upon detection vs 4503 to usual care; mean age was 74.7 ± 4.1 years and 2836 (47%) were women. AF detection was approximately triple for ILR vs usual care across TSH tertiles (adjusted P interaction = 0.44). In the first tertile, screening was associated with decreased risk of the primary outcome (hazard ratio [HR] 0.52, 95% CI 0.30-0.90; P = .02) and stroke, SE, or cardiovascular death (HR 0.54, 95% CI 0.34-0.84; P = .006) compared with usual care, while no effect was observed among participants with higher TSH (adjusted P interaction .03 and .01, respectively). There was no effect on other outcomes. Analyses of continuous TSH or excluding those with abnormal TSH or thyroid medication showed similar results.

AF screening and subsequent treatment was associated with decreased stroke risk among participants with low TSH, though the yield of screening was similar across TSH levels. TSH may be useful as a marker to indicate benefit from AF screening vs overdiagnosis and overtreatment. These findings should be considered exploratory and warrant further study.

Thermal ablation (TA) is an alternative to lobectomy for thyroid nodules (TNs). While it is believed that thyroid function remains stable after TA for cystic TNs, the impact of TA on solid TNs, especially the large ones, is less explored. This study investigates changes in thyroid hormones after TA in patients with solid-predominant TNs and identifies potential risk factors for thyroid dysfunction after TA.

Euthyroid patients with solid-predominant TNs (≥ 80% solid) were enrolled. The volume, diameter, and cytopathology of TNs were assessed before TA. TA was performed using either microwave or radiofrequency ablation. Thyroid hormone levels were measured at 1 week and 1, 3, 6, and 12 months after TA.

Seventy-seven euthyroid patients with TNs were included. The euthyroid rate dropped to 70.1% at 1 week after TA but improved to over 90% by 1 month and returned to 100% by 12 months. At 1 week after TA, subclinical hyperthyroidism and hyperthyroidism were observed, with elevated thyroxine, free triiodothyronine, free thyroxine, and thyroglobulin antibody levels, along with decreased thyroid-stimulating hormone (TSH) levels. The diameter and total volume of TNs were positively correlated with thyroid dysfunction, while TSH-baseline was negatively correlated with thyroid dysfunction 1 week after TA. A larger diameter and lower baseline TSH were identified as independent risk factors for thyroid dysfunction.

TA may cause short-term thyroid dysfunction, especially in patients with large TNs. Monitoring of thyroid hormone levels is recommended from 1 week to 3 months after TA to manage potential thyroid dysfunction effectively.

Subclinical thyroid dysfunction (ScTD), comprising subclinical hypothyroidism (SHypo) and subclinical hyperthyroidism (SHyper), has been associated with increased risk for cardiovascular events.

To assess associations between ScTD and cardiovascular risk factors (cvRFs) according to age and sex.

This analysis of pooled participant data from large prospective cohort studies from the Thyroid Studies Collaboration assessed cvRFs (blood pressure [BP], lipid levels, high-sensitivity C-reactive protein [hs-CRP]) among participants aged 18 to 103 years with SHypo (thyroid-stimulating hormone [TSH] > 4.50 mU/L, normal fT4) and SHyper (TSH < 0.45 mU/L, normal fT4) vs euthyroid (TSH 0.45-4.50 mU/L).

Of 69 006 participants (mean age 62 years, 55% women, 25% current smokers) from 16 international cohorts, 3748 (5.4%) had SHypo and 3428 (5.0%) had SHyper. In both women and men, systolic and diastolic BP were similar regardless of thyroid status. Exceptions were lower diastolic BP in women with SHyper compared to euthyroid participants (adjusted mean difference [aMD] -1.3 mmHg, 95% CI -2.0 to -0.5), and lower systolic BP in men with SHyper compared to euthyroid participants (aMD -3.1 mmHg, 95% CI -4.8 to -1.4). In both women and men, lipid levels (total, HDL, LDL-cholesterol, triglycerides) and hs-CRP were similar regardless of thyroid status. The only exception were women with SHyper who had lower LDL-cholesterol vs euthyroid (aMD -0.17 mmol/L, 95% CI -0.29 to -0.05).

Participants with ScTD and euthyroid participants have similar cvRFs and differences are arguably too small to explain the increased cardiovascular risk in ScTD observed in previous studies.

In recent years, the incidence of cardiovascular disease (CVD) has risen steadily, significantly impacting public health. Subclinical hypothyroidism (SCH) remains a controversial risk factor for CVD. This review examines the associations between SCH and dyslipidemia, carotid intima-media thickness (C-IMT), cardiac dysfunction, and cardiovascular event risk. Evidence suggests SCH may exacerbate atherosclerosis and cardiac dysfunction through mechanisms such as increased LDL synthesis, oxidative stress, and impaired vascular endothelial function. However, the causal link between SCH and cardiovascular outcomes remains unclear due to study design heterogeneity and overreliance on TSH levels. Elevated TSH may not solely reflect thyroid dysfunction but could also indicate compensatory responses to inflammation, aging, or stress. Large-scale studies like NHANES and IPD meta-analyses show a strong association between SCH and cardiovascular risk in younger populations, which diminishes in older adults due to physiological TSH increases. The cardiovascular benefits of levothyroxine (L-T4) therapy in SCH patients are limited, especially in older individuals, where a narrow therapeutic window increases side effect risks. Studies relying solely on TSH as a diagnostic and therapeutic target have significant limitations, as TSH cannot distinguish adaptive thyroid adjustments from pathological states and overlooks the role of free thyroid hormones (FT3/FT4). Future research should integrate multi-dimensional markers (such as oxidative stress indicators, vascular elasticity measures, and thyroid antibody status) and adopt longitudinal study designs to more accurately assess the clinical significance of SCH.

Thyroid stimulating hormone (TSH) is related to increased atrial fibrillation (AF) inducibility and plays an important role in a variety of cardiovascular diseases. However, the association of baseline TSH with in-hospital outcomes in patients with AF and coronary artery disease (CAD) is unknown. This study aimed to investigate the distribution of baseline TSH and its association with in-hospital outcomes (major adverse cardiovascular events, all-cause death, or heart failure [HF]) in AF patients combined with CAD.

A total of 19 725 patients with AF were included. The status of blood TSH was investigated. Patients with AF and CAD were divided into low, median, and high-TSH subgroups based on tertiles of baseline TSH levels. Clinical characteristics and in-hospital outcomes were compared. Logistic regression analysis was performed to determine the association of TSH with in-hospital outcomes. Subgroup analysis was also performed.

In patients with AF and CAD, compared with the low-TSH group, the median-TSH (OR 0.277, 95% CI 0.078-0.991, P = .048) and high-TSH (OR 0.163, 95% CI 0.036-0.750, P = .020) groups were associated with decreased all-cause death. Besides, high TSH showed a protective role for HF events, and the same results were seen in females, age ≥75, and non-non-hypertension subgroups.

Higher baseline TSH presented a protective effect on in-hospital all-cause death and HF in patients with AF combined with CAD.

Major depressive disorder (MDD) often presents alongside physical illnesses, such as a high incidence of subclinical hypothyroidism (SHypo) in patients, highlighting the common occurrence of these comorbidities. Recent research has indicated that the presence of comorbid SHypo in individuals diagnosed with MDD may result in notable alterations in both brain structure and function. This study aimed was to investigate the neurological mechanisms underlying this co-occurrence using a data-driven approach to analyze brain activity patterns.

Twenty-nine patients diagnosed with MDD without any comorbid conditions (nSHypo-MDD) were included in the study, along with 29 MDD patients who also had SHypo (SHypo-MDD), 26 patients with SHypo only, and 29 healthy individuals as controls (HCs). Each participant received resting-state functional magnetic resonance imaging scans and underwent neuropsychological evaluations.

We found significantly altered functional connectivity (FC) within the resting-state networks (RSNs) of the ventral and dorsal sensorimotor network (VSMN and DSMN) and occipital pole visual network (PVN) (p < 0.05, FDR corrected). A vital interaction effect between SHypo and MDD was detected in the PVN, showing that SHypo-MDD patients had higher FC values in the left cuneus than nSHypo-MDD patients. Serum-free triiodothyronine (FT3) levels in SHypo-MDD patients demonstrated an inverse relationship with FC values of the right supplementary motor area (SMA.R) (r = - 0.563, p = 0.003). Furthermore, the FC values in the left cuneus are positively associated with the Digit Symbol Substitution Test (DSST) scores (r = 0.507, p = 0.008).

Our study reveals significant FC changes in SHypo-MDD patients, particularly in the PVN, VSMN, and DSMN, suggesting compensatory mechanisms that mitigate cognitive deficits and highlighting the need for integrated management of SHypo and MDD to improve cognitive outcomes.

The American Heart Association (AHA), in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and metabolic syndrome) that contribute to cardiovascular health. The AHA Heart Disease and Stroke Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).

The AHA, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistical Update with review of published literature through the year before writing. The 2025 AHA Statistical Update is the product of a full year's worth of effort in 2024 by dedicated volunteer clinicians and scientists, committed government professionals, and AHA staff members. This year's edition includes a continued focus on health equity across several key domains and enhanced global data that reflect improved methods and incorporation of ≈3000 new data sources since last year's Statistical Update.

Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics.

The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

Abnormal fluctuations in thyroid function within the reference range were strongly associated with increased all-cause mortality. This study aimed to analyze the association between oxidative balance score (OBS) and free thyroxine (FT4) and thyrotropin (TSH) in euthyroid adults, as well as their interrelationships with mortality. 5727 euthyroid adults were selected from the National Health and Nutrition Examination Survey (NHANES). Weighted linear regression investigated the potential association of OBS with FT4 and TSH. In addition, COX proportional hazard models and restricted cubic spline (RCS) were used to investigate the association between OBS, FT4, TSH, and all-cause mortality. The results showed that OBS was negatively associated with serum FT4 concentrations in euthyroid adults (- 2.95%, 95% CI - 5.16%, - 0.92%). Additionally, the all-cause mortality rate was significantly higher in the fourth quartile (Q4) of FT4 compared to the first quartile (Q1) (HR 1.40, 95% CI 1.07-1.85). In the fourth quartile of OBS, the all-cause mortality rate was 31% lower than in Q1 (HR 0.69, 95% CI 0.52-0.92). Mediation analyses indicated that FT4 partially mediated the relationship between OBS and all-cause mortality. These results suggest a significant negative association between OBS and serum FT4, while both OBS and FT4 are strongly associated with mortality. However, the effect of OBS on serum FT4 is relatively limited, and therefore its clinical significance needs to be interpreted objectively.

Clinical studies have shown that thyroid stimulating hormone (TSH) is associated with increased cardiovascular disease risk and mortality. Even within normal ranges, elevated TSH levels have an impact on the cardiovascular system and have been associated with cardiac dysfunction. The aim of our study was to evaluate the predictive value of admission fasting serum TSH levels in patients with coronary heart disease in relation to long-term major adverse cardiovascular events (MACE) and all-cause mortality.

A total of 3515 patients with coronary heart disease who met the inclusion criteria were divided into four groups according to the quantile of TSH levels: Group 1 (TSH, 0.34-1.02 mIU/L, n=878); Group 2 (TSH, 1.03-1.71 mIU/L, n=886); Group 3 (TSH, 1.72-2.84 mIU/L, n=880); and Group 4 (TSH, 2.86-5.50 mIU/L, n=873). MACE and all-cause mortality were also compared. TSH concentrations associated with the risk of MACE, all-cause mortality were assessed using continuous scales (restricted quartic splines) and Cox proportional hazards regression models.

A total of 3515 patients with coronary heart disease were eligible for analysis. At a median follow-up of 70 months, patients in group 2 had a lower incidence of MACE compared to the other three groups. All-cause mortality was lower in the 3rd group. Restricted quartic spline analysis also revealed that TSH concentrations were associated with heart failure risk.

TSH levels have predictive value for adverse cardiovascular events and heart failure in patients with coronary heart disease.

Inflammation has been widely recognized as one of the major pathophysiological drivers of the development of atrial fibrillation (AF), which works in tandem with other risk factors of AF including obesity, diabetes, hypertension, and heart failure (HF). Our current understanding of the role of inflammation in the natural history of AF remains elusive; however, several key players, including the NLRP3 (NLR family pyrin domain containing 3) inflammasome, have been acknowledged to be heavily influential on chronic inflammation in the atrial myocardium, which leads to fibrosis and eventual degradation of its electrical function. Nevertheless, our current methods of pharmacological modalities with reported immunomodulatory properties, including well-established classes of drugs e.g., drugs targeting the renin-angiotensin-aldosterone system (RAAS), statins, and vitamin D, have proven effective in reducing the overall risk of developing AF, the onset of postoperative atrial fibrillation (POAF), and reducing overall mortality among patients with AF. This might bring hope for further progress in developing new treatment modalities targeting cellular checkpoints of the NLRP3 inflammasome pathway, or revisiting other well-known anti-inflammatory drugs e.g., colchicine, vitamin C, nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticosteroids, and antimalarial drugs. In our review, we aim to find relevant upstream anti-inflammatory treatment methods for the management of AF and present the most current real-world evidence of their clinical utility.

Excess thyroid hormone is a well-documented risk factor for the development of atrial fibrillation (AF). The purpose of the study is to assess incidence of AF in patients taking levothyroxine for hypothyroidism and correlate it with biochemical thyroid function.

This was a retrospective cohort study of patients aged 18 years and older who were treated with levothyroxine. Exclusion criteria were pre-existing diagnosis of AF and use of amiodarone in the prior year. Patients were followed 2012 through 2019 and stratified into 4 groups based on mean thyroid-stimulating hormone (TSH) value or mean fT4 value in 2012. Primary outcome was incidence of AF. Rates of AF between groups were assessed via Poisson regression with control of underlying confounders.

Of 21,035 patients, 1091 (5.2%) developed AF during follow-up. Thyroid-stimulating hormone at baseline was not significantly associated with incident AF. Higher fT4 levels at baseline were associated with increased AF risk in age- and sex-adjusted analyses (hazard ratio 1.22; 95% CI, 1.03-1.44) for the highest quartile versus the lowest quartile of fT4.

In hypothyroid patients treated with levothyroxine, higher circulating fT4 levels are associated with increased risk of incident AF. There is no association of serum TSH with risk of AF. In patients at risk for AF, consideration should be given to avoiding fT4 levels in the highest quartile.

Knowledge about the prevalence of atrial fibrillation (AF) in young stroke patients, as well as its associated factors and outcomes, is scarce. Our objective was to analyse it.

A retrospective analysis of the Spain Nationwide Minimum Basic Data Set (MBDS) (2016-2020), including ischaemic stroke (IS) patients aged 18 and 50 years, was conducted. Multivariate analyses were conducted to identify factors related to AF diagnosis.

Amongst 11,615 young IS patients, 426 (3.7%) had AF. Patients with AF were older (median age 45, interquartile range 42-48 vs. 44, interquartile range 40-47 years, p < 0.001) and displayed more incapacitating symptoms, higher in-hospital complications and were less often discharged home (p < 0.001). Multivariate analyses showed that older age (odds ratio [OR] 1.053, 95% confidence interval [CI] 1.032-1.074), obstructive sleep apnoea (OR 1.508, 95% CI 1.018-2.233), hyperthyroidism (OR 3.741, 95% CI 1.798-7.783), valvular heart disease (OR 6.094, 95% CI 4.261-8.716), congenital (OR 2.386, 95% CI 1.146-4.969) and non-congenital (OR 4.446, 95% CI 3.149-6.278) cardiopathies and heart failure (OR 3.098, 95% CI 1.905-5.037) were independently associated with higher probability of AF, whereas female gender (OR 0.647, 95% CI 0.516-0.812), diabetes mellitus (0.487, 95% CI 0.339-0.699), smoking (OR 0.617, 95% CI 0.501-0.759), patent foramen ovale (OR 0.210, 95% CI 0.111-0.396) and arterial dissection (OR 0.294, 95% CI 0.130-0.668) were associated with a lower probability.

In young IS patients, AF is associated with more in-hospital complications and disabling strokes. These findings emphasize the need to recognize AF in this demographic group, especially in patients with risk factors like hyperthyroidism and cardiomyopathies. Clinicians should assess these risk factors to ensure timely diagnosis and management of AF.

Objective: To study the link between free thyroxine (FT4) levels and mortality in hypertensive patients. Methods: Utilizing data from the National Health and Nutrition Examination Survey performed in the United States from 2007 to 2012. Results: This study included 3365 adults from the National Health and Nutrition Examination Survey (NHANES) 2007-2012. Weighted Cox regression model, Kaplan-Meier (KM) survival analysis, and restricted cubic spline (RCS) were used to analyze the link between FT4 levels and mortality in hypertensive patients. Furthermore, subgroup analyses and interaction analyses were carried out to evaluate the stability of links between FT4 levels and all-cause mortality across different subgroups of hypertensive patients. In the weighted Cox regression model, after adjusting for all covariates, FT4 levels treated as a continuous variable were positively linked to all-cause mortality in hypertensive patients (HR = 1.08,95% CI: 1.04-1.12, P < .001). When FT4 levels were treated as a categorical variable according to quartiles, the fully adjusted model found that the highest quartile of FT4 posed a greater all-cause mortality risk in hypertensive patients relative to the lowest quartile (HR = 1.47, 95% CI:1.01-2.15, P = .045). Based on the Kaplan-Meier survival curve, all-cause mortality was notably higher in groups Q3 and Q4 relative to FT4 levels in groups Q1 and Q2 (P < .001). The RCS curve revealed that the all-cause mortality in hypertensive patients exhibited a nonlinear increasing trend with rising FT4 levels (P for nonlinear = .033). The results were further validated by subgroup and sensitivity analyses, which confirmed their robustness and reliability. Conclusion: The level of FT4 is strongly linked to the all-cause mortality risk in hypertensive patients.

There is a paucity of data on the prognostic impact of thyroid dysfunction in patients with heart failure (HF). We aimed to examine the association between these two conditions in a nationwide cohort of patients with HF.

This Danish cohort study evaluated the thyroid function of patients diagnosed with first-time HF from 2000-2021. Patients were categorized according to laboratory-based thyroid function values (euthyroid, overt/subclinical hypothyroidism, or hyperthyroidism) recorded within one year before the HF diagnosis. The primary outcome was a composite of mortality and hospitalization for HF, examined using the cumulative incidence function. Cox proportional hazard analysis adjusted for major comorbidities was performed to investigate differences in outcomes among groups.

Of the 58,067 individuals included in this study (43.9% female, median age 75.7 years [p25-p75:66.4-83.5]), 54,319 (93.6%) were euthyroid, 1,669 (2.9%) had subclinical hypothyroidism, 239 (0.4%) had overt hypothyroidism, 1,633 (2.8%) had subclinical hyperthyroidism, and 207 (0.4%) had overt hyperthyroidism. Compared with euthyroid patients, the adjusted one-year HR of the composite outcome was 1.11 (95% CI, 1.02-1.20) in patients with subclinical hypothyroidism, 1.24 (95% CI, 1.02-1.51) in patients with overt hypothyroidism, 1.06 (95% CI, 0.98-1.15) in patients with subclinical hyperthyroidism, and 1.27 (95% CI, 1.00-1.60) in patients with overt hyperthyroidism. This positive association was mainly driven by the increased mortality rates.

In patients with incident HF, the presence of both hypo- and hyperthyroidism up to one year prior to HF diagnosis was associated with increased risk of the composite of mortality and hospitalization for HF. Our results demonstrate a high-risk group of patients in need of increased clinical awareness.

This study aims to establish a normal range for the thyroid uptake derived from 99mTc pertechnetate scans. In particular, variations of uptake with TSH stimulation and other factors such as urinary iodine concentration are taken into account and compared with the calculation of a raw uptake value.

Clinical multicentric (center A, B and C) prospective study on 125 consecutive healthy patients undergoing thyroid scans for thyroid nodules. Normal functional thyroid status was assured by normal TSH, normal thyroid size, no thyroid antibodies and no symptoms of thyroid functional disorders. Calculations of raw Tc-uptake (uptake) and modified uptake values regarding current TSH value (uptakeTSH1), urinary iodine concentration (uptakeTSH1&uic), gland volume, age, smoking status, weight and tissue thickness ventral to the thyroid were performed.

There is a positive correlation of thyroid uptake with TSH allowing for the calculation of a normalized uptake value (uptakeTSH1). The normal range for uptakeTSH1 compares favourable to that for raw uptake in that it yields a clear distinction from thyroid functional disorders. The additional normalization for urinary iodine concentration (uptakeTSH1&uic) may even improve the distinctive power whereas further normalizations such as for gland volume, age and others are not warranted by this study. The 95% CI of uptakeTSH1 for sites A, A&B, and A&B&C were 0.21%-2.06%, 0.22%-2.38% and 0.24%-2.40%.

A normal range for the thyroid uptake can be established with respect to the current TSH stimulation. This normalization (uptakeTSH1) overcomes the drawback of raw uptake by yielding a clinically useful parameter with obviously high distinctive power against functional thyroid disorders.

Thyroid hormones play a crucial role in cardiovascular physiology. Subclinical thyroid dysfunction has been associated with adverse cardiovascular outcomes, but evidence is mixed regarding causality.

The purpose of this study was to investigate the potential causal relationships of thyroid-stimulating hormone (TSH), free thyroxine, hypothyroidism, and hyperthyroidism with cardiovascular outcomes, including atrial fibrillation (AF), coronary artery disease, myocardial infarction, heart failure, and ischemic stroke, as well as their effect on cardiac structure and function assessed by cardiac magnetic resonance imaging.

A comprehensive 2-sample Mendelian randomization analysis was performed using summary data from large-scale meta-analyses of European ancestry individuals.

Genetically determined lower TSH levels (odds ratio 0.928; 95% confidence interval 0.884-0.974; P = .003) and genetic risk of hyperthyroidism (odds ratio 1.049; 95% confidence interval 1.016-1.083; P = .003) were associated with increased AF risk. These associations remained significant even after adjusting for cardiovascular risk factors. Colocalization and multivariable Mendelian randomization revealed height as a key mediator between TSH/hyperthyroidism and AF. These findings were further corroborated in the independent FinnGen cohort. However, no clear evidence was found for relationships between thyroid function and other cardiovascular outcomes and cardiac structure and function.

Our study shows that reduced TSH levels and hyperthyroidism heighten AF risk, with height serving as an important mediator in these associations. The primary focus of thyroid management in cardiovascular health should be on preventing and treating arrhythmias, particularly AF. Our research highlights the importance of routine screening and timely treatment of thyroid dysfunction to optimize the prevention and management of arrhythmias.

This study aimed to evaluate the impact of hypothyroidism and levothyroxine (LT4) treatment on arrhythmic risk by concurrently analyzing multiple electrocardiogram (ECG) parameters such as the Index of Cardio-Electrophysiological Balance (iCEB), frontal QRS-T angle, Tpeak-Tend (Tp-e) interval/QT interval ratio, and QT dispersion (QTd).

This cross-sectional study included 132 adult patients with primary hypothyroidism who had been receiving LT4 treatment, and 132 demographically matched healthy controls. The hypothyroid group was also stratified by thyroid-stimulating hormone (TSH) levels (subclinical <4.5 and overt ≥ 4.5). Participants underwent a series of thyroid function and ECG measurements.

The hypothyroid and healthy control groups were matched for age and gender (p = 0.080; p = 0.176). Participants with hypothyroidism had higher Tp-e/QT ratios, iCEB, median frontal QRS-T angle, and corrected QT dispersion (cQTd) than healthy controls (p = 0.004; p = 0.025; p = 0.004; p = 0.004, respectively). In the overt group, the Tp-e/QT ratio, iCEB, and median frontal QRS-T angles were all higher (p = 0.012, p = 0.037, and p = 0.016, respectively). Logistic regression analysis indicated that a higher iCEB score (β = 0.60, p = 0.003) was significant for the detection of arrhythmia risk. ROC analysis showed that iCEB had the highest sensitivity (0.80), moderate specificity (0.60), and AUC 0.70.

Patients with hypothyroidism have a higher risk of arrhythmia. To assess this risk, it is important to analyze the Tp-e interval, iCEB, frontal QRS-T angle, and QTd. Differentiating between patients with subclinical and overt hypothyroidism can help minimize the risk of arrhythmia. iCEB is the most effective method for identifying arrhythmic risk. Using all these parameters can improve the accuracy of arrhythmic risk detection in patients with hypothyroidism.

Physical activity (PA) plays an important role in human health. However, the relationship between the PA and dysthyreosis was not clear. This study aimed to explore this question.

We performed a population-based study on the basis of the participant's information that was collected from the National Health and Nutrition Examination Survey (NHANES) database. The association of the thyroid hormone and total PA metabolic equivalent task (MET) were assessed via linear regression analysis with adjusting for different covariates. Moreover, we also used path analysis to explore the causality between PA, thyroid hormone index, and dysthyreosis. The restricted cubic spline analysis was used to explore the non-linear relationship between the thyroid hormone index and the PA total MET.

A total of 2118 participants aged≥20, including 969 females and 1149 males, were collected from NHANES. The linear regression with multivariate adjustment suggested a linear relationship between the PA total MET and Thyroid-Stimulating Hormone Index (TSHI), and Thyroid Feedback Quantile-Based Index (TFQI), respectively. And TFQI and dysthyresis occurrence were significantly correlated (P<0.05). The path analysis showed that the PA total MET affected dysthyreosis occurrence by TFQI. In addition, we found a non-linear relationship between the total PA met and dysthyreosis via restricted cubic spline analysis.

PA was significantly correlated with dysthyreosis via thyroid hormone sensitivity. Therefore, it can be considered to prevent the occurrence of dysthyreosis by regulating thyroid hormone sensitivity through PA in daily life.

This study aims to explore the association between the triglyceride-glucose (TyG) index and vitamin D status to enhance our understanding of how vitamin D status relates to metabolic health and to provide evidence for the early diagnosis of vitamin D deficiency (VDD) using the TyG index.

We conducted a comprehensive search in various databases, including PubMed, Web of Science, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), China Biology Medicine disc, China Science and Technology Journal Database, and Wanfang Data to gather articles published from the inception of these databases until February 19, 2024. We assessed the quality of included studies using the Newcastle-Ottawa Scale (NOS) for case-control studies and the Agency for Healthcare Research and Quality (AHRQ) methodology checklist for cross-sectional studies. Statistical analyses in this study were conducted using conversion methods for non-standard data formats and consolidation techniques for combining multiple groups. The Fisher transformation method was used for correlation coefficients. We used a random-effects model considering the inherent clinical heterogeneity among the studies, and assessed statistical heterogeneity with the Cochrane Q test and I2 statistic, complemented by subgroup analyses and sensitivity analysis.

Our meta-analysis selected a total of nine studies. The analysis revealed that patients with vitamin D deficiency (VDD group) exhibited a significantly higher TyG index than those without deficiency (no-VDD group), with a mean difference (MD) of 0.16 (95% CI: 0.10 to 0.23, I2 = 93%). This association was particularly pronounced among patients with type 2 diabetes (T2DM), showing an MD of 0.15 (95% CI: 0.05 to 0.26, I2 = 55%). Additionally, a negative correlation was observed between the TyG index and vitamin D levels, with a correlation coefficient (r) of -0.236 (95% CI: -0.310 to -0.159, I2 = 91%). Excluding each study sequentially in the sensitivity analyses did not significantly alter the outcomes.

Our findings demonstrate a significant association between the TyG index and vitamin D status across diverse populations, including those with T2DM, subclinical hypothyroidism (SCH), and metabolic associated fatty liver disease (NAFLD). Our results reveal a notable disparity in the TyG index between vitamin D deficient and non-deficient groups, suggesting that vitamin D may play a critical role in metabolic health. These findings highlight the need for further research to explore the underlying mechanisms and clinical implications of vitamin D in the context of various metabolic disorders.

The association between thyroid function, coagulation and venous thromboembolism (VTE) has been reported in observational studies with conflicting findings. This study aimed to elucidate the causal effects of thyroid function on coagulation and VTE from a genetic perspective.

Two sample Mendelian randomization analysis was conducted using summary statistics from genome-wide association studies in a European population. Coagulation status was associated with nine coagulation-related factors (F VIII, F IX, F XI, Fibrinogen, Antithrombin-III, Thrombomodulin, Plasminogen activator inhibitor-1, Protein C and Protein S). Inverse variance weighting with random effect method was used as the main analytic approach with MR-Egger, weighted median, simple mode and weighted mode methods serving as complements. Sensitivity analyses including heterogeneity test, horizontal pleiotropy test and leave-one-out analysis were conducted to further assess the reliability of results.

No genetic causal effects of thyroid function on VTE (including pulmonary embolism and deep venous thrombosis) were found. Genetically, hyperthyroidism was suggestively related to decreased Antithrombin-III (β: -0.04 [95% CI: -0.06 to - 0.01], p = 0.010) and Protein C (β: -0.03 [95% CI: -0.06 to 0.00], p = 0.045). No notable associations were observed between other thyroid function parameters and coagulation-related factors.

We provide suggestive genetic evidence supporting the causal effect of hyperthyroidism on decreased level of anticoagulant factors including Antithrombin-III and Protein C. However, whether this genetic causality could lead to clinically significant hypercoagulable state and increased risk of VTE in hyperthyroid population needs to be further addressed.

Thyroid dysfunction's effects on those who have been diagnosed with atrial fibrillation have not been well investigated. We looked at how thyroid function among patients with pre-existing atrial fibrillation related to thromboembolic risk and clinical outcomes.

We gathered the medical information of patients diagnosed with nonvalvular atrial fibrillation (NVAF) between 2016 and 2020 at Dongguan People's Hospital. We then assessed the correlation between thyroid dysfunction and thrombotic risk (CHA2DS2-VASc) as well as the occurrence of clinical composite endpoint (all-cause death, heart failure, systemic embolism and hemorrhage events).

Of 1329 patients were admitted, 82.6% were euthyroid, 7.4% had subclinical hyperthyroidism, 4.2% had subclinical hypothyroidism, and 6.7% had low triiodothyronine (T3) syndrome. Lower levels of total triiodothyronine (TT3) were linked to an increased risk of thromboembolism (P < 0.005). During a median follow-up period of 1.84 years, there were 608 clinical composite endpoint occurrences. In the adjusted model, Low T3 syndrome was linked to a higher risk of the clinical composite endpoint (HR, 1.68; 95% CI, 1.20-2.37; P < 0.05) in comparison to euthyroidism. Specifically, low T3 syndrome was linked to a higher risk of heart failure (HR, 1.52; 95%CI, 1.01-2.30; P < 0.05) and all-cause death (HR, 3.34; 95% CI, 1.76-6.36; P < 0.001).

Low T3 syndrome are linked to an increased risk of heart failure and all-cause death in individuals with NVAF. And Patients with NVAF and low TT3 levels have a higher risk of thromboembolism.

Pulmonary vein (PV) antrum isolation (PVAI) that involves electrically isolating PV foci is a useful treatment strategy for atrial fibrillation (AF). However, non-PV triggers during/after the PVAI are observed in approximately 30 % of AF cases, contributing to AF recurrence. We present the case of an 84-year-old woman who underwent ablation of recurrent symptomatic paroxysmal AF in our hospital. AF was easily induced following spontaneous activity (SA) from non-PV triggers even after completing the PVAI, left atrial posterior wall isolation with roof and bottom lines, and superior vena cava isolation. Interestingly, the area of the earliest activation site of the SAs initiating AF and that with a fractionation mapping score of ≥4 corresponded. AF was steadily terminated during ablation of this fractionated area, and the programmed stimulation could no longer induce any SA or AF. This case report demonstrated that the area with a score of ≥4 points on the fractionation mapping calculated by EnSite™ (Abbott, Abbott Park, IL, USA) during sinus rhythm may contribute to the initiation and maintenance of paroxysmal AF. In patients whose AF does not resolve during ablation, physicians may consider performing an additional targeted ablation of the area with a fractionation mapping score of ≥4, even in patients with paroxysmal AF.

The area with a fractionation mapping score of ≥4 calculated by EnSite™ during sinus rhythm might play an important role in producing spontaneous activities and initiating and maintaining paroxysmal atrial fibrillation (AF). Thus, if the AF does not terminate during ablation, physicians should consider performing an additional targeted ablation of the area with a fractionation mapping score of ≥4, even if it is paroxysmal.

The relationship between thyroid dysfunction and measures of myocardial disease in older individuals remains to be defined.

To evaluate the impact of thyroid dysfunction on structure and function of the left heart chambers and blood markers of cardiac disease.

Cross-sectional analysis of the Cardiovascular Health Study, a community-based cohort of older individuals recruited from 4 urban areas in the United States. Of 3163 participants studied, 2477 were euthyroid, 465 had subclinical hypothyroidism (SCH), 47 overt hypothyroidism (OH), 45 endogenous (endo) subclinical hyperthyroidism (endo-SCT), and 129 had exogenous (exo) SCT due to thyroid hormone supplementation. Participants underwent clinical evaluation, blood sampling and biomarker measurement, 2-dimensional and speckle tracking echocardiography for assessment of left heart myocardial deformation, circulating biomarkers of diastolic overload (NT-proBNP), fibrosis (sST2, gal-3), and cardiomyocyte injury (hs-cTnT).

SCH was associated with higher NT-proBNP (beta = 0.17, P = .004), whereas OH was associated with higher hs-cTnT (beta = 0.29, P = .005). There were also suggestive associations of SCH with higher sST2, as well as endo-SCT with higher gal-3 and lower (worse) left atrial reservoir strain. Left ventricular longitudinal strain and end diastolic strain rate did not differ significantly from euthyroid participants in SCH, OH, or exo-SCT.

In this free-living elderly cohort, subclinical and overt hypothyroidism were associated with abnormalities of blood biomarkers consistent with diastolic overload and myocardial necrosis respectively, whereas subclinical hyperthyroidism tended to be associated with myocardial fibrosis and decreased left atrial strain. Our findings could represent stage B heart failure and illuminate distinct aspects of the pathobiology of heart disease related to thyroid gland dysfunction with potential clinical implications.

Obstructive sleep apnea (OSA) and thyroid dysfunction frequently overlap clinically and are risk factors for cardiovascular disease. The free triiodothyronine to free thyroxine (FT3/FT4) ratio as a novel biomarker of cardiovascular disease prognosis, but the impact of the FT3/FT4 ratio on the prognosis of OSA in patients with acute coronary syndromes (ACS) remains uncertain.

In this prospective cohort study, 2160 patients with ACS were recruited and underwent portable sleep monitoring at Beijing Anzhen Hospital from June 2015 to January 2020. OSA was diagnosed when apnea-hypopnea index of ≥15 events/h. Patients were further divided into tertiles according to FT3/FT4 ratio. All patients had scheduled follow-up visits at 1, 3, 6, 9 and 12 months after discharge, with subsequent outpatient visits or telephone follow-up visits every 6 months. The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE), including cardiovascular death, myocardial infarction (MI), stroke, ischemia-driven revascularization, or hospitalization for unstable angina or heart failure.

Among 1,547 euthyroid patients enrolled (mean age, 56.0 ± 10.5 years), 812 patients (52.5%) had OSA. The FT3/FT4 ratio between OSA and non-OSA patients was not significantly different. During 2.8 (1.4, 3.5) years follow up, the risk of MACCE increased with the decreasing FT3/FT4 tertiles in patients with OSA (tertile3 as reference, tertile2: hazard ratio (HR) 1.26, 95% CI: 0.85-1.86, P = 0.255; tertile1: 1.60, 95% CI 1.11-2.32; P = 0.013). After adjustment for confounders, the lowest FT3/FT4 tertile was still independently associated with an increased risk of MACCE (adjusted HR 1.66, 95% CI 1.11-2.50, P = 0.015).

Lower FT3/FT4 ratio associated with poor prognosis in patients with ACS and OSA.

Thyroid dysfunction is associated with characteristic changes in heart rate and arrhythmias. Thyroid hormones act through genomic and non-genomic effects on myocytes and influence contractility, relaxation and action potential duration through a variety of mechanisms. Atrial fibrillation is the most common arrhythmia associated with thyroid dysfunction, it occurs in both euthyroidism and hyperthyroidism in clear association with T4 levels. Mechanistically, in the hyperthyroid state, increased automaticity and triggered activity, together with a shortened refractory period and slowing of the conduction speed, lead to the initiation and maintenance of multiple intraatrial reentry circuits. Influences from the autonomic nervous system and hemodynamics controlled by thyroid hormones act as modulators for arrhythmias, which are promoted by a corresponding substrate (significant impact of comorbidities). Concerning therapy, in addition to treating hyperthyroidism, the initial therapeutic focus is on adequate rate control and anticoagulation in patients with a high risk of thromboembolism. Ablation of atrial fibrillation can be considered later on, although there is an increased likelihood of recurrence compared to patients without hyperthyroidism.Prolongation of the QT interval and increase in QT dispersion are involved in the formation of ventricular arrhythmias. Epidemiological data suggest an association of elevated T4 levels with ventricular arrhythmias and sudden cardiac death. However, this seems to be mainly relevant for patients with underlying cardiac disease (e.g. ICD users).

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. Its prevalence has increased due to worldwide populations that are aging in combination with the growing incidence of risk factors associated. Recent advances in our understanding of AF pathophysiology and the identification of nodal players involved in AF-promoting atrial remodeling highlights potential opportunities for new therapeutic approaches.

This detailed review summarizes recent developments in the field antiarrhythmic drugs in the field AF.

The current situation is far than optimal. Despite clear unmet needs in drug development in the field of AF treatment, the current development of new drugs is absent. The need for a molecule with absence of cardiac and non-cardiac toxicity in the short and long term is a limitation in the field. Improvement in the understanding of AF genetics, pathophysiology, molecular alterations, big data and artificial intelligence with the objective to provide a personalized AF treatment will be the cornerstone of AF treatment in the coming years.

This article includes a review of information primary care physicians need to know direct their evaluation and treatment of thyroid disorders that include sick euthyroid, hyperthyroidism, hypothyroidism, and subclinical thyroid disorders.

Background: Iodinated contrast is commonly used for radiological procedures, with one dose delivering several hundred-fold the daily requirements needed for normal thyroid hormone production. Risks of excess iodine include incident thyroid dysfunction, which is associated with adverse cardiac outcomes, yet there are no prospective studies investigating the changes in cardiac physiology following iodine contrast administration. This study was conducted to investigate the longitudinal relationships between the amount of iodinated contrast administration and changes in cardiac electrophysiology and structure. Methods: A longitudinal cohort study was conducted with prospectively enrolled participants who received iodine contrast for elective computed tomography or coronary angiography. Serum thyroid function tests, electrocardiograms (EKG), and transthoracic echocardiograms were obtained serially until 36 months. Trends of electrical and structural cardiac changes following iodine contrast administration were assessed using mixed effect models. Results: The cohort was composed of 129 patients (median age, 70 [interquartile range: 63, 75] years; 98% male). Larger amounts of iodine exposure were associated with increases in QRS and QTc durations and decreased ejection fraction (EF), and these associations were still observed for follow-up EF after additionally adjusting for baseline values (the high-iodine contrast group vs. the low-iodine contrast group, -4.23% [confidence interval, -7.66% to -0.79%]). Dose-response analyses also showed lower EF with larger amounts of iodine received; these trends were not significant for the EKG parameters studied. Conclusions: Over a period of up to 36 months, a larger amount of administered iodine contrast was associated with lower EF among participants. Further investigation is needed to elucidate the long-term trends of electrical and structural cardiac function after iodine contrast administration.

This study evaluates the association between vitamin A levels, AIP (the atherogenic index of plasma), and subclinical hypothyroidism.

A cross-sectional analysis was conducted involving a representative sample of 3530 Chinese adults. Linear and logistic regression models were utilized to evaluate the associations between AIP and subclinical hypothyroidism, stratified by vitamin A levels. These analyses were further differentiated by sex and age groups to identify any demographic-specific associations.

In the vitamin A-sufficient group, an increase in AIP was associated with elevated total triiodothyronine (TT3) levels (β = 0.26, 95%CI: 0.09, 0.41, p = 0.003). Conversely, in the group with severe vitamin A deficiency, higher AIP levels were linked to increased free triiodothyronine (fT3) and TT3 levels and decreased free thyroxine (fT4) levels (β = 0.12, 0.03, and -0.29, respectively). Additionally, severe vitamin A deficiency increased the risk associated with AIP and subclinical hypothyroidism (OR = 1.66, 95%CI: 1.07, 2.58, p = 0.025). This risk was notably more pronounced in women and older adults, with odds ratios of 2.44 (95%CI: 1.55, 3.86, p < 0.001) and 2.14 (95%CI: 1.36, 3.38, p = 0.001), respectively.

Vitamin A deficiency may increase the risk of the association between AIP and subclinical hypothyroidism, particularly among women and the elderly.