Cardiotoxicity, inflammation, and immune response after rattlesnake envenomation in the horse.

BACKGROUND

Cardiac abnormalities are reported in rattlesnake-bitten horses. The prevalence and cause are unknown.

OBJECTIVES

To detect cardiac damage in rattlesnake-bitten horses by measuring cardiac troponin I (cTnI) and evaluating ECG recordings for presence of arrhythmias, and explore causes of this cardiac damage by measuring venom excretion, anti-venom antibodies, and tumor necrosis factor alpha (TNFα).

ANIMALS: A total of 20 adult horses with a clinical diagnosis of rattlesnake bite and 6 healthy adult horses.

METHODS

In a prospective clinical study, bite site swabs, blood samples, and urine samples were collected at various time points from 20 horses with a clinical diagnosis of snake bite. Continuous ECG recordings were obtained on the 20 affected horses and 6 normal control horses using 24-hour holter monitors. Plasma samples were assayed for cTnI, serum samples were assayed for TNFα and anti-venom antibodies, and bite site swabs and urine were assayed for venom.

RESULTS

Forty percent of rattlesnake-bitten horses (8/20) experienced myocardial damage (increased cTnI). Seventy percent (14/20) experienced a cardiac arrhythmia. There was a positive correlation between cTnI and TNFα (P < .02). Horses with cTnI ≥ 2 ng/mL were more likely to have antibody titers >5,000 (P < .05). No correlations were found between venom concentration and cTnI, anti-venom antibody titers, TNFα, or presence of arrhythmias.

CONCLUSIONS AND CLINICAL

IMPORTANCE

Cardiac abnormalities in this population of horses indicate that cardiac damage after rattlesnake bite is common. Rattlesnake-bitten horses should be monitored for signs of cardiac damage and dysfunction. Long-term follow-up should be encouraged to detect delayed cardiac dysfunction.