Thyrotoxic Cardiomyopathy Research Articles

Takotsubo Cardiomyopathy Precipitated by Thyrotoxicosis

ThyroidVol. 20, No. 12 Letters to the EditorTakotsubo Cardiomyopathy Precipitated by ThyrotoxicosisFazil Alidjan, Mustafa Ezzhati, Wim Bruggeling, and Coen van GuldenerFazil AlidjanDepartment of Internal Medicine, Amphia Hospital, Breda, The Netherlands.Search for more papers by this author, Mustafa EzzhatiDepartment of Internal Medicine, Amphia Hospital, Breda, The Netherlands.Search for more papers by this author, Wim BruggelingDepartment of Cardiology, Amphia Hospital, Breda, The Netherlands.Search for more papers by this author, and Coen van GuldenerDepartment of Internal Medicine, Amphia Hospital, Breda, The Netherlands.Search for more papers by this authorPublished Online:29 Nov 2010https://doi.org/10.1089/thy.2009.0444AboutSectionsView articleView Full TextSupplemental MaterialPDF/EPUBView Supplemental Data ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"Takotsubo Cardiomyopathy Precipitated by Thyrotoxicosis." , 20(12), pp. 1427–1428FiguresReferencesRelatedDetailsCited ByThe association between Takotsubo cardiomyopathy and thyrotoxicosis: A systematic review26 August 2022 | Endocrine, Vol. 21Association of Endocrine Conditions With Takotsubo Cardiomyopathy: A Comprehensive ReviewJournal of the American Heart Association, Vol. 7, No. 19Congestive Heart Failure Secondary to a TSH-Secreting Pituitary Adenoma Aggravated by Takotsubo Cardiomyopathy in an Elderly PatientAACE Clinical Case Reports, Vol. 4, No. 2Recurrent Takotsubo Cardiomyopathy Related to Recurrent Thyrotoxicosis1 April 2016 | Texas Heart Institute Journal, Vol. 43, No. 2Takotsubo cardiomyopathy and transient thyrotoxicosis during combination therapy with interferon-alpha and ribavirin for chronic hepatitis C3 February 2014 | BMC Endocrine Disorders, Vol. 14, No. 1Takotsubo cardiomyopathy and endocrine disorders: a mini-review of case reportsThe American Journal of Emergency Medicine, Vol. 32, No. 11Takotsubo Cardiomyopathy Associated with Thyrotoxicosis: A Case Report and Review of the Literature11 February 2014 | Thyroid, Vol. 24, No. 2Pathophysiology of Takotsubo SyndromeCirculation Journal, Vol. 78, No. 7Broken heart syndrome triggered by an obstructive goiter not associated with thyrotoxicosis11 July 2013 | Canadian Journal of Anesthesia/Journal canadien d'anesthésie, Vol. 60, No. 8Takotsubo Cardiomyopathy Complicating Thyroidectomy for Graves' Disease27 August 2012 | Thyroid, Vol. 22, No. 9Thyroid Storm and Reversible Thyrotoxic Cardiomyopathy After Ingestion of Seafood Stew Thought to Contain Marine Neurotoxin10 June 2011 | Thyroid, Vol. 21, No. 6 Volume 20Issue 12Dec 2010 InformationCopyright 2010, Mary Ann Liebert, Inc.To cite this article:Fazil Alidjan, Mustafa Ezzhati, Wim Bruggeling, and Coen van Guldener.Takotsubo Cardiomyopathy Precipitated by Thyrotoxicosis.Thyroid.Dec 2010.1427-1428.http://doi.org/10.1089/thy.2009.0444Published in Volume: 20 Issue 12: November 29, 2010Online Ahead of Print:November 7, 2010PDF download

Chylous Ascites as a Manifestation of Thyrotoxic Cardiomyopathy in a Patient with Untreated Graves' Disease

Thyrotoxicosis is an uncommon cause of heart failure, and patients with heart failure rarely present with chylous ascites. In this report, we describe a patient with uncontrolled Graves' disease with thyrotoxicosis, heart failure, and chylous ascites. A 39-year-old woman with no previous cardiac disease presented with dyspnea, orthopnea, palpitations, exophthalmos, goiter, distended abdomen, and pedal edema. The thyroid function tests demonstrated hyperthyroid Graves' disease (serum-free triiodothyronine level, 7.12 pg/mL [reference range, 2.0-4.0]; free thyroxine level, 4.33 ng/dL [reference range, 0.54-1.40]; thyroid-stimulating hormone level, <0.015 microU/mL [reference range, 0.34-5.60]; and thyrotropin receptor antibodies, 84.5% [reference value, <15%]). The chest radiograph showed moderate cardiomegaly and bilateral pleural effusions, electrocardiogram revealed atrial fibrillation, and the abdominal sonography found ascites. Chylous ascites was diagnosed by paracentesis and analysis of the ascitic fluid (triglyceride level, 347 mg/dL). Laboratory and imaging studies demonstrated no apparent hepatic dysfunction, abnormal tumor, lymphadenopathy, or lymphatic drainage deficit. With aggressive treatment of the heart failure and hyperthyroid state, her dyspnea, pleural effusion, chylous ascites, and edema resolved completely within a few days. Chylous ascites may develop as a result of heart failure secondary to thyrotoxic cardiomyopathy and resolve promptly if treated appropriately.

Type 2 deiodinase Thr92Ala polymorphism impact on clinical course and myocardial remodeling in patients with Graves' disease

Patients with thyreotoxicosis have variable clinical manifestations and various degree of cardiomyopathy which severity depends on many factors. Last years the genetic factors predicting development and clinical features of thyrotoxic symptoms and thyreotoxic cardiomyopathy became more evident. It is known, that production of T3 in various tissues including cardiac muscle is limited by deiodinase 2 (D2). Resent studies showed that certain polymorphisms, including Thr92Ala of D2 gene, are implicated in the development of thyrotoxic symptoms and thyreotoxic cardiomyopathy. Individuals with Ala92Ala genotype have lower D2 activity in tissues compared to other genotypes. In our study we focused on codon 92 polymorphism of D2 gene in relation to clinical manifestations of thyreotoxic cardiomyopathy and Echo-cardiography parameters in patients with Graves’disease.

Thyrotoxic cardiomyopathy and encephalopathy in a paraplegic man

Case report. Thyrotoxicosis complicating spinal cord injury is more common than generally appreciated. To raise the level of awareness, the following case of fatal thyrotoxicosis is presented. A 77-year-old man, paralyzed at the T12 level for 46 years, developed a sudden 42 lb weight loss, dyspnea, interscapular pain, 120/40 mm Hg blood pressure, a nodular thyroid gland, atrial fibrillation, progressive cardiac enlargement, left ventricular ejection fraction diminishing from 30 to 10% and a persistently low level of thyrotropic hormone, 0.05-0.2 microU ml(-1) (normal 0.35-5.5 microU ml(-1)). As coronary artery bypass grafting had been carried out 6 years earlier and other signs of thyrotoxicosis-exophthalmos, lid lag, sweating, tremor and diarrhea-were absent, recurrent arteriosclerotic heart disease was assumed and a trial of thyroid suppression not attempted. He eventually developed depression and memory loss and died in heart failure after a 4-year course of this illness. This case probably represented a toxic multinodular goiter in an elderly paraplegic man with potentially treatable cardiovascular and nervous system complications.

Thyrotoxic heart disease

Patients with tachyarrythmias as a result of thyroid storm have been typically treated with beta-blockers to decrease the heart rate and alleviate beta-receptor mediated symptoms such as anxiety and tremulousness. We report an unusual case of a previously well young man presenting to the emergency department with atrial flutter and who was clinically hyperthyroid. The patient was treated with propanolol to control his heart rate but suffered cardiovascular collapse. Although the patient was successfully resuscitated, he required inotropic support and intra-aortic balloon pump. The use of propanolol should be carefully considered in patients with thyrotoxic cardiomyopathy especially in those with heart failure because of the risk of exacerbation.

Cardiomyopathy and thyrotoxicosis: tachycardiomyopathy or thyrotoxic cardiomyopathy?

Ischaemic heart disease is the most common cause of heart failure, but less common causes such as hyperthyroidism should be kept in mind.As a potential reversible cause of cardiomyopathy hyperthyroidism should be excluded in every new patient, young and old, especially in the absence of coronary artery disease. Inspired by an intriguing clinical case we address the question whether hyperthyroidism-related cardiomyopathy is due to tachycardiomyopathy or to thyrotoxic cardiomyopathy.

Thyrotoxic Heart Disease

The close link between the thyroid gland and the heart has been well recognized since the first description of thyrotoxicosis in nearly 200 years ago. Despite this well known association, there have been only a few population based studies performed on thyrotoxic heart disease except thyrotoxic atrial fibrillation. Even so, there has not been any consensus for the definition for "thyrotoxic heart disease". For other cardiac manifestations of thyrotoxicosis including thyrotoxic cardiomyopathy and thyrotoxic pulmonary hypertension, only occasion case reports can be found in the current medical literatures. Their natural history, clinical course and outcomes are largely unknown. On the other hands, there is an enlarging body of evidence suggesting a direct pathogenic role of thyrotoxicosis per se as the sole cause of these thyrotoxic heart diseases. In this review, we briefly discuss the three cardiac consequences of thyrotoxicosis, namely atrial fibrillation, congestive cardiac failure and pulmonary hypertension.

P082 - Cardiothyréoses : fréquence, étiologies, aspects nosologiques et prise en charge thérapeutique. à propos de 38 cas

Patients with tachyarrythmias as a result of thyroid storm have been typically treated with beta-blockers to decrease the heart rate and alleviate beta-receptor mediated symptoms such as anxiety and tremulousness. We report an unusual case of a previously well young man presenting to the emergency department with atrial flutter and who was clinically hyperthyroid. The patient was treated with propanolol to control his heart rate but suffered cardiovascular collapse. Although the patient was successfully resuscitated, he required inotropic support and intra-aortic balloon pump. The use of propanolol should be carefully considered in patients with thyrotoxic cardiomyopathy especially in those with heart failure because of the risk of exacerbation.

Left ventricle filling abnormalities prior to and following treatment of thyrotoxicosis -- is diastolic dysfunction implicated in thyrotoxic cardiomyopathy?

Despite cardiac failure being a well recognised complication of thyrotoxicosis, systolic function has generally been reported as maintained or enhanced. In this study, left ventricular diastolic function was assessed in 16 thyrotoxic patients and 18 age-matched controls by pulsed-Doppler echocardiography. Patients were re-studied after 3 and 12 months of treatment. Prior to treatment all standard Doppler-derived indices of diastolic function were significantly different to control (isovolumic relaxation time (IVRT) 63 +/- 18.9 vs 84.0 +/- 14.8 ms, peak early filling velocity (Emax) 79.2 +/- 15.2 vs 61.9 +/- 10.7 cm.s-1, peak atrial filling velocity (Amax) 68.2 +/- 17.9 vs 42.2 +/- 9.4 cm.s-1, deceleration of early filling (E/F slope) 6.1 +/- 1.8 vs 3.7 +/- 1.1 m.s-1, thyrotoxic vs control). However, these filling abnormalities appear likely to reflect the tachycardia and reduced systemic vascular resistance (SVR) found in the patients (heart rate 102 +/- 15 vs 76 +/- 9, SVR 874 +/- 207 vs 1293 +/- 362 dynes.s-1 x cm-5, both P < 0.001). After 3 months of treatment haemodynamics were similar in the two groups but filling remained abnormal in patients with a pattern suggesting increased transmitral pressure gradients (Emax 73.1 +/- 15.1 cm.s-1, Amax 55.8 +/- 19.2 cm.s-1, E/F slope 4.9 +/- 2.0 m.s-1, all P < 0.05 compared to controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Oxidative muscular injury and its relevance to hyperthyroidism

In experimental hyperthyroidism, acceleration of lipid peroxidation occurs in heart and slow-oxidative muscles, suggesting the contribution of reactive oxygen species to the muscular injury caused by thyroid hormones. This article reviews various models of oxidative muscular injury and considers the relevance of the accompanying metabolic derangements to thyrotoxic myopathy and cardiomyopathy, which are the major complications of hyperthyroidism. The muscular injury models in which reactive oxygen species are supposed to play a role are ischemia/reperfusion syndrome, exercise-induced myopathy, heart and skeletal muscle diseases related to the nutritional deficiency of selenium and vitamin E and related disorders, and genetic muscular dystrophies. These models provide evidence that mitochondrial function and the glutathione-dependent antioxidant system are important for the maintenance of the structural and functional integrity of muscular tissues. Thyroid hormones have a profound effect on mitochondrial oxidative activity, synthesis and degradation of proteins and vitamin E, the sensitivity of the tissues to catecholamine, the differentiation of muscle fibers, and the levels of antioxidant enzymes. The large volume of circumstantial evidence presented here indicates that hyperthyroid muscular tissues undergo several biochemical changes that predispose them to free radical-mediated injury.

Is there a thyrotoxic cardiomyopathy in children?

We measured left ventricular ejection fraction by radionuclide angiocardiography at rest and during graded exercise in eight thyrotoxic children. Five patients were reassessed after return to a clinically euthyroid state. In the thyrotoxic state the left ventricular ejection fraction was 69% +/- 8% at rest, and increased normally by 7% to 10% during exercise in four patients but did not change significantly or decreased by as much as 8% in the other four patients. The change in left ventricular ejection fraction during exercise correlated inversely with serum concentrations of thyroxine (r = -0.82, P less than 0.02) and triiodothyronine (r = -0.88, P less than 0.01). A comparison between patients who had normal left ventricular response to exercise with those who had abnormal response while thyrotoxic failed to uncover any significant differences between their resting ejection fractions or resting and exercise heart rates and systolic blood pressures. Three abnormal and two normal responders were reassessed after return to a clinically euthyroid state. The left ventricular ejection was 64% +/- 6% at rest, and increased during exercise in all patients. Our study suggests that thyrotoxicosis causes diminished left ventricular reserve (compensated functional cardiomyopathy) in some patients, but appears to be reversible. Severity of thyrotoxicosis, as measured by thyroid hormone blood levels, may be a determining factor in the development of functional cardiomyopathy.

Thyrotoxic Cardiomyopathy Complicated by Systemic and Pulmonary Embolism

Thyrotoxic Cardiomyopathy Complicated by Systemic and Pulmonary Embolism