Abstract

Abstract Disclosure: A. Elahi: None. R.I. Mateo: None. The cardiovascular system is a major target of thyroid hormone action in which subtle changes in thyroid function can lead to cardiac complications such as coronary vasospasm. There are many proposed mechanisms in how this occurs, but further studies are needed to understand the specific pathophysiology. This case illustrates the clinical relevance of encountering a hyperthyroid patient complaining of chest pain and how to address it in real work practice. A 62 year old African American male with history of Graves hyperthyroidism, type 2 diabetes, hypertension, peripheral artery disease, and stroke with residual aphasia presented with acute onset chest pain, shortness of breath, and palpitations. He was noncompliant with his methimazole (MMI) and subsequent labs were significant for free T4 of 2.5 ng/dL, undetectable TSH, and free T3 of 11.53 pg/mL. His high sensitivity troponins were elevated at 29,569 ng/dL. EKG showed sinus tachycardia with T-wave inversions in leads II, III, and AVF with a bedside echo showing inferior lateral wall motion abnormality. He was started on MMI 20mg daily and admitted to the intensive care unit for non-ST elevation myocardial infarction management. Left heart catheterization (LHC) was done after 1 dose of MMI with findings suggestive of vasospasm; specifically, decreased blood flow of the right coronary artery which improved when the catheter was withdrawn and significant dampening of the arterial wave form of the left main coronary artery. Given the unclear differentiation between true coronary artery disease and vasospasm he needed a repeat LHC once his hyperthyroidism was more controlled. His free T3 levels were monitored every 1-2 days with administration of escalating doses of MMI up to 40mg daily. By day 7 of admission, his free T3 level was 4.54 pg/mL, free T4 was 2 ng/dL and repeat LHC was performed showing open vessel lumens with multiple occlusions requiring 2 stents in the right coronary artery and 1 stent in the left circumflex artery. Given that thyroid hormone receptors are present in the myocardium and vascular tissue, alterations in thyroid hormone concentration can affect cardiovascular function. The documentation of coronary spasm, however, is rare and to date, there are only a few limited cases describing the underlying pathophysiology. This case illustrates via cardiac catheterization images and corresponding labs, the positive correlation of coronary vasospasm with thyroid hormone levels in hyperthyroidism. Presentation: Thursday, June 15, 2023

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call