A Case of Amitriptyline-induced Myocarditis

Abstract

Amitriptyline is a widely prescribed tricyclic antidepressant (TCA) with a very concerning cardiotoxicity profile, but it is one that has not been discussed much in literature. Here, we present a case of amitriptyline toxicity presenting as myocarditis with pericardial involvement. A 21-year-old male with no previous cardiac history presented to the emergency department (ED) with a decreased level of consciousness after an amitriptyline overdose as a suicidal attempt. For concerns with airway protection, the patient was intubated and subsequently admitted to the intensive care unit (ICU). An electrocardiogram (EKG) showed sinus tachycardia, prolonged QRS complex, prolonged QTc interval, and nonspecific ST-T wave changes. Intravenous fluid resuscitation and sodium bicarbonate were administered with a target blood pH of 7.5 to 7.55. Two days later, the patient was taken off mechanical ventilation and improved clinically. However, troponin levels began to rise with a peak level of 4.08 µg/L. He then began having fevers, elevated white blood cell counts (WBCs), and elevated inflammatory markers. Transthoracic echo (TTE) revealed an ejection fraction (EF) of 45%-50%, no wall segment motion abnormalities, and a mild-to-moderate pericardial effusion. Cardiac magnetic resonance (CMR) was done, which revealed changes indicative of acute myocarditis, moderate pericardial effusion, a calculated EF of 45% with a moderate left ventricular dilation, and no coronary artery stenosis or anomalous coronary artery origin. Given the patient’s age, the absence of cardiac risk factors, and the presence of an amitriptyline overdose along with his EKG, TTE, and CMR findings, we hypothesize that this myocarditis with pericardial involvement is due to amitriptyline-induced direct toxicity.

The Evaluation of Myocarditis in the Post-Covid-19 Era: Pearls and Perils for the Clinician

“…Damage is often by direct cytotoxic effect and/or immune-mediated but in many cases the concomitant mechanisms are poorly understood. Table 2 lists many of the currently identified drugs/toxins reported to induce myocarditis with a recent analysis of World Health Organization pharmacovigilance database recognizing five distinct categories of drugs: antipsychotics, cytotoxic drugs, immunotherapies, vaccines, and salicylates [11][12][13][14][15][24][25][26][27][28][29][30]. Although patients are not routinely screened, they share many distinct similarities in presentation and clinicians should have heightened awareness to such etiologies.…”

“…While immune activation has a prominent role in the pathophysiology of myocarditis secondary to infectious or selected drug-induced process as previously described, systemic immune-mediated diseases that include systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), vasculitis (such as eosinophilic granulomatosis and polyangiitis (EGPA)), sarcoidosis and even organ-based immune mediated diseases such as chronic inflammatory bowel diseases may be associated with myocarditis [33]. Drugs/toxins known to cause toxic myocarditis [11][12][13][14][15][24][25][26][27][28][29][30][31][32].…”