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Notes: GRADAUS, R., et al.: Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans. Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 ± 11 years, 19 coronary artery disease, NYHA 2.2 ± 0.4, left ventricular ejection fraction 0.42 ± 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 ± 3.6 J after 10.3 ± 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with ≤ 8 J. In these patients, the mean defibrillation threshold was 4.0 ± 2.1 J after 1.4 ± 0.3 seconds compared to 9.5 ± 3.1 J after 10.2 ± 1.1 seconds (P 〈 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.

Notes: Cardiac Output and ICD Implantation. Introduction: Perioperative mortality of patients undergoing implantation of automatic implantable cardioverter defibrillators (ICDs) has been reduced dramatically following the availibility of trans venous-subcutaneous defibrillation leads. However, patients with severely reduced left ventricular function show a substantial rate of nonsudden cardiac mortality within the first year. Whether repeated intraoperative inductions of ventricular tachycardia/fibrillation (VT/VF) during implantation lead to hemodynamic deterioration and thus might contribute to development of end-stage heart failure in these patients is unknown. The purpose of the present study was to determine cardiac output and hemodynamic performance during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction. Methods and Results: In 11 patients with a left ventricular ejection fraction (EF) ≤ 0.35, cardiac output was measured automatically with a combined continuous cardiac output/mixed venous oxygen saturation pulmonary artery catheter system. ICD implantation was performed during standardized general anesthesia. In the 11 patients (EF = 27 ± 2% [mean ± SEM]) a total of 95 episodes of VT/VF followed by defibrillation were induced (epsiodes per patient = 9 ± 1; range 6 to 11). Cardiac index was 2.2 ± 0.2 L·min-1·min-2 after induction of anesthesia (before start of surgery), and 1.9 ± 0.1 L·min-1·m-2 immediately before first induction of VT/VF. After the last episode of VT/VF, cardiac index was 2.1 ± 0.2 L·min-1·m-2. Cardiac index measured 1, 2, and 3 minutes after induction of VT/VF was not significantly different when compared to the preinduction value during any episode of VT/VF induction. Similarly, stroke volume index was 39 ± 5 mL·m-2 immediately before first induction of VT/VF and 36 ± 3 mL·m-2 after the last episode of VT/VF (NS). At the end of surgery, hemodynamic parameters did not exhibit any significant difference when compared to the data obtained before start of ICD implantation and testing. Conclusion: Extensive defibrillation tests during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction are not associated with acute deterioration of cardiac performance.

Notes: Abstract Kidney tumors and pheochromocytomas of the adrenal gland may extend into the inferior vena cava (IVC) or even the right atrium. In these cases, curative surgery frequently requires partial resection of the IVC. From 1992 to 1995, 8 patients (6 kidney tumors, 2 pheochromocytomas of the adrenal gland) underwent tumor surgery with concomitant IVC resection. Four patients had tumor growth into the right atrium. Surgery was carried out during hypothermic circulatory arrest (n=4) using veno-venous bypass from the IVC to the jugular vein (n=2), or by simply clamping the IVC (n=2). In 6 patients the IVC was reconstructed using a PTFE prosthesis (n=2) or patch (n=4), in 2 patients the IVC was closed by a running suture only. All patients were discharged home 10–23 days after surgery (mean 13 days). During the follow-up (mean 23 months), 6 patients were in good clinical condition and without evidence of tumor recurrence up to 44 months after surgery and 2 patients died of metastases (16 and 17 months). Refinements of surgical techniques combined with a multidisciplinary approach involving vascular surgeons, cardiac surgeons, and urologists allow successful treatment of advanced tumor stages with IVC involvement, formerly considered a contraindication for surgery. The aggressive surgical approach is warranted not only for relief of symptoms, and acceptable survival rates can be achieved; even cure of the disease is possible.