Case Reports in Endocrinology

Volume 2012 (2012), Article ID 318398, 3 pages

doi:10.1155/2012/318398

Case Report

Complete Heart Block in Thyrotoxicosis, Is It a Manifestation of Thyroid Storm? A Case Report and Review of the Literature

Rashed Al Bannay,¹ Aysha Husain,¹ and Saeed Khalaf²

¹Cardiology Unit, Internal Medicine Department, Salmaniya Medical Complex, Manama, Bahrain

²Endocrinology Unit, Internal Medicine Department, Salmaniya Medical Complex, Manama, Bahrain

Received 4 April 2012; Accepted 4 July 2012

Academic Editors: I. Broom, T. Cheetham, and N. Sakane

Copyright © 2012 Rashed Al Bannay et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

Thyrotoxicosis complicated by advance degree atrioventricular block, a rare complication of a common disease. The term apathetic thyrotoxicosis, where palpitations and cardiac involvement are the sole manifestations of disease, is well known. Thyroxin's ability to sensitize the catecholamine receptors causing tachyarrhythmias is well addressed. However, as an aetiology for advanced heart block, thyrotoxicosis is ranked as one of the rarest.

1. Case Presentation

Mrs. T.R.M. is a 37-yr-old Egyptian woman who presented with a history of shortness of breath, palpitations, and recurrent syncope that had lasted three days.

The patient has been thyrotoxic for the last 10 years with erratic follow-up appointments and poor adherence to her treatment program.

At presentation, she had progressive shortness of breath that had been occurring for the past 3 days and was associated with palpitations that she perceived as slow and heavy.

She reported recurrent, unprovoked syncopal attacks that coincided with her palpitations. She had no history of chest pain or ankle oedema.

In a review of systems, she reported diarrhoea associated with colicky abdominal pain and fever.

The patient is a housewife who has had six pregnancies, the most recent of which was in 2008. The mode of delivery was a lower segment Cesarean section due to a twin pregnancy that had been complicated by placenta previa and antepartum hemorrhage.

The remainder of her obstetric history was significant, including two abortions and two intrauterine deaths. Her first pregnancy was uneventful.

She justified her noncompliance with antithyroid medications by relating these drugs to her complicated obstetric history.

On examination, she was apprehensive, restless, mildly icteric, and had a low-grade fever.

Her blood pressure was 140/80 mmHg, and she had a heart rate of 54 beats/min.

Her extremities were moist, and she was sweating excessively.

She had a diffuse goitre with bruit. Thyrotoxicosis-related eye signs, such as lid retraction and lid lag, were evident.

Cannon A waves were visible in her jugular venous pressure (JVP).

Auscultation of the precordium demonstrated audible heart sounds with variable S1 intensity.

Her lungs were clear, and she was not experiencing congestive heart failure.

The abdominal examination was unremarkable except for diffuse, mild tenderness, and active bowel sounds.

The basic metabolic workup is shown in the Table 1.

Table 1: Results of blood investigations done during patient’s admission.

Laboratory investigation
Value
Reference range

White cell count
9.9 × 10⁹
3.6–9.6 × 10⁹/L

Hemoglobin
11.4 g/dL
12–14.5 g/dL

Platelets
431 × 10⁹
140–440 × 10⁹/L

Random blood sugar
7.1 mmol/L
3.6–8.9 mmol/L

Urea
3.6 mmol/L
3–7 umol/L

Creatinine
57 umol/L
53–118 umol/L

Calcium
2.44 mmol/L
2.13–2.63 mmol/L

Magnesium
0.79 mmol/L
0.74–1 mmol/L

Phosphorous
1.0 mmol/L
0.8–1.4 mmol/L

Sodium
135 mmol/L
140–148 mmol/L

Chloride
101 mmol/L
100–107 mmol/L

Potassium
4.8 mmol/L
3.6–5.2 mmol/L

Bicarbonate
23 mmol/L
21–30 mmol/L

Creatinine kinase
21 mmol/L
<67 u/L

Albumin
32 g/L
38–50 g/L

Globulin
50 g/L
15–30 g/L

Total bilirubin
56 umol/L
<18 umol/L

Alkaline phosphatase
102 u/L
50–135 u/L

Alanine aminotransferase
57 u/L
30–65 u/L

g-glutamyltransferase
32 u/L
5–85 u/L

ESR
60
0–20 mm/hr

Thyroid stimulation hormone
0.0 uIU/mL
0.25–5 uu/mL

Free T3
23.0 pmol/L
2.5–7.8 pmol/L

Free T4
94.6 pmol/L
6–24.5 pmol/L

Thyroglobulin
16.3 ug/L
3–42 ug/L

The septic workup and autoimmune profile were normal.

Her electrocardiogram showed complete heart block with narrow QRS complexes (Figure 1).

Figure 1: Electrocardiogram showing advance degree atrioventricular block at time of admission.

The echocardiogram showed preserved left ventricular systolic function with no valvular lesions.

She was admitted to the cardiac care unit for closer monitoring. She consented to transvenous temporary pacing in the event that it was required.

Antithyroid medications, in the form of propylthiouracil (PTU) with parenteral steroid therapy, were initiated.

The patient remained hemodynamically stable, and by the third day of antithyroid medication, her heart rhythm transited into second degree AV block (Figure 2); by the fifth day of medication, she was in first-degree atrioventricular block AV block (Figure 3).

Figure 2: Electrocardiogram showing second-degree heart block performed on third day of anithyroid medication.

Figure 3: Electrocardiogram showing first-degree heart block performed on fifth day of antithyroid medication.

She was discharged seven days after admission. Her antithyroid medications were upgraded, and the steroids were tapered.

At the follow-up appointment, her holter monitor showed normal sinus rhythms with physiological heart rate variability, and she was in an euthyroid state (Figure 4).

Figure 4: Holter rhythm strip showing normal sinus rhythm.

Due to her nonadherence to medications, she was offered iodine ablation of her thyroid, which she adamantly resisted.

The patient continued to figure prescribed medications and remained euthyroid for two months.

2. Discussion

Thyrotoxicosis is known to cause tachyarrhythmia, the leading example of which is atrial fibrillation [1]. A hyperthyroid status complicated by high-grade atrioventricular block (AV) has been well documented in the literature [2–10]. Its rarity renders it more difficult to recognize in daily practice. Because the treatment of hyperthyroidism includes a betablocking agent, recognizing high-grade atrioventricular block is critical before subjecting patients with concomitant bradyarrhythmia to the hazardous effects of betablockers. Syncopal attacks are an indication of such a diagnosis in the context of thyrotoxicosis [2, 3, 5, 10].

The collective evidence from the sporadic reported cases suggests that any part of the cardiac conduction system is vulnerable to the effects of high thyroxin [11–13].

The effects of high thyroxin can manifest as sick sinus syndrome, sinoatrial block, or various degrees of AV block [11–13].

The data in the literature that address the pathogenesis of high-grade AV block in the context of hyperthyroidism are primarily speculative. The positive chronotropic effect of thyroxin is well known; however, its negative dromotropic action is not widely recognized. The presence of interstitial inflammation in the AV node, the His-bundle and its branches, which are associated with the typical ECG changes in hyperthyroidism, is well recognized [9].

Focal inflammation of the myocardium is reported in patients subjected to high levels of thyroxin [14].

In our patient, the collective thyrotoxic signs and symptoms indicated the possibility of an impending thyroid storm. Ho et al. have previously reported the coexistence of thyroid storm with high-grade AV block [7]. In other words, a high-grade AV block can be a manifestation of severe thyrotoxicosis. Despite the sporadic existence of similar cases in the literature, at least 5 of the reviewed cases were either frank or impending thyroid storms [3, 6–9].

It may be worth considering high-grade AV block, which is a life-threatening emergency, to be one of the cardiovascular markers of a thyroid storm [15].

However, it has to be emphasized that in such a scenario, the treatment is identical to a severe thyrotoxic crisis, with the exception of avoiding beta-blocking agents. The mainstays of treatment are antithyroid medication with steroid therapy and monitoring the cardiac rhythm by telemetry. Temporary pacing is rarely indicated unless there is hemodynamic instability, and cardiac electrophysiology has no role in acute management [3, 6].

For cases in which the hyperthyroidism is intractable or the patient is poor complaint, thyroid iodine ablation or subtotal thyroidectomy are long-term alternatives [16].

Conflict of Interests

The authors state no conflict of interests, and they didnot receive any funding for this paper.

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