# Can Acute Neurological Disease Cause Cardiomyopathy in Horses?

## TL;DR

This case report explores whether neurological diseases in horses can lead to heart problems, similar to what is observed in humans.

## Contribution

The paper presents three equine cases of cardiomyopathy following neurological events, suggesting a potential link not previously documented in horses.

## Key findings

- Three horses developed cardiomyopathy after acute neurological events.
- Elevated troponin concentrations and myocardial damage were observed in affected horses.
- The report suggests neurological disease may induce myocardial injury in horses.

## Abstract

In human medicine, neurological diseases have been associated with transient cardiac abnormalities. Rodent and canine models of cardiac injury after brain trauma have been developed; however, this condition has not previously been reported in horses. In this case report, we describe three horses with a diagnosis of acquired cardiomyopathy following acute neurological signs due to different causes, thereby raising the question of whether myocardial injury in horses can be induced by neurological disease similar to that in humans. Although we cannot prove this theory, based on the human literature, a similar pathophysiology can also occur in the equine species. We suggest that horses with acute neurological diseases benefit from cardiac monitoring to identify the presence and severity of myocardial damage and apply further treatment if needed.

In human medicine, neurological diseases have been associated with transient cardiac abnormalities. In horses, myocardial disease is rarely diagnosed and has been associated with a wide variety of causes. The aim of this article is to describe three horses with no previous cardiac disease, which all developed severe cardiomyopathy following neurological disease. A 5-year-old Shetland pony stallion was diagnosed with cardiomyopathy with arrhythmias following an episode of seizures caused by an accidental intra-arterial xylazine injection. A 20-year-old crossbred mare was hospitalised for an open fracture of the left maxillary bone with copious epistaxis from both nostrils and developed acute cardiomyopathy with arrhythmias following a venous air embolism. Both had elevated troponin concentrations. Multifocal areas of haemorrhages and coagulative necrosis within the myocardium were found at the post-mortem examination of a 4-year-old thoroughbred gelding who died shortly after suffering acute brain injury following a backward fall. Based on this report, we suggest that myocardial injury can also occur in horses following neurological disease. Equine patients with acute neurological disease may benefit from cardiac monitoring; otherwise, patients with unspecific or mild symptoms of cardiomyopathy are likely to remain unidentified. The prognosis associated with this type of cardiac disease remains to be defined.