REVERSIBLE NONISCHEMIC CARDIOMYOPATHY SECONDARY TO CENTRAL HYPOTHYROIDISM

Abstract

SESSION TITLE: Cardiovascular Disease 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Thyroid hormones are well known to cause alterations in the cardiovascular hemodynamics. Hypothyroidism causes decreased contractility and cardiac output, bradycardia and increased systemic vascular resistance. This is secondary to changes in gene expression of enzymes involved in myocardial calcium shift, decrease beta adrenergic receptor expression and increase afterload induced by thyroid hormone deficiency. Although contractility and cardiac output are reduced in hypothyroidism, heart failure is rare due to the accompanying decrease in oxygen demand in the body. Here we are presenting a case of non-ischemic cardiomyopathy secondary to central hypothyroidism that improved with thyroid hormone replacement. CASE PRESENTATION: A 38-year-old female patient with history of adrenal insufficiency and central hypothyroidism secondary to panhypopituitarism secondary to Sheehan syndrome, presented with dyspnea and fatigue. She stated that she has not been taking her thyroid replacement therapy for a few months. On exam, BP was 128/100 and HR 66, she had distant heart sounds, no JVD and negative pulsus paradoxus, however, systolic BP dropped by 10 during inspiration. Labs showed TSH of 2 and fT4 of 0.16. EKG showed normal sinus rhythm without electrical alternans. Echo showed moderate pericardial effusion with RA collapse but no RV collapse, LVEF 30-35% and global hypokinesis of the left ventricle (Echo from 3 months earlier showed trivial pericardial effusion and LVEF 50%). She was started on her oral home dose of levothyroxine 125 mcg/day and had a nuclear stress test that showed no reversible perfusion defects. During her stay, she was hemodynamically stable and her symptoms started to improve. Repeat Echo showed marginal improvement in her LVEF with increase in RV systolic pressure. The size of the pericardial effusion was unchanged, however, respiratory variation in mitral and tricuspid inflow was less pronounced with less RA collapse. Later, her dyspnea and fatigue significantly improved and she was discharged home on oral levothyroxine 125 mcg/day. She was evaluated 5 weeks after discharge, with labs showing normal fT4 and Echo showing improved LVEF and decrease in the size of the pericardial effusion. DISCUSSION: Cardiac manifestations of hypothyroidism usually include dyspnea, fatigue, bradycardia, diastolic hypertension, edema and pericardial effusions. This is due to the effects of thyroid hormones deficiency on the heart and the vasculature. Systolic dysfunction is rare and only a few cases has been reported. Fortunately, it is usually reversible and improves with correcting the hypothyroidism. L-thyroxine (T4) is used to replace thyroid hormones and in this case, her home dose of 125 mcg/day was used. CONCLUSIONS: Thyroid function should be checked more frequently in patients presenting with cardiomyopathy specially if they have any concomitant signs and symptoms of hypothyroidism. Reference #1: Klein I, Ojamaa K. Thyroid Hormone and the Cardiovascular System. N Engl J Med. 2001 Feb 15;344(7):501-9. Reference #2: I Khochtali et al. Reversible dilated cardiomyopathy caused by hypothyroidism. Int Arch Med. 2011;4:20. Reference #3: Myung Do Seol et al. Dilated Cardiomyopathy Secondary to Hypothyroidism: Case Report with a Review of Literatures. J Cardiovasc Ultrasound. 2014 Mar; 22(1): 32-35. DISCLOSURES: No relevant relationships by Marsha Antoine, source=Web Response No relevant relationships by Housam Hegazy, source=Web Response No relevant relationships by Mili Shah, source=Web Response No relevant relationships by Bashar Sharma, source=Web Response No relevant relationships by Vikrant Tambe, source=Web Response