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CASE REPORT
Year : 2023 | Volume
: 24
| Issue : 3 | Page : 153-156
Dilated cardiomyopathy in hyperthyroidism can be reversed with treatment
Lama Alasmari1, Osama Khairoalsindi2, Abdulaziz Algethami3, Ahmed Jizeeri3
1 Department of Internal Medicine, NGHA; KAIMRC, Riyadh, Saudi Arabia
2 KAIMRC; Department of Neurology, NGHA, Riyadh, Saudi Arabia
3 KAIMRC; Department of Cardiology, NGHA, Riyadh, Saudi Arabia
Correspondence Address:
Dr. Lama Alasmari
Department of Internal Medicine, NGHA, Riyadh
Saudi Arabia
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/heartviews.heartviews_110_22
Abstract
The authors present a case of a 54-year-old male patient with a history of shortness of breath and orthopnea. The echocardiogram showed an ejection fraction (EF) of 35%–40%. Diagnosis of hyperthyroidism was missed initially although the patient had bilateral exophthalmos and thyroid function tests suggesting it. Medical treatment of the hyperthyroid state reversed the cardiomyopathy within 6 months of treatment. Repeated echocardiograms after hyperthyroidism treatment showed a normalized EF.
Keywords: Dilated cardiomyopathy, Grave's disease, hyperthyroidism
Introduction 
Cardiomyopathies are a spectrum of myocardial disorders that have been morphologically classified into dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular (RV) cardiomyopathy, and nonclassifiable cardiomyopathy.[1]
Hyperthyroidism has a prevalence of 2.8% among Saudis.[2] Causes of hyperthyroidism include Graves' disease, toxic multinodular goiter, and toxic adenoma.[2] The entity of cardiomyopathy secondary to thyroid disease has been a matter of controversy for a long time. Cases have been reported as early as 1825 when Parry reported eight cases presenting with goiter, exophthalmos, edema, palpitations, and cardiomegaly.[3]
Long-standing untreated hyperthyroidism affects the heart causing tachycardia and increased cardiac contractility, thus increasing cardiac output.[4]
DCM is a rare disease entity; a study conducted in 2018 showed its prevalence to be <1% of patients with overt hyperthyroidism.[4] Thyroid hormone receptors are present in the myocardial and endothelial tissues and are sensitive to the slightest changes in thyroid hormone concentrations, like those observed in subclinical thyroid diseases. Thus, they can directly affect the cardiovascular system.[5]
Case Presentation This case reports on a 54-year-old Saudi male patient, with a smoking habit and type II diabetes mellitus, hypertension, and dyslipidemia. The patient presented to the emergency department with shortness of breath and orthopnea.
He was recently diagnosed with DCM in an outside hospital with no available medical report. He reported taking the following medications for an unknown duration: sacubitril/valsartan, hydralazine/nitrate, metoprolol, aspirin, and spironolactone. He denied any drug or alcohol abuse.
In addition, he reported a negative family history of thyroid diseases or the use of medications like amiodarone, or any exposure to iodine contrast dyes. The patient presented to the emergency department with shortness of breath and orthopnea.
Vital signs were within normal ranges, and the body mass index was 24.02. The general assessment showed bilateral exophthalmos and upgaze palsy without goiter. Cardiopulmonary auscultation revealed normal heart and lung sounds. Besides a clear chest on auscultation, no signs of increased jugular venous pressure and no lower limb edema were found. In addition, the echocardiogram showed an ejection fraction (EF) of 30%–35%.
The patient was subsequently admitted to a cardiac monitored unit as a case of compensated cardiomyopathy for workup.
Diagnostic workup
Laboratory tests revealed the brain natriuretic peptide levels of 75.2 pmol/L, troponin I level of 13.9 pg/mL, free T3 levels of 5.39, free T4 levels of 18.09, thyroid-stimulating hormone (TSH) levels of 0.02, and TSH receptor antibody levels of 11.6 (normal range < 1.8). Both C-reactive protein and erythrocyte sedimentation rate levels were elevatedChest radiography was unremarkable, with no signs of pulmonary edema or cardiomegalyElectrocardiography showed a normal sinus rhythm with voltage criteria for left ventricular hypertrophy and nonspecific ST- and T-wave abnormalityEchocardiography showed mild dilatation of the left ventricle (LV) with concentric left ventricular hypertrophy. The left ventricular systolic function was moderately reduced, with an EF of 35%–40%. There was moderate global LV hypokinesis. The right ventricle was normal in size and function. No significant valvular dysfunctions were detected. The main echographic measurements were the following: M-mode/2D Measurements and calculations: Interventricular septal thickness in diastole (IVSd): 0.75 cm, left ventricular internal dimension in diastole (LVIDd): 5.2 cm, left ventricular internal dimension in systole (LVIDs): 4.3 cm, and left ventricular posterior wall thickness in diastole (LVPWd): 0.82 cm; LV mass (C) d: 143.7 g; and left atrial dimension: 4.3 cmCoronary angiography showed mild nonobstructive coronary diseaseCardiac magnetic resonance imaging revealed the following left chamber measurements: LVEF 35%, LV end-diastolic volume (LVEDV) index 112 mL/m2, LV end-systolic volume (LVESV) index 73 mL/m2, LV stroke volume 65 mL, and no evidence of prior myocardial injuryThyroid ultrasound revealed heterogeneous echogenicity with increased vascularity of both lobes. No discrete thyroid nodules or parathyroid adenomas were found.Compensated heart failure (HF) secondary to cardiomyopathy (Graves' disease with orbitopathy) was diagnosed based on the clinical and laboratory findings. The patient started methimazole treatment under the guidance of the endocrinology team (after discharge, he was followed up by the same team and managed as an outpatient for optimal treatment titration).
After diagnosis, the patient's symptoms greatly improved by enhancing his diuresis. He was discharged from the hospital after 6 days on sacubitril/valsartan, metoprolol succinate, and furosemide.
The patient was seen at the endocrine clinic 1 month after starting methimazole. He was euthyroid clinically, and thyroid function tests revealed: TSH levels of 0.01, free T4 levels of 14.29, and free T3 levels of 3.70; thus, the treating physician decided to continue within the same methimazole dose. The latest follow-up 5 months later showed TSH levels of 0.53, free T4 levels of 9.97, and free T3 levels of 4.10.
Eight months later, a follow-up with the cardiology department revealed the resolution of symptoms, and a repeat echocardiogram reviewed by two certified cardiologists blinded to the patient's condition showed a dramatically improved LV function with normalization of left ventricular EF (EF >55%). Using Simpson's method, given the LVEDV and LVESV before and after treating Grave's disease, his LVEF before treatment was 38% and after treatment was 62% [Figure 1].
Figure 1: Echocardiography of the apical four-chamber views showing improvement in the EF before and after treating Grave's disease. (a) Initial LVEDV at the time of diagnosis: 111 mL. (b) Initial LVESV at the time of diagnosis: 69 mL. (c) LVEDV after treatment: 97 mL. (d) LVESV after treatment: 37 mL. LVEDV: Left ventricular end-diastolic volume, LVESV: Left ventricular end-systolic volume, EF: Ejection fraction Discussion Our patient who was diagnosed with thyroid cardiomyopathy showed complete recovery after initiation of antithyroid medication. Our patient was treated for HF without significant improvement in LV function owing to a lack of diagnosis of thyroid disease.
The complete workup of cardiomyopathy should be entertained at the first presentation to acknowledge the cause and provide treatment of the cause at any center. In our case, the main difficulty in establishing the diagnosis was the low clinical suspicion for thyroid-associated cardiomyopathy considering its low incidence and rarity worldwide.
The underlying pathophysiology of Graves' disease depends on the activation of the TSH receptor by autoantibodies.[6] A clear association between the activity of these autoantibodies and the presence of cardiomyopathy is not well established in the literature, and it is thought that the cardiovascular effect in hyperthyroidism specifically is related to the direct effect of thyroid hormones on the cardiac muscle.[7] Higher rates of cardiovascular morbidity and mortality have been associated with untreated hyperthyroidism in cardiovascular patients, mainly due to the increasing incidence of HF; thus, systematic screening for thyroid dysfunction is recommended to prevent these outcomes.[8]
Umpierrez et al. mentioned that reversible DCM secondary to hyperthyroidism followed the initiation of thyroid-directed therapy and after achieving euthyroid status in seven patients.[9] Guideline-directed medical therapy of HF with the treatment of hyperthyroidism resulted in an immediate clinical improvement, as also attested by echocardiographic improvement after 6–12 months of follow-up in all patients.[9] Our patient reverted to normal cardiac function with the same timing. Moreover, our patient did not have any RV involvement. This might have led to a better prognosis for recovery; it also raises questions about RV involvement in thyroid disease.
The medical literature points toward antithyroid drugs and beta-blockers as the mainstay of treatment to control and possibly reverse cardiovascular complications in hyperthyroidism.[5] After the cardiomyopathy reversal and the resuming of normal cardiac function in our patient following the euthyroid state, we stopped HF medication as no longer necessary, except for beta-blocker. Previous literature reported cases whereby different types of cardiomyopathy, like peripartum cardiomyopathy, could discontinue HF medications and remain asymptomatic without disease recurrence following the resolution of the initial cause.[10]
Consent to the publication
Informed consent was obtained from the patient for the publication of this report.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published, and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References 
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