Epsilon Archive for Student Projects

Abstract

Atrial fibrillation is the most common performance-limiting arrhythmia in horses. In Sweden,
atrial fibrillation is treated medically with quinidine sulphate. The aim of this pilot study was
primarily to investigate if medical conversion with quinidine sulphate could cause damage to
myocytes identified as an increase of cardiac specific troponin I (cTnI) in plasma. In addition,
this study also investigated whether an association could be seen between concentrations of
cTnI in plasma and the outcome of the treatment. Furthermore, this study also investigated the
side effects of quinidine sulphate as well as electrocardiographic changes during treatment.

The study included information from six different medical cardioversion attempts including
five horses with atrial fibrillation treated at the University Animal Hospital in Uppsala, Sweden.
Blood samples were collected continuously during the cardioversion and the following 12 hours
after the end of the cardioversion for later analyze of cTnI concentrations.

Cardioversion was successful in five of six attempts. In three attempts, treatment was
discontinued due to serious adverse reactions, hypersensitivity to quinidine sulphate and in one
case due to the owner’s request. In two of these cases, the heart converted to sinus rhythm later
even though the treatment attempt was discontinued. All horses in the study showed a variety
of adverse reactions that could be associated to treatment with quinidine sulphate (depression,
tachycardia, flatulence, diarrhea, colic, sweating, muscle tremor and ataxia).

This study also investigated the effects of quinidine sulphate on heart rate, atrial, respiratory
rate and the width of the QRS complexes. Heart rate increased over time while atrial rate
decreased until sinus rhythm occurred. The width of the QRS complex increased during the
cardioversion in all horses, but never above 25%, which is considered a sign of toxicity
secondary to treatment with quinidine sulphate. No association could be seen between findings
on the ECG recording and plasma concentrations of cTnI.

During the study, the plasma concentrations of cTnI were low for all horses. Treatment with
quinidine sulphate did not result in any significantly increased concentrations of cTnI in plasma.
This indicated that medical cardioversion with quinidine sulphate did not cause extensive
damage to the myocytes. However, the initial concentration of cTnI seemed to have a value as
a prognostic indicator for whether the cardioversion was to be successful or not. The horses
whose plasma concentration of cTnI initially exceeded 2 ng/L and whose plasma concentration
increased over time, were those that in this study did not convert to sinus rhythm and
respectively, reoccurred to atrial fibrillation despite successful cardioversion to sinus rhythm.