Bifascicular block in a patient with Graves disease-rare manifestation of a common disease

Prashant Panda; Vikas Bhatia; Somesh Thakur; Kiran Mokta; Jitender K Mokta; Surender Thakur

doi:10.4103/0973-0354.129736

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CASE REPORT

Year : 2014 | Volume : 11 | Issue : 2 | Page : 78-80

Bifascicular block in a patient with Graves disease-rare manifestation of a common disease

Prashant Panda¹, Vikas Bhatia¹, Somesh Thakur², Kiran Mokta³, Jitender K Mokta¹, Surender Thakur⁴
¹ Department of Medicine, IGMC, Shimla, Himachal Pradesh, India
² Department of ENT, IGMC, Shimla, Himachal Pradesh, India
³ Department of Microbiology IGMC, Shimla, Himachal Pradesh, India
⁴ Department of Radio Diagnosis and Intervention Radiology, IGMC, Shimla, Himachal Pradesh, India

Date of Web Publication

31-Mar-2014

Correspondence Address:
Prashant Panda
Department of Medicine, IGMC, Shimla - 171001, Himachal Pradesh
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/0973-0354.129736

Abstract

There are many cardiovascular manifestations of hyperthyroidism. Rhythm disturbances commonly occur in the form of tachyarrhythmia's. Conduction block are not commonly found in the hyperthyroid patients. We report a rare manifestation of hyperthyroidism in the form of bifasciular block.

Keywords: Bifasciular block, Graves′ disease, thyrotoxicosis

How to cite this article:
Panda P, Bhatia V, Thakur S, Mokta K, Mokta JK, Thakur S. Bifascicular block in a patient with Graves disease-rare manifestation of a common disease. Thyroid Res Pract 2014;11:78-80

How to cite this URL:
Panda P, Bhatia V, Thakur S, Mokta K, Mokta JK, Thakur S. Bifascicular block in a patient with Graves disease-rare manifestation of a common disease. Thyroid Res Pract [serial online] 2014 [cited 2022 Jun 29];11:78-80. Available from: https://www.thetrp.net/text.asp?2014/11/2/78/129736

Introduction

Graves' disease is a common disorder of thyroid causing thyrotoxicosis. Usual manifestations are increased sweating,restlessness,hypersensitivity to heat, weight loss etc. Cardiovascular manifestation of Graves'disease are tachycardia, atrial fibrillation, precipitation of angina, heart failure and hypertension. Common ECG manifestations aresinus tachycardia and a shortPRinterval. Despite the improvement in atrioventricular conduction, intraatrial and intraventricular conduction disturbances occur occasionally. Most common is the prolongation in intra-atrial conduction manifested by an increase in the duration or notching of the P wave.A delay in intraventricular conduction with a right bundle-branch block morphology is encountered in as many as 15% of patients. ^[1] We report a rare Electrocardiographic manifestation in a patient of Graves'disease in the form of bifascicular block.

Case Report

A 27-year-old male presented with complaints of pain abdomen for4 years,more since 2 weeks,weight loss for 6months, increased stool frequency for 5 months, easy fatigability for 2 months and diminished visionfor 2 months.Pain abdomen was in the upper part of abdomen associated with burning sensation, it was non-radiating, there was no relation to food intake, it was intermittent for past 4 yearsdecreasing with medication. Painwas continuous since past 2weeks with varying intensity. There was no history of vomiting. There was history ofmelena in thepast.Weight loss was present for6 months in the form of loosening of clothes. There wasno history of loss of appetite. Increased stool frequency was present with a normal consistency. Easy fatigability was present for past 2 months because of whichhe wasnot able to do strenuous activity but was able to do activities of daily life. There was historyof diminished vision for far objects and more during the night time. There washistory ofpalpitation on minimal exertion and during night timesit was intermittent.

On examination, pulse was 104/min regular, high volume, collapsing,Blood pressurewas130/64 mm HgandRRrespiratory rate was20/min regular and he was afebrile. On general physical examination,pallor was present, there were bilateral cervical and axillarylymph nodes measuring 0.5 cm × 1.0 cm, 4-5 in no., discrete, firm, non-tender, mobile, skin overthe surface was normal.There was bilateral pitting pedal edema upto half ofthe leg.In the neck,there wasdiffuse thyroid enlargement and bruit was present. In the ocular examination, corneal opacity, corneal ulcer in left eye was present. In cardiovascular examination there was presence of systolic murmur in the pulmonary area and there was presence of Means-Lerman scratch. Rest of the systemic examination was within normal limits.

On investigations there was mild anemia with ahemoglobin of 9.5 g%, SGOT/SGPTaspartate aminotransferase/alanine aminotransferase were 139/113, and ALP was 511KAu,rest of the biochemical and haematological investigations were within normal limits. ECG showedarate 100/min, regular rhythm,prolonged PR interval (0.28s), rSR pattern V1 and I degAVatrioventricular block withRBBBright bundle branch block suggestive ofbifasicular block [Figure 1]. Echocardiography was normal. TFTs showed T3of 25.3ug/dl(Normal-5.2-12.5ug/dl), T4 of 495.2ng/dl(70-204ng/dl) and thyroid-stimulating hormone(TSH) of.01uIU/ml(0.35-5.5uIU/ml). TFT was done by chemiluminescence method. USG Doppler of thyroid showedRt lobe of 50mm × 22 mm andLt lobe of 53 mm × 18 mm. Both lobeswere enlarged in size and heterogenous in echotexture. On color Doppler, thyroid gland showed highly increased inferno type of vascularity.These findings were suggestive of Graves' thyrotoxicosis. Thyroid scan showed both lobes of thyroid enlarged with homogenous andincreased traceruptake in both the lobe,no photopenic area was visualised. These findings were suggestive of diffuse toxic goitre [Figure 2].TPO Thyroid peroxidise antibodies were 5000Iu/ml.So a diagnosis of Grave disease was made and patient was started on propranolol and carbimazole. He didn't have any episode of syncopeor preseycope so he was kept on observation.

Figure 1: Electrocardiography of the patient showing prolonged PR interval with rSR pattern in lead V1 suggestive of Bright bundle branch block indicating bifasciular block

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Figure 2: Thyroid scan of the same patient showing enlarged lobes and homogenous and increased uptake in both the lobes of thyroid

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Discussion

The cardiovascular manifestations of hyperthyroidism have been recognized for more than two centuries and are a cornerstone for clinical diagnosis. The action of thyroid hormone involves virtually all organ systems; in particular, the heart responds to minimal changes in serum thyroid hormone levels as seen in individuals with subclinical hyperthyroidism. This condition, characterized by normal T3 and T4 levels and suppressed TSH, causes measurable alterations in several cardiac parameters. These include an increase in resting heart rate, myocardial contractility, left ventricular muscle mass, and a predisposition to atrial arrhythmias. The wide range of hemodynamic changes and cardiovascular complications that accompany hyperthyroidismserve to emphasize the role of thyroid hormone in the physiology of the cardiovascular system. ^[2] Atrial fibrillation is the most common cardiac complication of hyperthyroidism. It occurs in approximately 15% of patients and is usually associated with a rapid ventricular response. It is more common among men, and its incidence increases significantly with advancing age. ^[3],[4] While it is rare in patients <40 years of age, 25-40% of hyperthyroid individuals over the age of 60 experience atrial fibrillation. The majority of patients with hyperthyroidism and atrial fibrillation have an enlarged left atrium on echocardiography, compared with less than 7% of hyperthyroid patients in sinus rhythm. ^[5] Thyrotoxicosis commonly causes sinus tachycardia. The development of heart block, though rare, is important to recognize.

Second or third degree heart block complicating hyperthyroidism is rare, and has most commonly been reported in association with acute inflammatory disease, hypercalcemia, administration of drugs (for example digoxin), or co-existing heart disease. ^[6] Interstitial inflammation of the AV node, the His-bundle and its branches in a hyperthyroid patient with PR prolongation on ECG has been reported. ^[7] Necropsies in patients with fatal hyperthyroidism have revealed dilated ventricles, myocyte hypertrophy, edema, interstitial and peri-vascular fibrosis, cellular infiltration and myocyte necrosis, ^[8] which could also affect the conducting system within the heart to generate varying and intermittent degrees of heart block. Focal myocarditis affecting the region around the AV node has also been postulated to result in heart block. ^[9]

Hyperthyroidism causing bifasciular block is very rare and very few case reports ^[10] have been published regarding this.Bifasciular block is a very rare manifestation of Graves' disease and whenever no cause is found TFTs should be done in such patients.

References

1.	Montereggi A, Marconi P, Olivotto I, Castelli G, Dolara A, Luisi ML, et al. Signal-averaged P-wave duration and risk of paroxysmal atrial fibrillation in hyperthyroidism. Am J Cardiol 1996;77:266-9.
2.	Fadel BM, Ellahham S, Ringel MD, Lindsay J Jr, Wartofsky L, Burman KD. Hyperthyroid heart disease. ClinCardiol 2000;23:402-8.
3.	Petersen P, Hansen JM. Stroke in thyrotoxicosis with atrial fibrillation. Stroke 1988;19:15-8.
4.	Iwasaki T, Naka M, Hiramatsu K, Yamada T, Niwa A, Aizawa T, et al. Echocardiographic studies on the relationship between atrial fibrillation and atrial enlargement in patients with hyperthyroidism of Graves' disease. Cardiology 1989;76:10-7.
5.	Shimizu T, Koide S, Noh JY, Sugino K, Ito K, Nakazawa H. Hyperthyroidism and the management of atrial fibrillation. Thyroid 2002;12:489-93.
6.	Sataline L, Donaghue G. Hypercalcemia, heart-block, and hyperthyroidism. JAMA 1970;213:1342. [PUBMED]
7.	Ortmann C, Pfeiffer H, Du Chesne A, Brinkmann B. Inflammation of the cardiac conduction system in a case of hyperthyroidism. Int J Legal Med 1999;112:271-4.
8.	Shirani J, Barron MM, Pierre-Louis ML, Roberts WC. Congestive heart failure, dilated cardiac ventricles, and sudden death in hyperthyroidism. Am J Cardiol 1993;72:365-8.
9.	Yusoff K, Khalid BA. Conduction abnormalities in thyrotoxicosis - A report of three cases. Ann Acad Med Singapore 1993;22:609-12.
10.	Kuo YC, Tseng YT, Lee TI, Hsieh MH. Chronic bifascicular block with intermittent complete atrioventricular block induced by hyperthyroidism. Int J Cardiol 2006;110:407-10. [PUBMED]