Infections Associated with Resterilized Pacemakers and Defibrillators.

BACKGROUND: Access to pacemakers and defibrillators is problematic in places with limited resources. Resterilization and reuse of implantable cardiac devices obtained post mortem from patients in wealthier nations have been undertaken, but uncertainty around the risk of infection is a concern. METHODS: A multinational program was initiated in 1983 to provide tested and resterilized pacemakers and defibrillators to underserved nations; a prospective registry was established in 2003. Patients who received reused devices in this program were matched in a 1:3 ratio with control patients who received new devices implanted in Canada. The primary outcome was infection or device-related death, with mortality from other causes modeled as a competing risk. RESULTS: Resterilized devices were implanted in 1051 patients (mean [±SD] age, 63.2±18.5 years; 43.6% women) in Mexico (36.0%), the Dominican Republic (28.1%), Guatemala (26.6%), and Honduras (9.3%). Overall, 85% received pacemakers and 15% received defibrillators, with one (55.5%), two (38.8%), or three (5.7%) leads. Baseline characteristics did not differ between these patients and the 3153 matched control patients. At 2 years of follow-up, infections had occurred in 21 patients (2.0%) with reused devices and in 38 (1.2%) with new devices (hazard ratio, 1.66; 95% confidence interval, 0.97 to 2.83; P = 0.06); there were no device-related deaths. The most common implicated pathogens were Staphylococcus aureus and S. epidermidis. CONCLUSIONS: Among patients in underserved countries who received a resterilized and reused pacemaker or defibrillator, the incidence of infection or device-related death at 2 years was 2.0%, an incidence that did not differ significantly from that seen among matched control patients with new devices in Canada.

Postnatal development of atrial repolarization in the mouse.

OBJECTIVES AND METHODS: This study examines postnatal development of action potential duration (APD) and voltage-dependent K(+) currents in mouse atrial myocytes and compares the expression levels of corresponding K(+) channels between adult and neonatal mouse atrial tissues. APD and K(+) currents were compared between atrial myocytes isolated from postnatal Day-1, Day-7, Day-20, and adult mice. RESULTS: All K(+) currents examined underwent significant up-regulation during postnatal life in mouse atrium, resulting in a dramatic shortening of the APD. The ultrarapid delayed rectifier (I(Kur)) was absent in the developing mouse heart and only contributed to repolarization in the adult mouse atrium, whereas the density of the other K(+) currents increased earlier during the developmental period. Indeed, the major changes in the expression of the inward rectifier current (I(K1)) occurred within the first week of life, the density of the Ca(2+)-independent transient outward K(+) current (I(to)) gradually increased while the development of the steady-state outward K(+) current (I(ss)) was completed within the first 3 weeks of life. Results of RNase protection assay and Western blot analysis confirmed that the postnatal development of the mouse atrial K(+) currents correlates with an increase in expression levels of underlying K(+) channel isoforms. CONCLUSION: These findings indicate that in mouse atrium, each K(+) current exhibits a specific postnatal development, suggesting that regulatory factors taking place during development are major determinants of the functional role of K(+) channels in cardiac repolarization. The mouse atrium is, therefore, a very interesting model to gain information on the mechanisms regulating K(+) channel activity.

Characterization of ventricular repolarization in male and female guinea pigs.

Since both components of the delayed rectifier K(+) currents (I(Kr) and I(Ks)) are present in guinea pig and human ventricle, the guinea pig appears as an interesting model to examine the contribution of these currents in sex-related difference of cardiac repolarization. Accordingly, we compared ventricular repolarization in adult male and female guinea pigs using electrophysiological protocols together with Western blots analysis and perfused heart preparation. Our results indicate that there was no sex-related difference in the expression levels of the different K(+) channels studied (ERG, KvLQT1, minK and Kir2.1), nor in the density of the K(+) currents (I(Kr), I(Ks) and I(K1)) encoded by these channels. Action potential durations and QTc intervals were also similar between males and females. In addition, we compared QTc intervals using Langendorff-perfused whole hearts in the presence of I(Kr) and/or I(Ks) blockers. The I(Kr) blocker (5 microM E-4031) prolonged QTc intervals to a similar extent in male (24+/-2%) and female (29+/-3%, p=0.1) hearts. Similarly, the degree of QTc prolongation induced by 0.1 microM HMR1556 (I(Ks) blocker) was similar in both sexes (males: 15+/-2% and females 18+/-2%; p=0.2). In addition to their QT prolonging effects, the I(Kr) and I(Ks) blockers significantly reduced heart rate in both male and female guinea pigs. These studies clearly demonstrate that adult guinea pigs do not display sex differences in ventricular repolarization.