br Conclusions Implantable monitoring devices have become hi

Conclusions Implantable monitoring devices have become highly useful diagnostic tools for AT/AF [32]. However, the accuracy of the obtained diagnostic information is influenced by several factors, including the presence of non-AT/AF events, such as RNRVAS or PMT, caused by VA conduction or by suboptimal settings of the atrial sensitivity and PVAB duration.
Conflict of interest
Introduction Multiple randomized trials (such as the Valsartan in Acute Myocardial Infarction trial: VALIANT) have demonstrated that angiotensin II Homoharringtonine blockers (ARBs), as well as the angiotensin-converting enzyme (ACE) inhibitor captopril, reduce mortality and cardiovascular morbidity among patients with myocardial infarction complicated by left ventricular systolic dysfunction [1]. In the canine heart, reperfusion arrhythmias (RAs) are usually sudden in onset and deteriorate to ventricular fibrillation (VF) within 5–30s, and instantaneous VF (onset at 0–1min) is known to occur in the midst of the recovery process, when electrical heterogeneity is increased [2]. Acute administration of an ACE inhibitor and an ARB increases the threshold of VF, which suppresses RA [3,4]. The intracoronary delivery of low doses of ACE inhibitor suppresses RA after primary percutaneous coronary interventions for acute myocardial infarction [5]. On the basis of these findings, it is hypothesized that angiotensin II (Ang II) has a direct accelerating action on the generation of RAs during the super-acute phase of reperfusion (within 60s of reperfusion), in addition to its well-known, long-term action, which is termed remodeling [6]. However, the short-term direct electrophysiological action of Ang II at the cellular level during the super-acute phase of reperfusion has not been clarified.
Methods
Results
Discussion The major results from this study are summarized here. (1) In the control, the incidence of conduction block was highest within the first 10s of RES and that of AT alternans after conduction block was the highest from 10 to 20s; subsequently, 1:1 conduction was resumed after 40s. (2) The conduction block progressively increased during RES under perfusion with Ang II, and its occurrence was significantly higher during the late stage of RES (40–60s) in the Ang II group than in the control, although the recovery of APD50 progressed at the late stage of RES. (3) Ang II induced conduction block, and AT alternans was suppressed by adding AT1 receptor blocker (CV-11974) or mito-KATP blocker (5-HD) to the perfusate after reoxygenation.
Funding This study was supported by Takeda Pharmaceutical Company, Osaka, Japan.
Conflict of interest
Acknowledgments
Introduction Several experimental studies utilizing animal models of atrial fibrillation (AF) have shown a suppressive effect of angiotensin II receptor blockers (ARBs) on the process of atrial remodeling serving as the arrhythmogenic substrate for AF [1,2]. We have previously reported that olmesartan suppresses the increase in AF inducibility in a canine AF model by the suppression of tissue fibrosis and downregulation of connexin 43. Even in clinical patients with AF, several sub-analyses of mega-trials have highlighted the potential of using ARBs as upstream therapeutic agents for the suppression of AF [3–5]. However, recent prospective clinical trials on ARBs with suppression of AF as the primary endpoint have failed to document positive results [6,7]. These results clearly indicate that the suppression of AF using upstream ARB therapy is complicated and that its effect should be evaluated by a specific method of determining whether there is any positive effect in clinical AF cases. In the present study, we focused on the long-term effect (in years) of ARBs on the AF substrate. However, evaluation of the atrial electrophysiological properties of clinical patients is technically difficult because an invasive cardiac electrophysiological study using electrode catheters cannot be repeated frequently. Instead, we measured the fibrillation cycle length (FCL) by the spectral analysis of the fibrillation waves in the surface electrocardiogram (ECG) [8–11] since it is a non-invasive and easy method for evaluating the electrophysiological properties of the atria [12–16]. Therefore, factors influencing the atrial electrophysiological properties, if present, might be detected by the observation of the FCL. In this study, we evaluated a change in the fibrillation cycle length (FCL) in patients with chronic AF under long-term, i.e., 6-year, ARB therapy, and FCL and clinical data were compared between patients with and without ARB therapy.