Manifestation of non-ST elevation myocardial infarction due to hyperthyroidism in an anomalous right coronary artery

Abstract

IntroductionAnomalous origin of the right coronary artery (RCA) from the left coronary cusp of the aorta is a moderately rare but potentially life-threatening incident. Myocardial infarction (MI) and sudden cardiac death have been described with this anomaly, especially in those who engage in excessive exercise. However, this case study shows this incidence in association with hyperthyroidism.Case descriptionA previously healthy 51-year-old female with history of hypothyroidism presented with acute onset chest pain for 1 day. Patient’s electrocardiogram was normal, however, she had elevated troponins and given her typical chest pain, she was diagnosed with acute coronary syndrome (ACS). The patient had been on levothyroxine and was found to have a subnormal thyroid-stimulating hormone level suggesting hyperthyroidism. Echocardiogram was normal. Coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva and no evidence of atherosclerosis. A coronary computed tomography angiogram was done confirming this finding and showed a slit-like deformity of the coronary ostium with at least 50% luminal stenosis. The patient was referred to a cardiothoracic surgeon for potential coronary artery bypass graft.DiscussionThis case illustrates a rare presentation of ACS due to hyperthyroidism in an anomalous RCA. MI is a rare manifestation of hyperthyroidism, but in combination with an anatomical defect, it can potentiate adverse outcomes. The mechanisms by which thyroid hormones influence cardiovascular hemodynamics are by causing a hyperdynamic circulatory state, increasing myocardial oxygen demand, and increasing the risk of coronary vasospasm. The combination of anatomic and metabolic defects is what likely precipitated this patient’s outcome.

NON-ST-Segment Elevation Myocardial Infarction Associated with Inadvertent Thyroid Hormone Overdose

“…For this reason, cardiovascular hemodynamics are altered resulting in tachycardia, hyperdynamic precordium, diastolic relaxation, increased cardiac output, widened pulse pressure, myocardial oxygen consumption and a hypermetabolic state. [ 3 , 4 ]…”

“…Althought less common than the typical risk factors for coronary artery disease such as age, sex, presence of smoking, diabetes, hypertension, dyslipidemia, obesity, psychosocial factors, family history and prior MI, hyperthyroidism has been reported in many cases to be an independent risk factor as well. [ 3 ]…”

“…Increased thyroid hormone predisposes to ischemia is by raising the concentrations of von Willebrand Factor, Factor 8, and Factor 9; increase platelet plug formation and levels of plasma fibrinogen and plasminogen activator inhibitor; and decrease levels of tissue plasminogen activator. [ 3 ]…”

“…For this reason, cardiovascular hemodynamics are altered resulting in tachycardia, hyperdynamic precordium, diastolic relaxation, increased cardiac output, widened pulse pressure, myocardial oxygen consumption and a hypermetabolic state. [3,4] Molecular mechanisms of thyroid hormones action on the heart have been clearly defined. An uncontrolled hyperthyroid state has been shown to have deleterious repercussions on the hemodynamics of the heart via increased catecholamines and an overactive renin angiotensin aldosterone system.…”

“…Althought less common than the typical risk factors for coronary artery disease such as age, sex, presence of smoking, diabetes, hypertension, dyslipidemia, obesity, psychosocial factors, family history and prior MI, hyperthyroidism has been reported in many cases to be an independent risk factor as well. [3] Hyperthyroidism of any cause is related to an increased risk of a hypercoagulable state and a mild decrease of coronary reserve. Increased thyroid hormone predisposes to ischemia is by raising the concentrations of von Willebrand Factor, Factor 8, and Factor 9; increase platelet plug formation and levels of plasma fibrinogen and plasminogen activator inhibitor; and decrease levels of tissue plasminogen activator.…”