Scientific letter
Iatrogenic hyperthyroidism can be a triggering factor for takotsubo cardiomyopathy
Hipertiroidismo iatrogénico como factor desencadenante de miocardiopatía de estrés
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We describe a case of SCM in the setting of iatrogenic hyperthyroidism.</p><p id="par0010" class="elsevierStylePara elsevierViewall">A 60-year-old male with a previous history of chronic obstructive pulmonary disease, full remission laryngeal carcinoma treated with surgery and radiotherapy and primary hypothyroidism diagnosed 10 years ago under treatment with levothyroxine 100 micrograms per day, presented to the emergency service due to progressive increase of his baseline dyspnea and increased anxiety of 10 day-evolution, without symptoms of respiratory tract infection or chest pain. The initial physical examination highlighted sinus tachycardia and generalized pulmonary hypoventilation. Chest X-ray showed signs of mild fluid overload and vascular redistribution. At the emergency room he presented a sudden episode of tachypnea, respiratory worsening and desaturation up to 87% by pulse oximetry. An electrocardiogram demonstrated flattened T waves in V2 and V3 and shallow inverted symmetric T waves in precordial leads from V4 to V6 and in lower face. A transthoracic echocardiogram showed akinesia of the apex and medio-distal segments of all faces with hyperkinesia of basal segments and severely depressed left ventricular ejection fraction (LVEF), 30% visually estimated. Blood analyses revealed leukocytosis with neutrophilia, Nt-proBNP was 12788 ng/L and Troponin-I 429 ng/L with preserved renal function. Urgent coronary angiography was performed with no significant lesions in the coronary arteries. Treatment with furosemide, spironolactone and captopril was initiated. A control echocardiogram was repeated 24<span class="elsevierStyleHsp" style=""></span>hours after the onset of the symptoms in which normalization of LVEF and previous contractility alterations was observed. Troponin I levels dropped to 60 ng/L in the following 24<span class="elsevierStyleHsp" style=""></span>hours. The definitive diagnosis of stress cardiomyopathy (takotsubo syndrome) was established. During hospital admission ionogram, vitamins, hepatic, renal and ferric profile were within normal range. Thyroid hormone analyses showed an elevated T4 with supressed TSH (TSH 0.18 mIU/L; free T4 2.3 ng/dL). The administration of thyroid hormone was interrupted with close follow-up until normalization of the thyroid profile. Two months later, the patient evolution was favorable, with no new episodes of cardiomiopathy.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The Mayo Clinic diagnostic criteria for SCM include: transient akinesia, hypokinesia or dyskinesia of the left ventricle middle segments which may correspond to the territory of more than one epicardial artery; absence of obstructive lesions on angiography; new electrocardiographic alterations and/or troponin elevation. It is also necessary to rule out the existence of myocarditis and pheochromocytoma<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a>.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Although emotional stress was traditionally postulated as the most frequent triggering factor, recent reviews suggest that certain physical factors are more frequently identified as the causal agent of the SCM. In many cases a clear provoking factor is not identified<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a>. In this context, some case series have related alterations of thyroid function, especially hyperthyroidism states, with the development of stress myocardiopathy<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3,4</span></a>.</p><p id="par0025" class="elsevierStylePara elsevierViewall">In recent years there has been an increase in the incidence of SCM probably related to an improvement in the awareness and diagnosis of the disease<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a>. Although, several mechanisms have been proposed, the exact etiopathological mechanism of SCM remains unknown. The most accepted theory is based on the direct effect of catecholamines on the cardiac muscle. Catecholamines excess induces a direct toxic effect on the myocyte (mediated by B intracellular calcium overload) resulting in the band necrosis histologycal pattern most frequently observed in SCM biopsies. Thyroid hormones stimulate peripheral vascular resistance, increase cardiac chronotropism and inotropism and increase the expression of adrenergic receptors in many tissues, including the heart, predisposing to a greater susceptibility of myocardial tissue to the action of catecholamines. Both, the up-regulation of receptor-expression and a direct effect of thyroid hormones at an intracellular level, have been proposed in the pathogenesis of SCM<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a>.</p><p id="par0030" class="elsevierStylePara elsevierViewall">There is no specific treatment for SCM other than supportive measures and avoidance of triggering factors. In a recent review, the use of inhibitors of the renin-angiotensin system was associated with an increase in the overall survival. The use of beta-blockers showed no benefit in the survival or in the reduction of recurrences<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a>.</p><p id="par0035" class="elsevierStylePara elsevierViewall">In conclusion, different mechanisms of thyroid hormone may lead to the development of SCM. The systematic evaluation of thyroid profile and hyperadrenergic states, such as catecholamine-producing tumors, is important in these patients.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflict of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">Authors declare no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflict of interest" ] 1 => array:1 [ "titulo" => "Bibliografía" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "Bibliografía" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "A. 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Jaguszewski" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1056/NEJMoa1406761" "Revista" => array:6 [ "tituloSerie" => "N Engl J Med" "fecha" => "2015" "volumen" => "373" "paginaInicial" => "929" "paginaFinal" => "938" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/26332547" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0040" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Takotsubo cardiomyopathy associated with thyrotoxicosis: a case report and review of the literature" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "M. Eliades" 1 => "D. El-Maouche" 2 => "C. Choudhary" 3 => "B. Zinsmeister" 4 => "K.D. 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