Impact of thyroidectomy on cardiac manifestations of <scp>G</scp>raves' disease

Gauthier, Jason M.; Mohamed, Hassan Ibrahim; Noureldine, Salem I.; Nazari-Shafti, Timo Z.; Thethi, Tina K.; Kandil, Emad

doi:10.1002/lary.25687

Cited by 15 publications

(11 citation statements)

References 32 publications

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“…It is therefore important to exclude Graves' disease-related cardiac disease in those developing significant cardiorespiratory symptoms inconsistent with their thyroid status and under appropriate clinical circumstances. The majority of patients respond well to thionamides and specific cardiac intervention with complete or partial reversal of cardiac abnormalities (18), but definitive treatment should be discussed early to avoid Graves' disease relapse and a potential recurrence of cardiac decompensation (19).…”

Section: Discussionmentioning

confidence: 99%

Significant cardiac disease complicating Graves’ disease in previously healthy young adults

Witczak

Ubaysekara

Ravindran

et al. 2020

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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Summary Graves’ disease is associated with tachydysrythmia, cardiac ischaemia and cardiomyopathy – all uncommon in young adults without previous cardiac disease. We present three young individuals who developed cardiac complications after periods of uncontrolled Graves’ disease. Subject 1: A 34-year-old female had severe thyrotoxic symptoms for weeks. Investigations showed fT4: 98.4 (11–25 pmol/L), fT3: 46.9 (3.1–6.8 pmol/L), TSH <0.01 (0.27–4.2 mU/L) and thyrotrophin receptor antibody (TRAb): 34.8 (<0.9 U//l). She had appropriate treatment but several weeks later she became breathless despite improving thyroid function. Echocardiography showed a pericardial effusion of 2.9 cm. She responded well to steroids and NSAIDs but developed active severe Graves’ orbitopathy after early total thyroidectomy. Subject 2: A 28-year-old male developed thyrotoxic symptoms (fT4: 38 pmol/L, fT3: 13.9 pmol/L, TSH <0.01 (for over 6 months) and TRAb: 9.3 U/L). One month after starting carbimazole, he developed acute heart failure (HF) due to severe dilated cardiomyopathy – EF 10–15%. He partially recovered after treatment – EF 28% and had early radioiodine treatment. Subject 3: A 42-year-old woman who had been thyrotoxic for several months (fT4: 54.3; fT3 >46.1; TSH <0.01; TRAb: 4.5) developed atrial fibrillation (AF) and heart failure. Echocardiography showed cardiomegaly – EF 29%. She maintains sinus rhythm following early total thyroidectomy (EF 50%). Significant cardiac complications may occur in previously fit young adults, who have had uncontrolled Graves’ disease for weeks to months. Cardiac function recovers in the majority, but early definitive treatment should be discussed to avoid Graves’ disease relapse and further cardiac decompensation. Learning points: Cardiac complications of Graves’ disease are uncommon in young adults without previous cardiac disease. These complications may however occur if Graves’ disease had been poorly controlled for several weeks or months prior to presentation. Persistent symptoms after adequate control should alert clinicians to the possibility of cardiac disease. Specific treatment of Graves’ disease and appropriate cardiac intervention results in complete recovery in the majority and carries a good prognosis. Early definitive treatment should be offered to them to prevent cardiac decompensation at times of further relapse.

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Section: Discussionmentioning

confidence: 99%

Significant cardiac disease complicating Graves’ disease in previously healthy young adults

Witczak

Ubaysekara

Ravindran

et al. 2020

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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“…The rate of intra-and extra-thyroidal conversion of T 4 to T 3 is elevated in Graves' disease mostly due to an increased deiodase-1 activity. Thyroidectomy in Graves' disease has been reported to abolish the AF load [77]. It is worthwhile to note that the occurrence of AF in this condition is associated with concomitant autoantibodies toward the β1-adrenergic and the M2 muscarinic receptors [79][80][81][82][83].…”

Section: Thyroid Status Imbalance Promoting Afmentioning

confidence: 96%

“…Maximum P-wave duration and P-wave dispersion (indicators for the risk of paroxysmal AF) were longer in patients with endogenous and exogenous subclinical hyperthyroidism [72]. The incidence of paroxysmal AF is higher in toxic nodular goiter [75] and in patients suffering from Graves' disease [76,77], which is caused by the presence of TSH autoantibodies directed toward the G protein-coupled TSH receptor [78]. The rate of intra-and extra-thyroidal conversion of T 4 to T 3 is elevated in Graves' disease mostly due to an increased deiodase-1 activity.…”

Section: Thyroid Status Imbalance Promoting Afmentioning

confidence: 99%

“…Nevertheless, ventricular tachycardia has been registered in hyperthyroid patients suffering from Grave's disease and it has been associated with the interaction of autoantibodies of the β1-adrenergic, the M2 muscarinic, and the TSH-receptors [75]. While thyroidectomy in Graves' disease attenuates the occurrence of ventricular arrhythmias [77], it seems likely that VF may occur in individuals with an altered thyroid status when accompanied by the presence of the autoantibodies.…”

Section: Thyroid Status Imbalance Promotes Vfmentioning

confidence: 99%

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Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism

Tribulová

Kurahara

Hlivák

et al. 2020

IJMS

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A perennial task is to prevent the occurrence and/or recurrence of most frequent or life-threatening cardiac arrhythmias such as atrial fibrillation (AF) and ventricular fibrillation (VF). VF may be lethal in cases without an implantable cardioverter defibrillator or with failure of this device. Incidences of AF, even the asymptomatic ones, jeopardize the patient’s life due to its complication, notably the high risk of embolic stroke. Therefore, there has been a growing interest in subclinical AF screening and searching for novel electrophysiological and molecular markers. Considering the worldwide increase in cases of thyroid dysfunction and diseases, including thyroid carcinoma, we aimed to explore the implication of thyroid hormones in pro-arrhythmic signaling in the pathophysiological setting. The present review provides updated information about the impact of altered thyroid status on both the occurrence and recurrence of cardiac arrhythmias, predominantly AF. Moreover, it emphasizes the importance of both thyroid status monitoring and AF screening in the general population, as well as in patients with thyroid dysfunction and malignancies. Real-world data on early AF identification in relation to thyroid function are scarce. Even though symptomatic AF is rare in patients with thyroid malignancies, who are under thyroid suppressive therapy, clinicians should be aware of potential interaction with asymptomatic AF. It may prevent adverse consequences and improve the quality of life. This issue may be challenging for an updated registry of AF in clinical practice. Thyroid hormones should be considered a biomarker for cardiac arrhythmias screening and their tailored management because of their multifaceted cellular actions.

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“…Thyroid ablation reduces the incidence of AF [ 7 ] in patients with thyroid disease such as Graves’ disease [ 8 ], nodular goiter [ 9 ], and hyperthyroidism [ 10 ]. Cardiac disorders associated with thyroid disease are characterized by electrophysiological changes such as increased P wave duration, pulmonary vein ectopy, and sinoatrial (SA) node automaticity [ 11 ]. Altered regulation of thyroid gland can potentiate AF inducibility, particularly in older individuals in which lower thyroid stimulating hormone (TSH) has been shown to be associated with increased AF occurrence [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms and Management of Thyroid Disease and Atrial Fibrillation: Impact of Atrial Electrical Remodeling and Cardiac Fibrosis

Takawale

Aguilar

Bouchrit

et al. 2022

Cells

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Atrial fibrillation (AF) is the most common cardiac arrhythmia associated with increased cardiovascular morbidity and mortality. The pathophysiology of AF is characterized by electrical and structural remodeling occurring in the atrial myocardium. As a source of production of various hormones such as angiotensin-2, calcitonin, and atrial natriuretic peptide, the atria are a target for endocrine regulation. Studies have shown that disorders associated with endocrine dysregulation are potential underlying causes of AF. The thyroid gland is an endocrine organ that secretes three hormones: triiodothyronine (T3), thyroxine (T4) and calcitonin. Thyroid dysregulation affects the cardiovascular system. Although there is a well-established relationship between thyroid disease (especially hyperthyroidism) and AF, the underlying biochemical mechanisms leading to atrial fibrosis and atrial arrhythmias are poorly understood in thyrotoxicosis. Various animal models and cellular studies demonstrated that thyroid hormones are involved in promoting AF substrate. This review explores the recent clinical and experimental evidence of the association between thyroid disease and AF. We highlight the current knowledge on the potential mechanisms underlying the pathophysiological impact of thyroid hormones T3 and T4 dysregulation, in the development of the atrial arrhythmogenic substrate. Finally, we review the available therapeutic strategies to treat AF in the context of thyroid disease.

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Impact of thyroidectomy on cardiac manifestations of Graves' disease

Abstract: 4. Laryngoscope, 126:1256-1259, 2016.

Cited by 15 publications

References 32 publications

Significant cardiac disease complicating Graves’ disease in previously healthy young adults

Significant cardiac disease complicating Graves’ disease in previously healthy young adults

Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism

Mechanisms and Management of Thyroid Disease and Atrial Fibrillation: Impact of Atrial Electrical Remodeling and Cardiac Fibrosis

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