# A case report of sodium azide-induced myopericarditis

## TL;DR

A 31-year-old patient developed myopericarditis after ingesting sodium azide and was successfully treated with colchicine.

## Contribution

This is the first reported case of sodium azide-induced myopericarditis with preserved ejection fraction treated with colchicine.

## Key findings

- Sodium azide ingestion led to myopericarditis 48 hours later with preserved left ventricular ejection fraction.
- Colchicine treatment resolved symptoms within four days.
- Colchicine's mechanism of action may be relevant due to its effect on ATP-dependent functions.

## Abstract

Sodium azide exposures are rare but can be lethal as the substance inhibits complex IV in the electron transport chain, blocking adenosine-triphosphate (ATP) synthesis. Sodium azide is mostly used as a propellant in vehicular airbags but is also used in laboratory, pharmacy, and industrial settings. No known antidote exists and its cardiotoxic effects are poorly described in the literature.

We describe the case of a 31-year-old patient with major depressive disorder presenting with altered mental status after ingestion of an unknown amount of sodium azide. Although initially chest pain free, she developed pleuritic chest pain 48 h after ingestion. This was accompanied by new diffuse ST elevations on the electrocardiogram and serum troponin elevations concerning for myopericarditis. Treatment was pursued with a 14-day course of colchicine resulting in complete symptom resolution within 4 days of treatment initiation. The patient’s transthoracic echocardiogram was only notable for a preserved left ventricular ejection fraction (LVEF).

Cardiac toxicity after sodium azide ingestion usually occurs days after ingestion and has been previously described in the forms of heart failure with reduced ejection fraction complicated by cardiogenic shock. We describe the first case of sodium azide-induced myopericarditis with a preserved LVEF treated with colchicine. Colchicine is an established treatment for pericarditis, but its inhibition of endocytosis, an ATP-dependent cellular function, could be mechanistically relevant to this case.