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Background: Transvenous implantable cardioverter-defibrillators (ICD) have been implanted in Poland since 1995. As the method spreads it is important to consider its long-term benefits and disadvantages., Aim: To assess survival, efficacy and complication rate in ICD patients, who received the device more than ten years earlier., Methods: Retrospective analysis of 60 ICD patients implanted between 1995-1999., Results: There were 42 (70%) males, mean age 50.6 ± 16.4 years. In 59 patients ICD was implanted for sudden cardiac death (SCD) secondary prevention. Thirty eight patients (34 M, 63.3%) had coronary artery disease (CAD). The CAD was diagnosed in 89.5% of males and 10.5% of females (p〈 0.0001). Mean follow-up time was 75.4 ± 34.7 months. During this time 22 patients died (37%, 19 M, 3 F). Three deaths were SCD. Mean one-year mortality was 6.7%. Deaths were more frequent among males: 45.2% vs 16.7%, p〈 0.005. In CAD mortality was higher than in non-CAD patients (50% vs 13.6%, p〈 0.005). Appropriate ICD discharges in the ventricular fibrillation (VF) zone occurred in 35 (58%) patients, and in ventricular tachycardia (VT) zone - in 26 (43%) patients. Mean intervention rate per year was 3.7 for VF and 0.6 for VT. Complications occurred in 27 (45%) patients and 5 (8%) of them had no ICD intervention during follow-up. In 5 patients more than one complication was diagnosed. There were inappropriate discharges in 15 (25%) patients, 11 (18%) had electrical storm, and ICD-related infections were noted in 3 (5%) patients. During the perioperative period, lead revisions were done in 4 patients; in 3 with discharges induced by T-wave oversensing and in one with lead dislocation. Four cases of lead failure occurred during follow-up, requiring new lead implantation. In 4 patients, electrical storm (3 patients) and supraventricular tachycardia with ICD discharges (1 patient) were treated with radiofrequency ablation. Only 10 (17%) patients did not demonstrate any ICD interventions or ICD-related complications., Conclusions: 1. ICD interventions caused by malignant ventricular arrhythmias occurred in 75% patients with the device implanted more than 10 years earlier. 2. Almost a half of the analysed population suffered from complications and side effects related to implanted ICD and they were present in 8% of subjects without ICD intervention. Neither ICD interventions nor device-related adverse events were recorded in 17% of patients.

SDF-1, a chemokine secreted by injured tissues, may be instrumental in chemoattracting CXCR4(+) stem cells (SCs) for repair of infarcted myocardium. We hypothesize that the myocardial SDF-1 expression determines also the engraftment and beneficial effects of SCs transplanted into the infarcted heart. Myocardial infarction (MI) was induced in rats by coronary artery ligation. The animals were either sacrificed at 2, 7, 16, 21 or 28 days after MI or were re-operated at 2, 7 or 14 days after MI to receive SCs transplantation, and were sacrificed 14 days later. SCs transplantation consisted of 3 x 15 microl injections of SCs isolated from foetal rat liver (FLSCs) into the myocardium bordering the infarction zone (5 x 10(6) cells/heart, labelled with PKH2 Green Fluorescent Cell Linker, approximately 20% CXCR4(+)). In the MI border zone, SDF-1 and CXCR4 immunostaining was transiently increased after MI, picking at 2 days and down regulating to the sham level by 21 days after MI. Simultaneously, an increased incorporation of CXCR4(+) and CD133(+) cells into capillaries was evident. AMD1300, a blocker of CXCR4, prevented the post-MI expression of CXCR4. In the MI border zone, the cardiomyocyte cross-sectional diameter increased and capillary/cardiomyocyte ratio decreased systematically during the 28 post-MI days, while an interstitial collagen accumulation demonstrated transient increase. FLSCs did not survive in the non-infarcted hearts. In infarcted hearts, FLSCs survived best when they were injected at 2 days after MI. The survival was negligible again when the injection was performed at 14 days after MI. FLSCs transplanted at 2 days after MI caused a further rise in SDF-1, CXCR4, and CD133 expression, compared with the untreated infarcted hearts. Only FLSCs transplanted at 2 days, but not later, attenuated cardiomyocyte hypertrophy and increased capillary/cardiomyocyte ratio in the MI border zone. These results suggest that myocardial signalling for homing of the endogenous and the exogenous SCs is transiently activated early after MI, that SDF-1 is instrumental in this process, and that there is only a narrow time-window after MI when SCs transplantation results in their efficient myocardial engraftment and beneficial anti-remodelling effect.