Transient ST-segment elevation due to iatrogenic hyperthyroidism in a patient with normal coronary arteries
Cetìn Mustafa1, Uçar Ozgül, Güven Cetìn Zehra
1Department of Cardiology, Atatürk Chest Disease and Chest Surgery Education and Research Hospital, Sanatoryum caddesi, Turkey. mdmustafacetin@yahoo.com
Insights
Thyrotoxicosis from L-thyroxine overdose can induce coronary vasospasm, leading to acute myocardial ischemia. This case highlights the importance of monitoring thyroid hormone levels to prevent cardiac events.
Area of Science:
- Cardiology
- Endocrinology
Background:
- Acute myocardial ischemia can manifest with ST-segment elevation.
- Coronary vasospasm is a potential cause of myocardial ischemia, even with normal epicardial coronary arteries.
Observation:
- A 53-year-old male presented with angina pectoris and ST-segment elevation, indicative of acute myocardial ischemia.
- Symptoms resolved promptly with nitroglycerine, suggesting a vasospastic etiology.
- Coronary angiography showed normal epicardial coronary arteries.
Findings:
- The patient was found to be in a thyrotoxic state due to a recent increase in L-thyroxine dosage.
- The clinical presentation and diagnostic findings strongly suggested L-thyroxine-induced coronary vasospasm.
- Withholding L-thyroxine and initiating diltiazem treatment led to symptom resolution.
Implications:
- This case highlights a rare but serious adverse effect of L-thyroxine over-replacement.
- Clinicians should consider thyroid hormone levels in patients presenting with unexplained myocardial ischemia, especially those on L-thyroxine.
- Thyroid hormone-induced coronary vasospasm is a reversible cause of acute myocardial ischemia.
Abstract:
A 53-year-old man presented with angina pectoris and ST-segment elevation in V(1)-V(4) leads. Electrocardiogram changes and chest pain were completely resolved with nitroglycerine infusion. Coronary angiogram revealed normal epicardial vessels. These findings suggest that the acute myocardial ischemia was secondary to coronary vasospasm. From his medical history we learned that he was taking L-thyroxine and the dose had been increased two months previously. He was found to be in thyrotoxic state at admission. L-thyroxine treatment was withheld and diltiazem was given. He had no further symptoms. In conclusion we think that acute myocardial ischemia was likely secondary to L-thyroxine-induced coronary spasm.
Related Concept Videos
Acute Coronary Syndrome I: Introduction
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
Hyperthyroidism I: Introduction
Acute Coronary Syndrome III: Diagnostic Studies
Hyperthyroidism II: Pathophysiology
Transient Ischemic Attack l: Introduction


