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Second degree AV block and severely impaired contractility in cardiac myxedema: a case report
Apostolos Chatzitomaris1, Michael Scheeler2, Michael Gotzmann3
1Department of Endocrinology and Diabetes, Medical Hospital I, Bergmannsheil University Hospitals, Ruhr University of Bochum, Bochum, NRW Germany.
Insights
Severe hypothyroidism can cause significant heart problems, including heart failure and heart block. Prompt thyroid hormone replacement therapy can reverse these cardiac issues, highlighting the importance of thyroid testing in heart failure patients.
Area of Science:
- Cardiology
- Endocrinology
Background:
- Thyroid hormones significantly impact cardiac function.
- Severe overt hypothyroidism can lead to various cardiac manifestations, including diastolic dysfunction, reduced cardiac output, and bradycardia.
Observation:
- A 20-year-old male presented with syncope due to second-degree atrioventricular block (Mobitz 2) and heart failure with reduced ejection fraction (38%).
- Laboratory results indicated severe overt hypothyroidism (TSH >100 mIU/L) with low fT3 and fT4 levels, attributed to hypothyroid Graves' disease.
- Cardiac MRI revealed decreased contractility and pericardial effusion, but cardiac biomarkers (BNP, troponin I) were low, and viral testing was negative.
Findings:
- Treatment with intravenous levothyroxine normalized left ventricular ejection fraction and resolved pericardial effusion.
- Bradycardiac episodes improved, though intermittent atrioventricular block persisted nocturnally.
- The case demonstrates that overt hypothyroidism can cause cardiac myxedema affecting both electrophysiology and contractility.
Implications:
- Thyroid dysfunction should be considered in the differential diagnosis of heart failure.
- Early diagnosis and treatment of hypothyroidism are crucial for reversing cardiac abnormalities.
- This case underscores the necessity of thyroid testing in patients presenting with diverse phenotypes of heart failure.
Abstract:
The heart is a major target organ for thyroid hormone action. Severe overt hypothyroidism can result in diastolic hypertension, lowered cardiac output, impaired left ventricular contractility and diastolic relaxation, pericardial effusion and bradycardia. However, the function of the atrial pacemaker is usually normal and the degree by which the heart rate slows down is often modest. Here we report the case of a 20 year old male Caucasian with severe overt hypothyroidism. He presented with syncopation due to second degree atrioventricular block type Mobitz 2 and heart failure with reduced ejection fraction (38 %). Laboratory testing revealed a severe overt hypothyroidism with markedly elevated TSH (>100 mIU/L) and reduced fT3 and fT4 levels. The condition was caused by hypothyroid Graves' disease (Graves' disease with Hashimoto component). Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low. A possible infectious cause was unlikely, since testing for cardiotropic viruses was negative. The patient was treated with intravenous levothyroxine and after peripheral euthyroidism had been achieved, left ventricular ejection fraction returned to normal and pericardial effusion dissolved. Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night. In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.
