Related Experiment Videos
Platelet function, antithrombin-III activity, and fibrinogen concentration in heartworm-infected and
1Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849-5519.
Insights
Thiacetarsamide treatment in dogs, particularly those without heartworm, can increase blood clot risk by enhancing platelet aggregation. This procagulatory effect may contribute to thromboembolism during heartworm treatment.
Area of Science:
- Veterinary Medicine
- Hematology
- Parasitology
Background:
- Heartworm (Dirofilaria immitis) infection affects platelet function.
- Thiacetarsamide is an adulticidal drug used to treat heartworm disease.
- Understanding drug-induced hemostatic changes is crucial for patient safety.
Purpose of the Study:
- To investigate the effects of thiacetarsamide treatment on platelet aggregation and other hemostatic parameters in heartworm-infected and heartworm-negative dogs.
- To determine if thiacetarsamide itself induces procoagulant changes.
Main Methods:
- Evaluated platelet aggregation, platelet count, mean platelet volume, antithrombin-III activity, and fibrinogen concentration.
- Compared heartworm-negative dogs with heartworm-infected dogs at baseline and at 3, 10, and 21 days post-thiacetarsamide treatment.
- Utilized laboratory Beagles implanted with Dirofilaria immitis to assess long-term effects and treatment response.
Main Results:
- Thiacetarsamide enhanced adenosine diphosphate (ADP)-induced platelet aggregation in heartworm-negative dogs.
- A significant increase in fibrinogen concentration was observed on day 10 post-treatment.
- A significant decrease in antithrombin-III activity was noted 21 days after treatment in heartworm-infected dogs.
Conclusions:
- Thiacetarsamide exhibits procoagulatory effects in heartworm-negative dogs, indicated by enhanced platelet aggregation.
- These findings suggest thiacetarsamide may contribute to thromboembolic complications associated with adulticidal therapy.
- Further research is warranted to elucidate the precise mechanisms and clinical implications.
Abstract:
Platelet aggregation and release, platelet number, mean platelet volume, antithrombin-III activity, and fibrinogen concentration were evaluated in heartworm-negative and heartworm-infected dogs at baseline and on days 3, 10, and 21 after treatment with thiacetarsamide. Platelet reactivity was enhanced in a group of dogs naturally infected with Dirofilaria immitis, compared with 2 groups of heartworm-negative dogs, but platelet reactivity was not further enhanced after treatment with thiacetarsamide. A significant decrease in antithrombin-III activity was detected 21 days after treatment. The platelets from a group of laboratory Beagles implanted with 50 adult D immitis displayed enhanced reactivity 6 months after implantation, but by 18 months, platelet reactivity had returned to near, or less than, baseline. Platelet reactivity was enhanced after thiacetarsamide treatment in this group. Thiacetarsamide-associated changes were not observed in platelet number or size; antithrombin-III activity decreased, but the change was not significant. Fibrinogen concentration was increased significantly (P less than 0.05) on day 10. Enhanced adenosine diphosphate (ADP)-induced platelet aggregation was observed on days 3, 10, and 21 after treatment in heartworm-negative dogs. This change was not observed in 6 control Beagles not treated with thiacetarsamide. Although antithrombin-III activity was decreased on day 3 and fibrinogen concentration was increased on day 10, paralleling changes observed in the heartworm-infected dogs, the changes were not statistically significant. In this study, thiacetarsamide was procagulatory in heartworm-negative dogs and may be an important contributing factor to the thromboembolism observed with adulticidal therapy.