Because of limited knowledge about natural history and outcomes of medical or surgical intervention for TR, the treatment decision making is often challenging

Because of limited knowledge about natural history and outcomes of medical or surgical intervention for TR, the treatment decision making is often challenging. to dilated right ventricle (RV), moderate resting pulmonary hypertension, and preserved biventricular systolic function. Interventions and outcomes: After 6 months of antithyroid treatment, her thyroid function was restored euthyroid state and she was fully recovered from right heart failure. Follow-up echocardiography showed complete disappearance of severe TR and pulmonary hypertension and normalization of RV dimension. Lessons: Severe TR can be rarely associated with thyrotoxicosis, but this is reversible and can be completely recovered with normalization of thyroid function. strong class=”kwd-title” Keywords: Graves disease, heart failure, tricuspid regurgitation 1.?Introduction Graves disease is the most common cause of thyrotoxicosis and can cause cardiovascular complications. Thyroid hormones are closely related to the function and the structure of the heart. Excess thyroid hormones induce significant cardiovascular hemodynamic changes.[1] Arterial Sclareolide (Norambreinolide) hypertension and atrial fibrillation (AF) are the most common complications. Heart failure (HF) and valvular dysfunction have also been rarely reported.[2] Right heart failure (RHF) is a more uncommon presentation than left-sided HF in patients with hyperthyroidism.[3] Here, we present a case of uncontrolled thyrotoxicosis-related severe TR with RHF, fully recovered with the attainment of euthyroid state. 2.?Case presentation A 41-year-old woman presented to the emergency department with worsening generalized edema and dyspnea for a month. She was diagnosed with Graves disease at a primary clinic 18?months ago. Methimazole was prescribed for 10?months and has been discontinued for 8?months after restoration to normal thyroid function. However, Graves disease relapsed and methimazole was resumed since last month. Despite treatment, worsening pedal edema and dyspnea brought her to the emergency room. At presentation, her blood pressure was 116/73?mmHg, heart rate 91?beats/min, respiratory rate 20/min, and body temperature 36.2?C. Physical examination Sclareolide (Norambreinolide) revealed exophthalmos, a diffuse goiter, irregular heartbeats with grade 3/6 systolic murmur at the left lower sternal border, and grade 3 pitting edema at both lower legs. Chest radiographs showed cardiomegaly with a cardiothoracic ratio of 0.56 (Fig. ?(Fig.1A)1A) and small amount of fluid shift on bilateral decubitus views. An electrocardiogram (ECG) exhibited AF at a rate of 87?bpm. Laboratory test revealed suppressed thyroid-stimulating hormone (TSH, 0.007?IU/mL), elevated levels of free thyroxine (T4, 37.63?pmol/L) and anti-TSH receptor antibody (27.12?IU/L), and Mouse monoclonal to PRKDC negative anti-thyroid peroxidase (anti-TPO Ab, 21.23?IU/mL) and anti-thyroglobulin (anti-TG Ab, 14.70 IU/mL) antibodies. The levels of liver enzymes were mildly increased (aspartate aminotransferase, 50?IU/L; alanine aminotransferase, 45?IU/L) and N-terminal pro-brain natriuretic peptide was also elevated to 1007?pg/mL. Technetium-99m thyroid scan showed bilateral diffuse enlargement of thyroid gland and intense homogeneous radiotracer uptake, consistent with Graves disease (Fig. ?(Fig.1B).1B). Transthoracic echocardiography was performed to assess the etiology of HF and exhibited severe tricuspid regurgitation (TR) associated with incomplete systolic coaptation of tricuspid valve due to dilated right ventricle (RV) (Fig. ?(Fig.2A,2A, B), moderate resting pulmonary hypertension with pulmonary artery systolic pressure of 59?mmHg (Fig. ?(Fig.2C,2C, D), normal left ventricular (LV) dimension, normal LV systolic function with ejection fraction of 59%, borderline elevation of LV end-diastolic pressure with em E /em / em E /em ratio of 12.5, and preserved RV systolic function. She underwent enhanced chest computed tomography to identify the presence of pulmonary thromboembolism as a cause of RHF, which showed bilateral pleural effusion, minimal ascites, and no evidence Sclareolide (Norambreinolide) of pulmonary embolism. Generalized edema and dyspnea were gradually improved with administration of furosemide, propranolol, and methimazole. After 6 months, euthyroid state was restored. In addition, follow-up ECG showed spontaneous conversion to normal sinus rhythm. Echocardiography revealed scanty TR with normalization of RV dimension and pulmonary artery systolic pressure of 27?mmHg (Fig. ?(Fig.3).3). Diuretics and beta-blocker were discontinued and methimazole was gradually tapered. She has been doing well and thyroid hormone levels have been maintained within the normal range for 6?months. Open in a separate window Physique 1 A, A chest radiograph showing moderate Sclareolide (Norambreinolide) cardiomegaly and blunted costophrenic angle. B, Technetium-99m thyroid scan demonstrating diffuse bilateral enlargement of thyroid gland with intense homogeneous radiotracer uptake suggesting Graves disease. Open Sclareolide (Norambreinolide) in a separate window Physique 2 Transthoracic echocardiography at the time of diagnosis of severe tricuspid regurgitation (TR) showing (A) dilated right ventricle, (B) severe TR (arrow) on a color Doppler image, and (CCD) moderately increased pulmonary artery systolic pressure of 59?mmHg with inferior vena cava plethora. IVC?=?inferior vena cava, LA?=?left atrium, LV?=?left ventricle, RV?=?right ventricle; asterisk?=?pleural effusion. Open in a separate window Physique 3 Six-month follow-up echocardiographic images after attainment of euthyroid state showing (A) normalized size of the right ventricle, (B) near complete resolution of tricuspid regurgitation (arrow), and (CCD) normalization of pulmonary artery systolic pressure and inferior vena cava diameter. IVC?=?inferior vena cava, LA?=?left atrium, LV?=?left ventricle, RV?=?right ventricle. 3.?Discussion Graves disease is an autoimmune disorder characterized by hyperthyroidism or thyrotoxicosis,.