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Published on: September 19, 2019
A case of hypothyroidism mimicking acute coronary syndrome
Huseyin Gunduz1, Huseyin Arinc, Mustafa Yolcu
1Department of Internal Medicine and Cardiology, Izzet Baysal Medical Faculty, Izzet Baysal University, Bolu, 14100, Turkey. drhuseyingunduz@yahoo.com
Insights
Hypothyroid patients can show elevated cardiac enzymes, mimicking heart attacks. This case highlights that elevated troponin I in hypothyroidism may not always indicate myocardial infarction, complicating diagnosis.
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Hypothyroidism can elevate creatine kinase (CK) levels, primarily CK-MM.
- Elevated CK-MB in hypothyroid patients without myocardial damage can mimic cardiac injury.
- Troponin I is a preferred marker for myocardial infarction (MI) in hypothyroid individuals.
Observation:
- This report details a 47-year-old male hypothyroid patient presenting with chest pain.
- The patient exhibited abnormal ECG findings and elevated cardiac enzymes, suggestive of acute coronary syndrome.
- Coronary arteriogram revealed no significant coronary artery disease.
Findings:
- The case demonstrates that troponin I can be elevated in hypothyroid patients even without myocardial damage.
- This finding challenges the exclusive reliance on troponin I for diagnosing MI in this patient population.
- The observed elevation in cardiac enzymes was not attributable to acute coronary syndrome.
Implications:
- Accurate diagnosis of myocardial injury in hypothyroid patients requires careful consideration of thyroid status.
- Relying solely on cardiac biomarkers like troponin I may lead to misdiagnosis in hypothyroid patients.
- Further research is needed to understand the mechanisms behind elevated cardiac biomarkers in hypothyroidism.
Abstract:
Hypothyroid patients have increased concentrations of creatinine kinase that is mostly due to increased CK-MM. However, CK-MB has also been reported to increase above reference values in hypothyroid patients without apparent myocardial damage. This may create confusion during the evaluation of myocardial injury in a hypothyroid patient presenting with chest pain. Troponin I is considered as a superior marker for the diagnosis of myocardial infarction in hypothyroid patients. However, there are some reports showing an increase in the level of troponin I without any myocardial damage in hypothyroid patients as in our case. In this report, we present a 47 years old male hypothyroid patient who had chest pain, abnormal electrocardiographic findings and increased cardiac enzymes suggesting acute coronary syndrome although he had normal coronary arteriogram.
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