Abstract

Takotsubo cardiomyopathy is a disorder characterized by acute, transient left ventricular apical ballooning precipitated by emotional or physiologically stressful stimuli (1). We describe a rare case of Takotsubo cardiomyopathy following total thyroidectomy for Graves' disease in order to highlight an unusual complication of thyrotoxicosis and the difficulties associated with perioperative management of thyrotoxicosis.
A 40-year-old woman presented for a total thyroidectomy for known Graves' disease. A diagnosis of Graves' disease had been made following symptoms and biochemical evidence of thyrotoxicosis. The diagnosis was corroborated with a thyroid receptor antibody level of 10 (0–1 IU/L). Antithyroid medication had been commenced; however, difficulty controlling clinical toxicity over a period of 7 months (despite increasing doses of carbimazole and the addition of propranolol) led to the scheduling of thyroid surgery. Obtaining the euthyroid state preoperatively was difficult; the preoperative thyroid function tests were a thyroid stimulating hormone (TSH) of <0.005 (0.4–4 mIU/L), a free thyroxine (T4) of 15.8 (9–22 pmol/L), and a free triiodothyronine of 7.9 (2.6–6 pmol/L).
A total thyroidectomy was performed without complications. Twelve hours postoperatively the patient reported feeling anxious, short of breath, and complained of mild chest pain. Clinically the patient was tachycardic (140 beats/min) with tachypnea (27 breaths/min). An electrocardiogram demonstrated sinus tachycardia with inverted T waves in V1–2. Blood tests showed a baseline high sensitivity troponin-T of 81 (0–14 ng/L), a TSH level of 0.005 (0.4–4 mIU/L), and an elevated free T4 at 33.2 (9–22 pmol/L). Concern regarding an acute coronary syndrome led to an angiogram that demonstrated normal coronary arteries. A ventriculogram however showed moderate diffuse left ventricular apical hypokinesis and ballooning consistent with Takotsubo cardiomyopathy.
The patient was maintained on metoprolol and clinical symptoms were resolved. On follow-up the patient remains well. Histopathology was consistent with treated Graves' disease.
Associations between thyrotoxicosis and cardiac complications are well recognized (2). The development of thyrotoxicosis-induced Takotsubo cardiomyopathy, however, is a rare association (3), and until now it has never been reported in the postoperative thyroidectomy setting.
The clinical syndrome was originally described by Iga et al. within the context of phaeochromocytoma (cited in 1), but Sato et al. were the first group to liken the characteristic left ventriculogram morphology to a Japanese octopus pot, known as a Takotsubo, in 1990 (cited in 1). The typical clinical scenario generally involves emotional or physiological stress leading to elevated cardiac enzymes, normal coronary angiography, and left ventricular apical ballooning on ventriculography (1).
Multivessel epicardial coronary artery spasm, coronary microvascular impairment, catecholamine cardiotoxicity, and neurogenic stunned myocardium are all hypotheses that have been promoted to explain the disorder's pathogenesis (1). Akashi et al. have proposed a pathogenic schema beginning with a response to sudden physiological or emotional stimuli leading to autonomic neuronal activation and a surge in release of catecholamines. Increased systemic vascular resistance leads to elevated end-diastolic pressure and cardiac afterload. High circulating catecholamine levels induce increased mechanical wall stress, stunning of the myocardium, and result in apical ballooning.
Catecholamine cardiotoxicity is of interest within the context of thyrotoxicosis and phaeochromocytoma specifically. Takotsubo cardiomyopathy has previously been recognized in the presence of pheochromocytoma, highlighting the contribution of catecholamines to its pathogenesis. Associated elevations in plasma catecholamines have been shown to induce reversible cardiomyopathy, and furthermore, myocardial histological changes have been shown to be similar between cases of Takotsubo cardiomyopathy and catecholamine toxicity. A higher density of left ventricular apical adrenoreceptors leads to a greater sympathetic response in this region and may explain focal dyskinesia and characteristic ballooning.
Similar theories have been proposed for the clinical setting of thyrotoxicosis; the majority of previous case reports have occurred in patients with Graves' disease (3). While there is no direct evidence, it may be plausible to suggest that antithyroid antibodies also play a role.
The present case could be considered a complication of thyrotoxicosis and therefore warrants review of perioperative measures. Pursuing a euthyroid state with carbimazole was employed and is supported by recent guidelines for perioperative management of Graves' disease (4). Potassium iodide may also be given in the immediate preoperative period but was not deemed necessary in this case. Ongoing clinical and/or biochemical toxicity before surgery should lead to the addition of a beta-blocker. Where surgery cannot be avoided, anesthetic and surgical experience is required given the possibility of toxicosis-related sequelae.
In conclusion, Takotsubo cardiomyopathy is a disorder of great potential significance, particularly within the realm of thyrotoxicosis. All clinicians caring for patients with hyperthyroidism should be alert to the possibility of cardiac complications and specifically, Takotsubo cardiomyopathy.
Footnotes
Disclosure Statement
The authors have nothing to disclose.
