Iatrogenic embolization and transcatheter retrieval of a ventricular septal defect occluder in a dog.

A 7-month-old Irish Setter underwent transcatheter therapy of a muscular ventricular septal defect (VSD) and pulmonary valve stenosis. Standard devices for muscular VSD closure could not span the interventricular septum due to right ventricular hypertrophy, and an Amplatzer post-infarction muscular VSD occluder with a wider waist was successfully implanted. Following VSD closure, inflation of the balloon dilation catheter during balloon pulmonary valvuloplasty resulted in iatrogenic embolization of the VSD occluder to the left ventricular outflow tract. Retrieval and reimplantation of the device was achieved using a snare catheter. This report describes a potential complication and management during intracardiac device implantation in a dog. Additionally, the case illustrates that the Amplatzer post-infarction muscular VSD occluder holds potential value in animals with a hypertrophied interventricular septum that cannot be spanned using a conventional device.

In vitro effects of the glycoprotein IIb/IIIa receptor antagonists abciximab and eptifibatide on platelet aggregation in healthy cats.

OBJECTIVE: To determine effects of the glycoprotein IIb/IIIa receptor antagonists abciximab and eptifibatide on in vitro inhibition of cat platelets. SAMPLE: Venous blood samples from 10 healthy cats. PROCEDURES: Blood samples were anticoagulated with hirudin. Aliquots of whole blood from each cat were allocated to 5 treatments (baseline, 50 µg of abciximab/mL, abciximab volumetric control treatment, 4 µM eptifibatide, and eptifibatide volumetric control treatment). Impedance platelet aggregometry was performed with 6.5 µM ADP or 32 µM thrombin receptor activator peptide (TRAP). Magnitude of platelet aggregation was determined by measuring the area under the curve 15 minutes after addition of ADP or TRAP. RESULTS: Eptifibatide caused a significant reduction in platelet aggregation, compared with baseline values, for aggregometry with both ADP (median, 50.0; range, 8 to 122 [baseline median, 306.0; baseline range, 130 to 664]) and TRAP (median, 75.5; range, 3 to 148 [baseline median, 219.0; baseline range, 97 to 578]). There was no significant difference in platelet aggregation with abciximab, the abciximab volumetric control treatment, or the eptifibatide volumetric control treatment for aggregometry with ADP or TRAP. CONCLUSIONS AND CLINICAL RELEVANCE: Eptifibatide caused a significant reduction in platelet aggregation in vitro, but there was no identifiable antiplatelet effect for abciximab. Eptifibatide and abciximab have different binding and inhibitory actions; therefore, it can be hypothesized that abciximab would be ineffective in cats because of a lack of receptor binding, reduced binding kinetics, or lack of downstream signaling. Eptifibatide may be useful in identifying hyperreactive platelets in cats in an in vitro platelet inhibitory assay.