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Published on: August 18, 2016
Thyrotoxicosis and lactate-producing angina pectoris with normal coronary arteries
Insights
Thyrotoxicosis can cause cardiac pain mimicking myocardial infarction, even with normal coronary arteries. Early diagnosis and management are crucial for patients presenting with angina-like symptoms.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Thyrotoxicosis, a condition of excess thyroid hormones, can present with diverse symptoms.
- Cardiac manifestations of thyrotoxicosis are well-documented but can be complex.
- Distinguishing thyrotoxicosis-induced cardiac pain from myocardial infarction is clinically important.
Observation:
- Three patients with thyrotoxicosis experienced severe cardiac pain, leading to suspected myocardial infarction.
- Coronary arteriography revealed no significant coronary artery disease in these patients.
- Electrocardiographic evidence of ischemia and myocardial lactate production under stress were observed in all patients.
Findings:
- One patient developed myocardial infarction and a left ventricular aneurysm.
- All patients exhibited electrocardiographic ischemia and myocardial lactate production.
- Thyrotoxicosis was confirmed by thyroid function tests.
Implications:
- Thyrotoxicosis should be considered in the differential diagnosis of cardiac pain, especially in younger women.
- The cardiac pain may stem from the direct cellular effects of excess thyroid hormones on the myocardium.
- A guarded prognosis and ongoing medical follow-up are recommended for thyrotoxicosis patients with angina, even with normal coronary arteries.
Abstract:
Three patients with thyrotoxicosis are described, in whom the presenting symptom was severe cardiac pain at rest or on effort and who were admitted to hospital with suspected or proven myocardial infarction. All patients were studied by selective coronary arteriography and left ventriculography after thyroid function tests which confirmed thyrotoxicosis. There was no demonstrable disease of the major coronary arteries in any of the patients, yet myocardial infarction and left ventricular aneurysm were shown to be present in 1, and there was definite electrocardiographic evidence of ischaemia in all 3. In addition, under stress the myocardium of all 3 patients produced lactate. It is recommended that thyrotoxicosis be seriously considered in the differential diagnosis of cardiac pain, particularly in younger women. The cause of the pain seems related to the cellular effects of thyrotoxicosis on the myocardium and current views of these effects are summarised. Of the 3 patients, 1 died suddenly 6 months after becoming euthyroid, indicating that the disease may not be as benign as expected. A guarded prognosis and continued medical follow-up are recommended when thyrotoxicosis presents with angina pectoris even when normal coronary arteries have been demonstrated.
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