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Atrioventricular block in patients with thyroid dysfunction: Prognosis after treatment with hormone supplementation or antithyroid medication

Open ArchivePublished:June 27, 2012DOI:https://doi.org/10.1016/j.jjcc.2012.05.012

      Abstract

      Background

      Hypothyroidism is a reversible cause of atrioventricular (AV) block. Few reports have described reversible AV block caused by hyperthyroidism. However, it is unknown whether patients with AV block are expected to have a benign course after the initiation of appropriate therapy for thyroid dysfunction.

      Methods

      The study group consisted of patients with II or III degree AV block and bradyarrhythmia (≤40 bpm) excluding patients with myocardial infarction, electrolyte abnormalities, digitalis toxicity, and vasovagal syncope. Thyroid dysfunction is diagnosed when thyroid stimulating hormone and thyroxine levels are not in defined normal ranges. AV block was determined by surface electrocardiogram (ECG). The cause and effect relation between AV block and thyroid dysfunction was evaluated.

      Results

      Of 668 patients, 29 (4.3%) had hypothyroidism (19 overt) and 21 (3.1%) had hyperthyroidism (8 overt). The most frequent ECG finding was complete AV block (27 of 50 patients). Ten patients had bradyarrhythmia and 13 had second-degree AV block. Euthyroid state was achieved in 10 hypothyroidic (34%) and in 7 hyperthyroidic patients (33%) with hormone replacement and antithyroid therapy, respectively, during the follow-up period (≤21 days). Thyroid dysfunction was found to be not related with AV block in 40 patients (80%). However, in 4 of 10 patients with AV block related to thyroid dysfunction the resolution of AV block occurred after the placement of pacemaker (>21 days). Overall, 44 of 50 (88%) patients with AV block in association with thyroid dysfunction were implanted with a permanent pacemaker. Of 6 patients who did not receive a pacemaker, 2 had complete AV block and 4 had bradyarrythmia.

      Conclusion

      AV block associated with thyroid dysfunction needs great attention regardless of type of the thyroid disease. Patients with II and/or III degree AV block in the setting of thyroid dysfunction almost always need permanent pacemaker insertion even after normalization of thyroid status.

      Keywords

      Introduction

      Hypothyroidism is not an uncommon cause of complete atrioventricular (AV) block in clinical practice. Also, hyperthyroidism is thought to be a reversible cause of AV block [
      • Kramer M.R.
      • Shilo S.
      • Hershko S.
      Atrioventricular and sinoatrial block in thyrotoxic crisis.
      ,
      • Topaloglu S.
      • Topaloglu O.
      • Ozdemir O.
      • Soylu M.
      • Demir A.D.
      • Korkmaz S.
      Hyperthyroidism and complete atrioventricular block: a report of 2 cases with electrophysiologic assessment.
      ,
      • Karakaş C.Y.
      • Topaloğlu C.
      • Canbolant E.
      • Seyfeli E.
      • Akgül F.
      Hyperthyroidism as a rare cause of complete AV block.
      ]. According to contemporaneous guidelines pacemaker implantation is generally considered unnecessary in patients with “thyroid dysfunction associated with AV block” (TDAB) [
      • Epstein A.E.
      • DiMarco J.P.
      • Ellenbogen K.A.
      • Estes 3rd, N.A.
      • Freedman R.A.
      • Gettes L.S.
      • Gillinov A.M.
      • Gregoratos G.
      • Hammill S.C.
      • Hayes D.L.
      • Hlatky M.A.
      • Newby L.K.
      • Page R.L.
      • Schoenfeld M.H.
      • Silka M.J.
      • et al.
      ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons.
      ]. However, it is not known whether patients with TDAB can expect a benign course after the initiation of appropriate medical therapy. Moreover, the time course between the initial therapy for thyroid dysfunction and recovery of AV block is not clear. Hence, the appropriate strategy for patients with AV block in association with thyroid dysfunction remains challenging for physicians. We examined the clinical course of consecutive patients admitted to our institution with the diagnosis of “AV block” and hypo/hyperthyroidism.

      Methods

      We reviewed patients who had second-degree or third-degree AV block, and bradyarrhythmia (average heart rate ≤40 bpm on 24-h Holter monitoring) from our institution between January 2008 and June 2009. In addition, using the same criteria for patient selection, we collected patients prospectively beginning from June 2009. Shortly, all hospitalized patients to the department of cardiology with symptomatic AV block between January 2008 and July 2010 were evaluated. Patients with concomitant myocardial infarction, electrolyte abnormalities, digitalis toxicity, and vasovagal syncope were excluded. Also, patients who were taking beta-blockers, nondihydropyridine calcium-channel blockers, and class I and III antiarhythmics were excluded from this study. Thyrotropin (thyroid stimulating hormone, TSH) and thyroxin levels were studied from all hospitalized patients with AV block. Thyroid dysfunction was defined according to the value of the TSH and thyroxin. TSH level above the normal range (≥5 mIU/L), with or without thyroxin depletion (<2 ng/L) was defined as overt or subclinical hypothyroidism, respectively. Decreased level of TSH (<1 mIU/L), with or without elevated thyroxin (>5 ng/L) level was defined as overt or subclinical hyperthyroidism, respectively. Etiology of thyroid dysfunction was not sought for inclusion or exclusion. Patients who were on treatment for thyroid dysfunction before admission with AV block are classified as hypo or hyperthyroidic, according to their previous diagnosis irrespective of the level of TSH during the index hospitalization. All of the patients with abnormal TSH level were consulted by the endocrinologist and appropriate treatment with antithyroid medication or hormone supplementation have been started in hospital. Twelve of 29 hypothyroidic and 2 of 21 hyperthyroidic patients had been treated before the admission with AV block, and they all had normal TSH value during admission. Permanent pacemaker was implanted to all of the patients who had been treated for thyroid dysfunction before the admission with AV block.
      The type and level of AV block were determined by the surface electrocardiogram (ECG) [
      • Rosen K.M.
      • Gunnar R.M.
      • Rahimtoola S.H.
      Site and type of second degree AV block.
      ,
      • Olgin J.E.
      • Zipes D.P.
      Specific arrhythmias: diagnosis and treatment.
      ,
      • Narula O.S.
      • Samet P.
      • Wenckebach
      • Mobitz type I.I.
      AV block due to block within the His bundle and bundle branches.
      ,
      • Chung E.K.
      His bundle electrocardiography and other electrophysiologic studies.
      ,
      • Langerdorf R.
      • Cohen H.
      • Gozo E.G.
      Observations on second degree atrioventricular block, including new criteria fort the differential diagnosis between type I and type II block.
      ] (Table 1). Patients were classified into two groups to define a relationship between thyroid dysfunction and AV block: (1) AV block related to thyroid dysfunction: TDAB that resolved after the appropriate treatment and did not recur during the follow-up period (≤21 days); (2) AV block not related to thyroid dysfunction-incidental block (IB): AV block that never resolved within 3 weeks after initiation of medication or resolved but relapsed in spite of continuation of the therapy and normalization of TSH level. All patients were monitored continuously until they had improved AV conduction or received an implanted pacemaker. If AV block did not resolve within 4–6 days a pacemaker implantation was decided. Patients with resolved AV block were followed in hospital up to 3 weeks. Recurrent cases were identified by routine ECG that was obtained twice a day or by ECG that was obtained in case of bradycardia-related symptoms. Permanent pacemaker was implanted for all of the patients with recurrence of AV block during follow-up. Patients who recovered apparent normal AV conduction after normalization of the thyroid status were recommended to visit arrhythmia polyclinic, for evaluation of AV conduction with surface ECG, within one month after discharge. Patients who had abnormal TSH level at the time of pacemaker placement have been followed until they had normal TSH level to reveal the exact relation between the thyroid dysfunction and an AV block. Patients with improved AV conduction and no pacemaker dependency at pace rate of 40 bpm were classified as an AV block related to thyroid dysfunction. Those who had persistent AV block and/or pacemaker dependency at pace rate ≤40 bpm were defined as IB. Collection and analyses of data were authorized by the ethics committee of the hospital.
      Table 1Classification of second- or third-degree AV block and bradyarrhythmia based upon electrocardiographic characteristics.
      AV-nodal blockInfranodal AV blockUndetermined level of AV block
      Second-degree AV blockPR increment preceding a blocked P (Wenckebach) and narrow QRSConstant PR interval preceding blocked PPR increment (Wenckebach) preceding a blocked P and wide QRS
      Third-degree AV blockEscape rhythm has narrow QRS and rate ≥40 beats/minEscape rhythm has wide QRS and rate <40 beats/minEscape rhythm has wide QRS and rate ≥40 beats/min
      Bradyarrhythmiaf waves with irregular narrow QRSf waves with regular wide QRSf waves with irregular wide QRS
      AV, atrioventricular; f, fibrillatory.

      Statistical analysis

      Quantitative variables were expressed as mean value ± SD, and qualitative variables were expressed as percent (%). Categorical data were compared using the Chi-square test or Fisher's exact test. Logistic analysis was applied for multivariate analysis. A p-value < 0.05 was considered statistically significant. All statistical studies were carried out using NCSS 2007 (Number Cruncher Statistical System) and PASS 2008 Statistical Software Program (NCSS, Kaysville, UT, USA).

      Results

      Among the 668 study patients (mean age 68.2 ± 15.4 years, 337 women), 50 patients (7.4%) had the diagnosis of thyroid dysfunction during the hospitalization for AV block. Of these 19 patients (2.8%) had overt hypothyroidism (mean age 67.73 ± 9.04 years, 17 women), 8 patients (1.1%) had overt hyperthyoidism (mean age 67.75 ± 11.27 years, 6 women), 10 patients (1.4%) had subclinical hypothyroidism (mean age 69.10 ± 11.10 years, 4 women), and 13 patients (1.9%) had subclinical hyperthyroidism (mean age 71.92 ± 15.56 years, 9 women). In 36 of 50 (72%) patients with thyroid dysfunction, the diagnosis was established during the index hospitalization. The AV block type was similar in all four subclinical or overt hypo/hyperthyroidism groups (Table 2). Although there was no effect of comorbidities on the reversibility of AV block, diabetes mellitus and hypertension were common in patients with hypothyroidism (Table 3).
      Table 2The level of AV block based upon the surface electrocardiographic findings in patients with thyroid dysfunction.
      Subclinical hypothyroidismSubclinical hyperthyroidismOvert hypothyroidismOvert hyperthyroidismp
      n (%)n (%)n (%)n (%)
      AV-Nodal4 (40)8 (61.5)7 (36.8)4 (50)0.568
      Infranodal4 (40)3 (23.1)11 (57.9)3 (37.5)
      Undetermined2 (20)2 (15.4)1 (5.3)1 (12.5)
      Mean values (SD) and % (n) are reported for continuous and categorical variables, respectively.
      AV, atrioventricular.
      Table 3Major comorbidities in patients with thyroid dysfunction.
      Thyroid dysfunctionp
      HypothyroidismHyperthyroidism
      n (%)n (%)
      DM12 (41.4%)3 (14.3%)0.039
      p<0.05.
      HT22 (75.9%)10 (47.6%)0.040
      p<0.05.
      CRF3 (10.3%)2 (9.5%)1.000
      Mean values (SD) and % (n) are reported for continuous and categorical variables, respectively.
      CRF: chronic renal failure; DM: diabetes mellitus; HT: hypertension.
      * p < 0.05.
      TSH level was normalized in 10 patients with hypothyroidism after the hormone supplementation therapy. While, AV block was resolved and never recurred in 5 patients, 3 patients had sustained AV block and 2 patients had recurrence of AV block despite the continuation of therapy (Fig. 1). A permanent pacemaker was implanted for these five patients. Euthyroid state was achieved in 7 of 21 patients with hyperthyroidism with the antithyroid therapy, but AV block was resolved in only 3 of them. However, 2 out of these 3 patients experienced recurrence of AV block, and remaining 4 patients had sustained AV block. As a result 6 of 7 hyperthyroidic patients who achieved euthyroid state had implanted a pacemaker (Fig. 2). Seven patients with hypothyroidism and 12 patients with hyperthyroidism had abnormal TSH level while implanting a pacemaker. Overall 24 of 29 hypothyroidic and 20 of 21 hyperthyroidic patients with AV block underwent a permanent pacemaker placement. However, 4 out of 44 pacemaker implanted patients were detected as having AV block secondary to thyroid dysfunction according to the extended follow-up with the ECG, TSH level, and device's memories. In these 4 patients two had AV block related to hypothyroidism and two related to hyperthyroidism (Fig. 1, Fig. 2).
      Figure thumbnail gr1
      Fig. 1Clinical course in patients with atrioventricular (AV) block and hypothyroidism. AV conduction was improved and never recurred in 5 patients with normalized thyroid stimulating hormone (TSH) level after the hormone supplementation therapy during the follow-up period (≤21 days). Any patient with abnormal TSH level experienced AV conduction improvement during the follow-up period. Extended follow-up of these patients revealed two additional AV blocks related to hypothyroidism.
      Figure thumbnail gr2
      Fig. 2Clinical course in patients with atrioventricular (AV) block and hyperthyroidism. AV conduction was improved and never recurred in only one patient with normalized thyroid-stimulating hormone (TSH) level after the antithyroid therapy during the follow-up period (≤21 days). Any patient with abnormal TSH level experienced AV conduction improvement during the follow-up period. Extended follow-up of these patients revealed two additional AV blocks related to hyperthyroidism.
      In conclusion, only 7 (24%) patients with hypothyroidism and just 3 (14%) patients with hyperthyroidism have had an AV block secondary to the thyroid disease. AV block in association with thyroid dysfunction was not suggested as being secondary to the disease in 40 of 50 patients (80%).

      Discussion

      Thyroid hormone exerts a major influence on the cardiovascular system by a number of direct and indirect mechanisms and, not surprisingly, its cardiovascular effects are prominent in both hypothyroidism and hyperthyroidism. It has direct inotropic, chronotropic, and dromotropic effects that are similar to those seen with adrenergic stimulation such as tachycardia and increased cardiac output [
      • Awtry E.H.
      • Colluci W.S.
      Disorders of the cardiovascular system: cardiac manifestations of systemic disease.
      ].
      Conduction block from the atrium to the ventricle may occur because of various reasons in a number of clinical situations. The etiologies may be classified as functional or structural. Those that are functional (metabolic disorders including hypothyroidism) are stated to be reversible in textbooks of internal medicine [
      • Tomaselli G.E.
      Disorders of the cardiovascular system: the bradyarhythmias.
      ]. However, the association of disturbances of intracardiac conduction with adult hypothyroidism is not well known. To our knowledge, the rate of resolution of AV block with hormone supplementation therapy in hypothyroidic patients has not been studied before. In the literature, there are some case reports of improved AV block with the normalization of TSH level after treatment of hypothyroidism. Schoenmakers et al. reported an elderly woman with complete AV block due to severe hypothyroidism which was resolved after supplementation therapy with levothyroxine [
      • Schoenmakers N.
      • de Graaff W.E.
      • Peters R.H.
      Hypothyroidism as the cause of atrioventricular block in an elderly patient.
      ]. Reversible AV block in association with myxedema was also presented in the literature as a case report [
      • Singh J.B.
      • Starobin O.E.
      • Guerrant R.L.
      • Manders E.K.
      Reversible atrioventricular block in myxedema.
      ]. It is postulated to be caused by edema by compressing on AV node and levothyroxine is thought to have an indirect effect on improving AV conduction by resolving edema. Not only overt hypothyroidism but also subclinical hypothyroidism is reported to be a possible cause of reversible AV block. Nakayama et al. reported a middle-aged man with transient 2/1 AV block and subclinical hypothyroidism. A conduction disturbance was improved completely after two weeks of thyroxine supplementation [
      • Nakayama Y.
      • Ohno M.
      • Yonemura S.
      • Uozumi H.
      • Kobayakawa N.
      • Fukushima K.
      • Takeuchi H.
      • Aoyagi T.
      A case of transient 2:1 atrioventricular block, resolved by thyroxine supplementation for subclinical hypothyroidism.
      ]. A case of AV block induced by hypothyroidism complicating long-term therapy with amiodarone was reported by Mangiardi et al. [
      • Mangiardi L.
      • Gaita F.
      • Brun S.
      • Presbitero P.
      • Nademanee K.
      • Singh B.N.
      Atrioventricular block complicating amiodarone-induced hypothyroidism in a patient with pre-excitation and rate-dependent bilateral bundle branch block.
      ]. Although amiodarone-induced hypothyroidism might cause AV block, the amiodarone itself could cause conduction defect by directly affecting cardiac conduction system [
      • Kawabata M.
      • Hirao K.
      • Hachiya H.
      • Higuchi K.
      • Tanaka Y.
      • Yagishita A.
      • Inaba O.
      • Isobe M.
      Role of oral amiodarone in patients with atrial fibrillation and congestive heart failure.
      ]. As stated above, all forms of hypothyroidism could cause an AV block which may resolve with levothyroxine therapy. Hence, herein all patients with hypothyroidism irrespective of primary etiology were included.
      Since, there is no obvious study to confirm a levothyroxine as the drug of hypothyroidism-related AV block, it is challenging for clinicians to manage patients with AV block in association with hypothyroidism. The question “Does the hormone supplementation improve both the AV conduction and hypothyroidism?” remains controversial. In one study from Lardoux et al., 14 of 42 non-treated hypothyroidic patients had conduction disturbances on routine ECG evaluation, and there was no evident effect of hormone therapy on conduction disturbances [
      • Lardoux H.
      • Cénac A.
      • Perlemuter L.
      • Bernheim R.
      • Hazard J.
      Disorders of intra-cardiac conduction and hypothyroidism in adults. A systematic study of 42 cases.
      ].
      Since in our research hypothroidism was detected in 4.3% of all patients with AV block which is similar to the ratio of hypothyroidism in the general population, it can be postulated that AV block does not have increased incidence in patients with hypothyroidism [
      • Jameson J.L.
      Endocrinology and metabolism: principles of endocrinology.
      ]. Additionally, the resolution of AV block occurred in only 24% of hypothyroidic patients despite the treatment with levothyroxine and normalization of TSH. These findings are distinct and controversial to the general belief that “AV block in association with hypothyroidism is reversible”.
      Cardiovascular manifestations are frequent in hyperthyroidism and, it is commonly associated with sinus tachycardia and atrial fibrillation. A rare complication of thyrotoxicosis is impaired AV conduction [
      • Topaloglu S.
      • Topaloglu O.
      • Ozdemir O.
      • Soylu M.
      • Demir A.D.
      • Korkmaz S.
      Hyperthyroidism and complete atrioventricular block: a report of 2 cases with electrophysiologic assessment.
      ,
      • Stern M.P.
      • Jacobs R.L.
      • Duncan G.W.
      Complete heart block complicating hyperthyroidism.
      ,
      • Rosenblum R.
      • Delman A.J.
      First degree heart block associated with thyrotoxicosis.
      ,
      • Davis A.C.
      • Smith H.L.
      Complete heart block in hyperthyroidism following acute infections: a report of 6 cases with necropsy findings in 1 case.
      ,
      • Muggia A.L.
      • Stejernholm M.
      • Houle T.
      Complete heart block with thyrotoxic myocarditis.
      ,
      • Campus S.
      • Rappelli A.
      • Malavasi A.
      • Satta A.
      Heart block and hyperthyroidism.
      ,
      • Sataline L.
      • Donaghue G.
      Hypercalcemia, heart block and hyperthyroidism (letter).
      ]. Complete AV block associated with thyrotoxicosis has generally been seen in patients with additional risk factors such as infectious diseases [
      • Davis A.C.
      • Smith H.L.
      Complete heart block in hyperthyroidism following acute infections: a report of 6 cases with necropsy findings in 1 case.
      ], rheumatic fever [
      • Stern M.P.
      • Jacobs R.L.
      • Duncan G.W.
      Complete heart block complicating hyperthyroidism.
      ], hypercalcemia [
      • Sataline L.
      • Donaghue G.
      Hypercalcemia, heart block and hyperthyroidism (letter).
      ], or digitalis treatment. Although complete heart block is usually the result of the primary insult, thyrotoxicosis may aggravate the condition. On the other hand, in the literature some patients with AV block are reported to have thyrotoxicosis as their only underlying disease, and in these patients control of thyroid disease has restored the normal AV conduction [
      • Muggia A.L.
      • Stejernholm M.
      • Houle T.
      Complete heart block with thyrotoxic myocarditis.
      ,
      • Campus S.
      • Rappelli A.
      • Malavasi A.
      • Satta A.
      Heart block and hyperthyroidism.
      ,
      • Kramer M.R.
      • Shilo S.
      • Hershko C.
      Atrioventricular and sinoatrial block in thyrotoxic crisis.
      ,
      • Toloune F.
      • Boukili A.
      • Ghafir D.
      • Hadri L.
      • Chaari J.
      • Akheddiou B.
      • Ohayon V.
      • Archane M.I.
      Hyperthyroidism and atrioventricular block. Pathogenic hypothesis. Apropos of case and review of the literature.
      ]. A 53-year-old woman with Graves’ disease while being euthyroid with propylthiourasil therapy was reported to have second-degree AV block and, the authors hypothesized that the most likely mechanism was an autoimmune response causing infiltration of the cardiac conduction pathways [
      • Singer Y.
      • Shvartzman P.
      Second-degree atrioventricular block in Graves’ disease.
      ]. Almange et al. suggested that a direct effect of thyroid hormone on the myocardium was responsible for a conduction disturbance [
      • Almange C.
      • Turnel F.
      • Badoual P.
      • Murie N.
      • Leborgne P.
      Hyperthyroidism and atrioventricular heart block.
      ]. The autonomic nervous system is also postulated to act by reciprocal excitation and exacerbate patent or latent hypervagatonia that was preexistent to the hyperthyroidism under the influence of thyroid hormone in excessive amount [
      • Toloune F.
      • Boukili A.
      • Ghafir D.
      • Hadri L.
      • Chaari J.
      • Akheddiou B.
      • Ohayon V.
      • Archane M.I.
      Hyperthyroidism and atrioventricular block. Pathogenic hypothesis. Apropos of case and review of the literature.
      ]. Complete AV block may even develop in a patient with thyrotoxicosis occurring during thyroid hormone therapy for clinical hypothyroidism [
      • Eraker S.A.
      • Wickamasekaran R.
      • Goldman S.
      Complete heart block with hyperthyroidism.
      ]. As mentioned above, in this report only 3 of 21 patients with hyperthyroidism-associated AV block returned to normal sinus rhythm with medical therapy. However pacemaker implantation was done in 2 of these patients due to persistency of AV block more than 6 days after the initiation of therapy. In these 2 patients, ventricular stimulation based upon devices’ memories occurred only 8% and 15% of the time. We assume that stimulation occurred in the initial several weeks of pacemaker implantation and/or at nights if heart rate dropped below the device's stimulation lower-rate.

      Study limitations

      We evaluated elderly symptomatic patients who were hospitalized. Our observations cannot be generalized to ambulatory or younger patients with asymptomatic AV block. An AV block is generally detected by the surface ECG, but sometimes especially in paroxysmal or intermettent AV block it is difficult to detect the block even by 24-h Holter monitoring [
      • Minamiguchi H.
      • Nanto S.
      • Onishi T.
      • Watanabe T.
      • Uematsu M.
      • Komuro I.
      Low atrial septal pacing with dual-chamber pacemakers reduces atrial fibrillation in sick sinus syndrome.
      ]. In our study, the surface ECG was used to detect AV block, although patients with paroxysmal or intermittent nature of block may possibly be underdiagnosed. Although, there were reports of improved AV conduction after six weeks of therapy for hypo/hyperthyroidism, we investigated over a relatively short time (≤21 days) to detect AV nodal conductance changes in period of normalization of TSH levels, hence the effect of thyroid disease on AV conduction might be underestimated. Inclusion of patients with bradyarrythmia might be inappropriate because of the close relation between thyroid hormone and heart rate response. Irrespective of the accuracy of electrocardiographic characteristics in defining the level of AV block, electrophysiologic studying was not performed in our series.

      Clinical implications

      Hypothyroidism is usually associated with bradycardia, and AV block occurring in patients with such a disorder is thought to be reversible and curable with levothyroxine therapy. Our findings suggest that a hypothyroidism-related AV conduction disease is really caused by hormone insufficiency in less than one quarter of patients. Patients with symptomatic AV block and either overt or subclinical hyperthyroidism almost always need a permanent pacemaker. We studied a small number of patients and our findings are preliminary. The results must be confirmed with findings that will be obtained from large populations in the future. One can argue that if AV block is not improved by the treatment of thyroid dysfunction, there are two possibilities; no relation to thyroid dysfunction or irreversible damage induced by the disease. However, defining the exact cause of irreversible AV block is not of clinical importance because a pacemaker should be placed in both situations.

      Conflicts of interest

      The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

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