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Serial histopathologic myocardial findings in a patient with ectopic atrial tachycardia-induced cardiomyopathy
M Tomita1, S Ikeguchi, K Kagawa
1Second Department of Internal Medicine, Gifu University School of Medicine.
Insights
Ectopic atrial tachycardia can mimic dilated cardiomyopathy and lead to permanent heart damage, even after successful treatment. Early diagnosis and intervention are crucial for managing this condition.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiomyopathy
Background:
- Ectopic atrial tachycardia (EAT) is a rare arrhythmia.
- EAT can present with symptoms mimicking other cardiac conditions.
- The long-term effects of untreated EAT on cardiac structure and function are not fully understood.
Observation:
- A 17-year-old woman presented with EAT and echocardiographic findings suggestive of dilated cardiomyopathy.
- Initial treatment with atenolol controlled the tachycardia.
- Recurrent EAT at age 22 necessitated catheter ablation.
Findings:
- Catheter ablation successfully treated the persistent EAT.
- Left ventricular dimensions and function normalized within one year post-ablation.
- Despite successful treatment, myocardial fibrosis was evident, indicating permanent cardiac damage.
Implications:
- EAT can cause significant cardiac remodeling and damage, even when controlled.
- Catheter ablation is effective for treating persistent EAT.
- Long-term cardiac monitoring is essential for patients with EAT, even after successful treatment, due to the risk of permanent myocardial fibrosis.
Abstract:
A 17-year-old woman was found to have ectopic atrial tachycardia by her physician. Echocardiography and cardiac catheterization revealed findings resembling dilated cardiomyopathy at the time of initial presentation. The tachycardia was controlled with atenolol only at a dose of 50 mg/day. However, at the age of 22, the presence of ectopic atrial tachycardia was once again confirmed. We successfully performed catheter ablation for persistent ectopic atrial tachycardia. Serial echocardiographic findings showed the left ventricular dimension and function appeared to return to normal 1 year postablation. However, despite pharmacologic control and catheter ablation therapy, histopathology revealed myocardial fibrosis presumably representing permanent damage of the heart secondary to tachycardia 1 year postablation.