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Thyrotoxic Dilated Cardiomyopathy: Personal Experience and Case Collection from the Literature

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Thyrotoxic Dilated Cardiomyopathy: Personal Experience and Case Collection from the Literature ID: 20-0068 -20-0068 G Molinaro and others Thyrotoxic dilated ID: 20-0068; December 2020 cardiomyopathy DOI: 10.1530/EDM-20-0068 Thyrotoxic dilated cardiomyopathy: personal experience and case collection from the literature Giuseppina Molinaro1, Renato De Vecchis2, Elio Badolati3 and Raffaele Giannattasio3 Correspondence should be addressed 1UOC Internal Medicine, The Pellegrini Hospital, Naples, Italy; 2Medical and Polyspecialist Centre, Department of to R De Vecchis Cardiology, DSB 29 “S.Gennaro dei Poveri Hospital”, Naples, Italy; 3Medical and Polyspecialist Centre, Department of Email Endocrinology and Metabolic Disorders, DSB 29 “S.Gennaro dei Poveri Hospital”, Naples,Italy [email protected] Summary The authors examine several reports of the literature concerning thyrotoxic dilated cardiomyopathy. In particular, it is pointed out that this clinical manifestation of hyperthyroidism is rare in readily diagnosed and properly treated hyperthyroidism. Case reports are analyzed comparatively. A case deriving from the direct experience of the authors is also presented. Learning points: • Dilated cardiomyopathy has been reported as the initial presentation of hyperthyroidism in only 6% of patients although <1% developed severe LV dysfunction. • Clinical picture of thyrotoxic dilated cardiomyopathy can degenerate into an overt cardiogenic shock sometimes requiring the use of devices for mechanical assistance to the circulation, or extracorporeal membrane oxygenation. • For thyrotoxic dilated cardiomyopathy, evidence-based pharmacologic measures valid for heart failure should alwaysbesupplementedbytheadministrationofspecificthyroidtherapiessuchasthionamides(methimazole, carbimazole or propylthiouracil), whose relatively long latency of action should be supported by the i.v. administration of small doses of beta-blocker. • In cases of cardiogenic shock, the administration of beta-blocker should be carried out only after the restoration of satisfactory blood pressure levels- with the prudent use of synthetic catecholamines, if necessary. The present article illustrates a collection of cases from Case presentation the literature plus one case deriving from the Authors’ direct experience, all of them having thyrotoxic The report by Abbasi et al. (7) is centered around the case of a cardiomyopathy as their subject. It describes a collection 34-year-old Hispanic male, diagnosed with Graves’ disease of cases characterized by unusual presentation of three years before, who presented to the emergency room the hyperthyroidism with the clinical picture of with complaints of generalized weakness, palpitations, thyrotoxic cardiomyopathy (1, 2, 3, 4, 5, 6), albeit a fair chest pain and multiple episodes of nausea and vomiting. polymorphism emerges from the case comparison due On presentation, the patient was tachycardiac and had a to comorbid conditions, able to mislead the diagnostic precordial systolic flow murmur, while the ECG showed work-up. atrial flutter. In addition, cardiac troponin was 0.04 ng/mL This work is licensed under a Creative Commons © 2020 The authors https://edm.bioscientifica.com/ Attribution-NonCommercial-NoDerivatives 4.0 PublishedbyBioscientificaLtd International License. Downloaded from Bioscientifica.com at 09/27/2021 03:00:13PM via free access G Molinaro and others Thyrotoxic dilated ID: 20-0068; December 2020 cardiomyopathy DOI: 10.1530/EDM-20-0068 and echocardiogram revealed severely depressed left administered for 2 days. On the 6th day of treatment, ventricular function with an ejection fraction of 26–30%. hydrocortisone and Lugol’s solution were stopped, and Of note, the prospect of thyroid function was markedly methimazole was reduced by half. The patient was altered due to the steep rise of triiodotyronine with discharged with almost complete recovery. This report subnormal TSH: thyroid-stimulating hormone (TSH) is suggestive of a patient’s failure to adhere to the 0.02 µIU/mL, Free Triiodothyronine (T3) 25.14 pg/mL previously prescribed insulin therapy, in conjunction and free thyroxine (T4) 5.23 ng/dL. In addition, physical with the triggering of a thyrotoxic crisis due to previously examination showed upper and lower extremity weakness undiagnosed nodular goiter. In fact, the clinical picture graded with a three out of five on the strength scale. The is dramatically improved by the administration of therapy included propranolol, along with propylthiouracil methimazole, that is, a drug not previously prescribed and hydrocortisone to prevent thyroid storm. Since blood to patient because he had never received the correct work showed a potassium of 1.8 millimoles per liter diagnosis of ‘toxic nodular goiter’. (mmol/L), a central line was placed for rapid potassium In the report by Alam et al. (9) the case of a 65-year- repletion. Management was continued with methimazole old woman referred urgently from primary care with plus propranolol. Physical exam showed an increase worsening breathlessness, tachyarrhythmia as per atrial in the upper and lower extremity muscle strength to fibrillation and newly diagnosed left bundle branch five out of five. The patient discharged on day nine block (LBBB) is described. She had a background of with methimazole, propranolol and lisinopril, with an type 2 diabetes, asthma and hypertension. Initial ECG outpatient follow-up appointment. This report is very revealed atrial fibrillation with fast ventricular rate on the remarkable because it encompasses two life-threatening background of LBBB. ECHO findings were consistent with complications of Flajani–Graves–Basedow disease: the a state of systolic impairment. Initial testing including truly rare thyrotoxic periodic paralysis and the thyrotoxic checking thyroid function test revealed hyperthyroidism. dilated cardiomyopathy. It became evident that this patient had thyrotoxic dilated In the description made by Meregildo Rodriguez cardiomyopathy. Chest X-ray: cardiomegaly, left-sided et al. (8) a case of simultaneous presentation of pleural effusion, prominent pulmonary hila, X-ray image decompensated thyrotoxicosis, diabetic ketoacidosis suggestive of early pulmonary edema. Echocardiogram: (DKA) and frank thyrotoxic dilated cardiomyopathy is showed severely dilated left atrium with severe impairment reported. A patient presented to emergency department to overall left ventricle systolic function (ejection fraction with drowsiness, alteration of breathing (tachypnea and 24% using biplane Simpson method). Moderate tricuspid Kussmaul’s breathing) and severe hypotension. He had a regurgitation and mild mitral regurgitation. The thyroid history of malaise, headache, fever, and generalized body function test revealed: thyroid-stimulating hormone pain during the last 6 days. Laboratory findings were (TSH): <0.01 (0.35–3.50 mU/L), thyroxine (free T4): 28.5 serum glucose: 460 mg/dL, urea: 115 mg/dL, creatinine: (7.5–21.1 pmol/L), triiodothyronine (free T3): 8 (3.8– 1.3 mg/dL, hemoglobin: 12.9 g/dL, hematocrit: 40%, 6.0 pmol/L). Thus, thyrotoxic dilated cardiomyopathy platelets: 198,000/mm3, white blood cells: 10,100/ was diagnosed. The patient was started on antithyroid mm3, pH: 6.99, TSH: 0.024 μIU/L, free-T4: 2.16 ng/ medications (carbimazole 20 mg once daily), beta-blocker dL (reference range (RR): 0.82–1.63 ng/dL), total-T3: (bisoprolol 2.5 mg once daily), ramipril 2.5 mg once daily 0.18 ng/mL (RR: 0.5–2.0 ng/mL), free-T3: 0.42 pg/mL (RR: and i.v. furosemide 80 mg twice daily. As the patient 2.1–3.8 pg/mL) Echocardiography showing borderline developed bronchospasm, bisoprolol was later switched to pulmonary artery systolic pressure (35 mmHg), severe ivabradine 2.5 mg twice daily which was slowly uptitrated LV systolic dysfunction (LV ejection fraction 35%), with to 7.5 mg × twice daily. The dose of i.v. furosemide was left ventricular global hypokinesia and mitral inflow decreased and switched to bumetanide 1 mg once daily. pattern of restrictive type. Based on these results, normal In the further course of hospitalization, the patient’s saline, insulin infusion plus potassium chloride, sodium condition improved over the next 3–4 days, with complete bicarbonate, norepinephrine, hydrocortisone 100 mg resolution of fluid overload, and heart rate slowed down every 8 h, methimazole 20 mg every 8 h, and Lugol’s to 70 b.p.m. solution 10 drops every 8 h, were prescribed. Based on She turned back to sinus rhythm, maintaining her physical examination, chest X-ray (CXR), and progressive heart around 50–60 b.p.m. decrease in partial oxygen pressure compatible with Her repeat echocardiogram showed moderate to acute lung edema, i.v. furosemide 20 mg every 12 h was severe left ventricular (LV) impairment with a decrease in https://edm.bioscientifica.com/ 2 Downloaded from Bioscientifica.com at 09/27/2021 03:00:13PM via free access G Molinaro and others Thyrotoxic dilated ID: 20-0068; December 2020 cardiomyopathy DOI: 10.1530/EDM-20-0068 tricuspid and mitral regurgitation. Her ejection fraction was improved to 37% (biplane Simpson method). In the report by Allencherril et al. (10) there is a description of the dramatic picture that occurs in the presence of thyrotoxic heart failure with severe hypotension. The patient described was already known as an individual affected by Graves’ disease, however, he had omitted to take the previously prescribed methimazole for the last 45 days. The clinical scenario was initially characterized by dyspnoea and palpitations with an electrocardiographic picture of atrial flutter 2:1 with a ventricular
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