A decontamination and sterilization protocol employed during reuse of cardiac electrophysiology catheters inactivates human immunodeficiency virus.

OBJECTIVE: To assess the effect of a standard decontamination and sterilization protocol employed during reuse of cardiac electrophysiology (EP) catheters on human immunodeficiency virus (HIV). SETTING: Public health viral research laboratory. METHODS: Studies were performed on distal, electrode-containing segments of 40 EP catheters previously used in up to 10 clinical EP procedures. EP catheter segments were immersed for 1 hour in blood contaminated with a high titer of HIV. After air drying for 2 hours, subgroups of 8 EP catheters were subjected to either (1) no treatment, (2) washing in general purpose detergent, (3) washing in enzyme cleaner, (4) sterilization in ethylene oxide, or (5) the full protocol of sequential detergent-enzyme cleaner-ethylene oxide exposure. HIV infectivity after treatment was determined by measuring HIV RNA and, in cell culture studies, assessing HIV-induced cytopathic effects (CPEs) and supernatant HIV-specific p24 antigen content RESULTS: With no treatment, all catheters had high HIV RNA levels associated with CPEs and high p24 antigen levels. After washing in detergent, 5 of 8 catheters had HIV RNA detected, but without CPEs or p24 antigen. HIV RNA was detected in all catheters after washing in enzyme cleaner, with CPEs and a high p24 antigen level in 1 of 8 catheters. HIV RNA, CPEs, and p24 antigen were absent after ethylene oxide. After the full protocol, HIV RNA levels were undetectable (n = 7) or low (n = 1), without evidence of CPEs or p24 antigen. CONCLUSION: Appropriate decontamination and sterilization of EP catheters during reuse is highly effective in inactivating HIV.

Chronic threshold testing of implantable cardioverter defibrillators does not increase coagulation activity or platelet activation.

It is unknown if the brief periods of circulatory statis occurring with induction of VF during DFT testing in patients with an ICD activate blood coagulation processes. To address this question, coagulation activity and platelet activation were measured in peripheral venous blood samples obtained from 12 patients undergoing DFT testing under general anesthesia, 3 (n = 11) or 6 months (n = 1) after ICD implantation for recurrent ventricular arrhythmias. Five patients were anticoagulated with warfarin and two to six episodes of VF (median five) were induced per patient. Blood samples were drawn at baseline, after each DFT test and on the following morning. Coagulation activity was assessed by measuring prothrombin fragment 1 + 2 (F1 + 2) (a marker of thrombin generation), soluble fibrin (a marker of fibrin production), and D-dimer (a breakdown product of cross-linked fibrin). Platelet activation was evaluated by measuring the expression P-selectin on the platelet surface using flow cytometry. No significant changes in F1 + 2, soluble fibrin, D-dimer, or P-selectin expression occurred during DFT testing, or between baseline and morning after samples. Moreover, results were unaffected by warfarin. These findings suggest that chronic threshold testing of implantable cardioverter defibrillators is not associated with activation of blood coagulation processes.