SUMMARYDuring implantable cardioverter-defibrillator (ICD) implantation, ventricular defibrillation testing (DFT) is considered a standard procedure. This procedure often requires multiple ventricular fibrillation (VF) inductions. These repeated short episodes of circulatory arrest with global cerebral ischemia may cause neurological damage. In the present study, patients undergoing initial ICD implantation and limited induction of VF for defibrillation safety margin testing were evaluated for pre-and postoperative cognitive and neurologic functions. In addition, the serum neuron specific enolase (NSE) level, which is a biochemical marker of cerebral injury, was evaluated.The study was performed on 16 patients undergoing initial elective transvenous insertion of an ICD. A neurologic examination and cognitive assessment tests were performed 24 to 48 hours before and after ICD. NSE was determined before (NSE 1) and at the end of the surgery (NSE 2), as well as 2 hours (NSE 3), 24 hours (NSE 4), and 48 hours (NSE 5) after implantation.A total of 29 internal shocks (average, 1.8 ± 0.4) with energy ranging from 14 to 41 J (mean, 20 ± 5; median, 20 J ) were delivered in the ICD group patients. In one patient, 3 external (50, 200 and 360 J) shocks were required for fast VT induced during ICD lead positioning. The mean duration of VF was 10 ± 4 seconds and the mean cumulative time in VF was 16 ± 5 seconds. The mean recovery time between VFs was 5.3 ± 0.6 minutes. NSE levels were not different from the baseline at any time point in the patients of the group that completed the 48-hour observation period (P > 0.05). The patients did not report any new neurological symptoms after ICD implantation, and repeat examination after the procedure showed no abnormal findings other than those detected in the previous one. There were no statistically significant differences between the preoperative and postoperative scores obtained in the cognitive assessment.Single or two VF inductions and the brief arrest of cerebral circulation during ICD implantation are not associated with permanent neurological injury. However, further studies are needed to confirm this finding. (Int Heart J 2008; 49: 553-563)

Acute infection causes transient endothelial dysfunction. It increases inflammatory markers and generates an atherogenic lipid profile. Among the parameters evaluated, only the change in Apo-A1 level was associated with acute infection-induced endothelial dysfunction.

The present study showed that hs-CRP and WBC count were higher in patients with syndrome X than in control subjects. Furthermore, endothelial function was impaired significantly in patients with syndrome X.The increased levels of hs-CRP and WBC count may suggest that these markers may be used in clinical practice for the assessment of the inflammatory status of the endothelium in syndrome X.

RF delivery inside the CVS is less likely to produce detectable LGE on CMRI compared to RVOT. This may partially explain less than ideal long-term results after ablation of LVS IVAs from within the great cardiac vein/anterior interventricular vein.

Ablation of premature ventricular complexes (PVCs) originating from left ventricular outflow tract (LVOT)/left ventricular summit (LVS) is challenging with considerable rate of failure. Recently, in a novel approach to ablation of these arrythmias, application of radiofrequency energy to anatomically opposite sites of presumed origin of arrythmia, has been associated with moderate procedure success. Although late elimination of PVCs that are persistent following an ablation procedure has been previously reported, this observation has not been studied sufficiently. In this report, firstly, we present three cases of lately eliminated LVS PVCs, then, we discuss possible mechanism of this observation and conclude that after an initial failed attempt of anatomic ablation, operators may choose a period of watchful waiting before attempting a redo procedure.