The methods used for this purpose are substantially the

The methods used for this purpose are, substantially, the analyses of atrial potentials, evoked atrial potentials [10], and ventricular rhythm in cases of stable spontaneous AV conduction [11].
Materials and methods
Results
Discussion This is the first report on the current ACAP Confirm® release. This study investigated the accuracy and applicability of the ACAP Confirm® algorithm in pacemakers and ICDs. The results showed that the algorithm operates as intended, and that ACAP-determined thresholds are similar to manually measured atrial thresholds. Polarization values gradually increase with pulse width as previously described by Luria [13]. One important finding is the reliability of ACAP at different pulse widths, which enables current drain to be minimized in the event of pacing threshold increase by avoiding voltage multipliers [14]. Indeed, this feature differs across manufacturers, being available only in SJM and Biotronik devices, and can enable automatic voltage/duration adjustment in the event of a threshold increase, thereby maximizing device longevity. A previous study conducted on the old ACAP algorithm [12] found that the system was activated only in 1% of patients in the acute phase, and that this figure increased to 50% after two weeks. In contrast, the new algorithm displayed a significantly higher percentage of activation immediately after BMN673 in our experience. However, the system was activated in a significantly higher percentage of patients during the first follow-up examination than immediately after implantation (p<0.001) similar to the previous study [12].
Conclusions
Author contributions
Conflicts of interest
Introduction Abnormal local conduction is a key mechanism of arrhythmogenesis, often complicating acute myocardial infarction (MI) [1]. The accompanying autonomic dysfunction, modulated by the release of endothelin-1 (ET-1) [2], exerts a prominent role [3], but their relative effects on the electrophysiological milieu remain unclear [4]. Here, we recorded ventricular tachyarrhythmias (VTs), monophasic action potentials (MAPs) and local activation sequences in rats. To identify the effects of central sympathetic activity, we used the “subtraction-model” offered by clonidine, whereas the effects of ET-1 were examined in ETB-deficient rats.
Material and methods Sustained inhibition of sympathetic preganglionic neurons was induced by clonidine, administered at 0.5mg/kg in wild-type and ETB-deficient rats 1h prior to MI; the latter well-characterized rat-strain, kindly provided by Professor M. Yanagisawa (University of Tsukuba, Japan), displays 10-fold higher ET-1 levels [5]. The study protocol conformed to EU Directive 2010/63/EU, and was approved by the regulatory authorities (6003, 19/04/2013). Under 2.5% sevoflurane anesthesia, exerting minimal effects on sympathetic activation [6], acute MI was induced by ligation of the mid-left coronary artery. VTs were recorded by implanted telemetry transmitters in conscious rats (n=24) for 24h, and infarct size was measured at the end of the experiment, as previously [7]. No major bleeding occurred during surgery. In another similar animal cohort (n=32), MAPs were recorded from the antero-lateral left ventricular (LV) and right (RV) ventricular epicardium; voltage rise (dV/dtmax) was measured, providing information on sodium-channels. Measurements were carried out in anesthetized animals (as above) at baseline and at 5and 30min (phase I) and at 6 and 24h (phase II) post-ligation. Unipolar electrograms were recorded from the LV and RV with a 32-electrode array, in reference to Wilson׳s central terminal. We measured RR intervals and activation delay, defined as the time difference between the onset of the first and last electrograms in each recording. Variables are reported as mean±standard error of the mean. Differences were assessed with one-way analysis of variance (ANOVA) or with ANOVA for repeated measures, as appropriate, followed by Duncan׳s test. Significance was set at p<0.05.