Thyroid hormones exert their influence on nearly all nucleated cells and are indispensable for regulating normal processes of growth and energy metabolism. Both insufficient and excessive iodine levels can result in hyperthyroidism, a condition characterized by an overactive thyroid gland. In populations with adequate iodine intake, autoimmunity is the primary cause of thyroid dysfunction. These autoimmune thyroid disorders include Graves' disease, Hashimoto's thyroiditis, and postpartum thyroiditis, which are distinguished by the presence of thyroid-targeting autoantibodies in circulation [1]. Based on a prior academic study, the prevalence of hyperthyroidism in iodine-sufficient nations exhibited a range of 0.1% to 2.5%, with an incidence rate spanning from 25.8 to 81.6 per 100,000 individuals within the population [2]. However, in 2015, both the prevalence and incidence rates of hyperthyroidism experienced a substantial increase, reaching 2.76 and 0.55 per 1,000 individuals within the population, respectively [3]. Within the context of South Asia, specifically in Taiwan, a retrospective academic investigation involving a cohort of one million randomly selected individuals unveiled a persistent upward trend in the prevalence of overt hyperthyroidism. As a consequence of Taiwan's modifications in iodine intake regulations, the incidence rate of hyperthyroidism surged from 0.27% in 2004 to 0.37% in 2010. Furthermore, the incidence of hyperthyroidism increased from 0.97 cases per 1,000 individuals in 2004 to 1.06 cases per 1,000 individuals in 2010 [4].

Hyperthyroidism can disrupt the normal electrical signaling of the heart, thereby increasing the risk of atrial fibrillation (AF). The prevalence of atrial fibrillation among individuals with hyperthyroidism exhibits a variable range, spanning from 2% to 20%.There is a significant disparity in the prevalence of AF between individuals with normal thyroid function and those with overt hyperthyroidism. While the incidence of atrial fibrillation among those without thyroid abnormalities hovers around 2.3%, it increases considerably to 13.8% among those with overt hyperthyroidism [5]. Hyperthyroidism is a reversible underlying cause of AF with a relatively favorable prognosis. More than three-quarters of patients with thyrotoxic AF without concurrent cardiac or valvular disease experience spontaneous restoration of a normal sinus rhythm within three to six months of initiating antithyroid drug therapy. In addition, hyperthyroidism-related AF is more amenable to maintaining sinus rhythm after cardioversion and a 36% lower recurrence rate compared to non-hyperthyroidism-related AF [6, 7].

Following the normalization of free thyroxine (fT4) levels in the thyroid, predicting the occurrence of AF or cardiovascular diseases remains a challenge. Across the spectrum of subclinical thyroid disease, an association between thyroid stimulating hormone (TSH) levels and the risk of atrial fibrillation is observed [8, 9]. Nevertheless, contradictory evidence exists in some research findings, where elevated circulating fT4 levels, as opposed to TSH levels, have been linked to an increased risk of incident AF in euthyroid individuals [10].

Thyrotropin-binding inhibitory immunoglobulin (TBII) antibodies are significant in Graves' disease, an autoimmune condition characterized by immune cell infiltration, T cell activation, and autoantibody production targeting the thyroid-stimulating hormone receptors (TSH-R) on thyroid cells [11]. This TSH-R-Ab demonstrates distinct functionality in comparison to the TSH-R, encompassing both stimulatory and inhibitory effects. Activation of stimulatory TSH-R-Ab initiates the 3’, 5’-cyclic adenosine 5’-monophosphate pathway, thereby stimulating the TSH-R and resulting in an augmented thyroid size and increased thyroid hormone production. Conversely, TSH-R-Ab antagonists act as inhibitors of the TSH-R [12, 13]. Two methods are employed for the detection of TSH-R-Ab: the competitive TBI assay and the thyroid stimulating immunoglobulin (TSI) bioassay. The TBII assay is capable of identifying immunoglobulins that hinder the binding of radiolabeled TSH to the TSH-R [14]. TBII titers reflect hyperthyroidism severity and predict remission or relapse. Anti-thyroid drugs often lower TBII levels, potentially by improving thyroid autoimmunity [15].

Clinical guidelines advocate the measurement of TBII levels as a prerequisite before discontinuing antithyroid medication therapy. In instances where TBII concentrations remain persistently elevated, the prudent course of action is to consider the continuation of antithyroid drug treatment [16, 17]. The prolonged elevation of TBII subsequent to treatment cessation may carry an augmented risk of Grave's ophthalmopathy or fetal hyperthyroidism [18]. However, the long-term repercussions of TBII on cardiovascular outcomes have hitherto remained unexplored. Therefore, the aim of study was to investigate the association between TBII levels and the incidence of AF and cardiovascular mortality.