A Case of Amitriptyline-induced Myocarditis.
Thamer Kassim1, Toufik Mahfood Haddad2, Amandeep Rakhra3
1Internal Medicine, Creighton University Medical Center, Omaha, USA.
Cureus
|November 16, 2018
Summary
Amitriptyline overdose can cause myocarditis and pericardial effusion, a rare but serious cardiotoxicity. This case highlights the need to consider direct toxic effects of tricyclic antidepressants on the heart.
Area of Science:
- Cardiology
- Toxicology
- Pharmacology
Background:
- Tricyclic antidepressants (TCAs), like amitriptyline, are widely prescribed but possess a significant cardiotoxicity profile that is under-discussed in medical literature.
- Amitriptyline overdose presents a serious risk, necessitating prompt recognition and management of potential cardiac complications.
Observation:
- A 21-year-old male with no prior cardiac history presented with decreased consciousness following an amitriptyline overdose.
- Initial EKG revealed sinus tachycardia, prolonged QRS, prolonged QTc, and non-specific ST-T wave changes, prompting aggressive management with fluid resuscitation and sodium bicarbonate.
- Despite clinical improvement, subsequent troponin elevation, fever, leukocytosis, and inflammatory markers indicated cardiac involvement.
Findings:
- Transthoracic echocardiography (TTE) showed reduced ejection fraction (45%-50%) and mild-to-moderate pericardial effusion.
- Cardiac magnetic resonance (CMR) confirmed acute myocarditis, moderate pericardial effusion, moderate left ventricular dilation, and preserved coronary arteries.
- The constellation of clinical presentation, EKG findings, and advanced cardiac imaging in the context of amitriptyline overdose strongly suggests direct drug-induced cardiotoxicity.
Implications:
- This case underscores the potential for amitriptyline to induce direct myocardial and pericardial toxicity, leading to myocarditis and effusion.
- Clinicians should maintain a high index of suspicion for cardiac involvement in amitriptyline overdose, even in young patients without prior cardiac history.
- Further research into the specific mechanisms of TCA cardiotoxicity is warranted to improve patient outcomes and treatment strategies.
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