Performance of an ICD algorithm to detect lead noise and reduce inappropriate shocks.

BACKGROUND: Implantable cardioverter-defibrillators (ICD) provide treatment for life-threatening ventricular tachyarrhythmias. Failure of the pace/sense conductor of an ICD lead can cause noise on the sensing electrogram (EGM) that may be misinterpreted as ventricular activity, triggering inappropriate therapy. An algorithm based upon the confirmation of ventricular activity from a far-field EGM has been developed to reduce inappropriate therapies resulting from this type of lead failure, while ensuring that appropriate therapy is delivered. The objectives of this study were to evaluate the algorithm's ability to discriminate lead noise from ventricular tachycardia/ventricular fibrillation (VT/VF) and to determine whether it inhibits inappropriate shocks without delaying appropriate shocks. METHODS: The algorithm was prospectively tested using near- and far-field EGM recordings from patients in three conditions: normal sinus rhythm with sustained and non-sustained lead noise via manipulation of the ICD pocket or lead system, and VT/VF induced during defibrillation threshold testing. The recordings were played through a bench-top device running the algorithm with the diagnosis, time to diagnosis, and inhibition of therapy documented. RESULTS: The algorithm detected noise and withheld inappropriate therapy in 231 of 238 recordings of sustained lead noise that would otherwise have been diagnosed as VT/VF (97.1%). Non-sustained lead noise was correctly diagnosed in 47 of the 52 recordings (90.4%). The device appropriately identified all 853 recordings of VT/VF (100%), without an increase in the time to detection (0.01 ± 0.14 s). CONCLUSIONS: The SecureSense(TM) algorithm correctly diagnosed sustained and non-sustained lead noise recordings without compromising detection of VT/VF. Use of the algorithm may reduce inappropriate shocks and alert clinicians to lead noise indicative of lead failure.

Spatial heterogeneity and oxygen dependence of glucose consumption in R3230Ac and fibrosarcomas of the Fischer 344 rat.

To examine the oxygen-dependence of glucose consumption in solid tumors, we monitored gradients of glucose, lactate, and hypoxia in R3230Ac and FSA tumors growing in Fischer 344 rats. Bioluminescence imaging, detection of Hoechst 33342, and immunostaining of the hypoxia marker EF5 [2-8-N-(2,2,3,3,3-pentafluoropropyl)acetamide] were done in serial tumor slices. Glucose and lactate levels were also determined in liver and blood. Cells were further tested for glucose consumption and lactate production in vitro. In both tumor types, EF5 staining indicated similar maximum levels of hypoxia; the most intense staining occurred in perinecrotic regions. Glucose concentrations were highest in liver, declined from blood to tumor edge, further into vital tumor regions, and were lowest close to necrosis. Glucose was significantly lower in FSA than in R3230Ac tumors. Glucose concentrations in R3230Ac tumors were consistently higher in nonhypoxic than in hypoxic areas, with maximum values equal to systemic blood levels. Glucose in FSA tumors was close to zero, regardless of the presence or absence of hypoxia. Lactate did not differ significantly between the tumor types. FSA cells in culture showed a trend towards higher aerobic glucose consumption versus R3230Ac. Both cell lines increased their lactate production to similar levels under hypoxia. We conclude that both R3230Ac and FSA tumors retain the Pasteur effect, i.e., hypoxia triggers increased glycolysis. However, our results imply that increased aerobic glucose utilization leads to low glucose levels in FSA and a situation where supply limits uptake. This explains the repeatedly observed correlation between tumor blood flow and 18F-deoxyglucose uptake.