Is the Heart Involvement in Graves’ Disease Actually an Autoimmune Effect in Some Patients? Report From Cogthy – A Prospective, Longitudinal Case-Controlled Study

source: Thyroid

authors: K. Tammelin, M. Holmberg, A. Lundgren, H. Filipsson Nystrom

In Graves’ disease (GD), hyperthyroidism per se may entail tachyarrhythmia, atrial fibrillation and heart failure. Known GD complications are, however, of autoimmune origin.

In GD patients with heart complications, stimulatory autoantibodies targeting the cardiovascular system (CardAbs) are frequent. Although previous studies were relatively small and used non-standardized methods, we hypothesize that CardAbs are frequent in GD in general and affect heart function.

We used standardized ELISA assays to determine if CardAbs 1) were more frequent in hyperthyroid GD patients than controls, 2) were influenced by antithyroid drugs (ATD), 3) correlate with heart related symptoms or biomarkers. Our preliminary data with higher beta1 adrenergic receptor antibody (anti-B1) levels in GD that decreased after ATD strengthen our hypotheses. Premenopausal women (n = 60) with FT4 > 50 pmol/L (ref 12-22) were evaluated at diagnosis and after 7.5 months for CardAbs (anti-B1, muscarinic type 2 receptor (anti-M2) and angiotensin II type 1 receptor (anti-AT1) antibodies), symptom score, NTproBNP (marker of heart failure) and Troponine-I (TNI, marker of cardiac myocyte damage).