Background: Recently, it has been reported that frequent premature ventricular contractions (PVCs) may be associated with causing heart failure in patients with left ventricular (LV) dysfunction. However, the prognostic significance of frequent PVCs in asymptomatic patients with a normal LV function is unclear.

BackgroundThe antiarrhythmic or reverse remodeling effects of bepridil, a multi-ion channel blocker, have been recently reported, but inhomogeneity of the electrical remodeling and effects of bepridil have been observed in previous reports. In this study, the effect of long-term administration of bepridil on atrial electrical remodeling was evaluated in a comparison of the right and left atrium (RA and LA) in a canine rapid atrial stimulation model. Methods and ResultsIn 10 beagle dogs, rapid atrial pacing (400 beats/min) was delivered for 6 weeks and the atrial effective refractory period (AERP), conduction velocity (CV) and inducibility of atrial fibrillation (AF) were evaluated every week. In 5 of the pacing dogs, bepridil (10 mg·kg -1 ·day -1 ) was administered orally, starting 2 weeks after the initiation of the rapid pacing. At the end of the protocol, the hemodynamic parameters and extent of tissue fibrosis were evaluated and the mRNA of SCN5A, Kv4.3, the L-type Ca 2+ channel (LCC) and connexin (Cx) 40, 43, and 45 in both atria were examined by quantitative real-time reverse transcriptase-polymerase chain reaction. In the pacing control group, AERP shortening, decreased CV, increased AF inducibility and downregulation of the expression of SCN5A and LCC were observed. In the bepridil group, the AERP exhibited a relatively quick recovery after bepridil was started in the first week and continued to recover gradually until the end of the protocol, but that recovery was smaller in the LA than in the RA. The CV was not affected by bepridil administration. AF inducibility was well suppressed in the RA in the bepridil group, but the induction of short-duration AF could not be suppressed in the LA. The mRNA downregulation of the LCC and SCN5A was negated by bepridil administration in the RA; but not in the LA; however, the data showed similar tendencies. There were no significant differences in the hemodynamic parameters or tissue fibrosis and the mRNA expression of Kv4.3, Cx40, 43, and 45 between the pacing control and bepridil groups. Conclusion Bepridil exhibited an anti-electrical remodeling effect in this study as previously reported, but the effect was inhomogeneous between the RA and LA, with the LA appearing to be more resistant to the effect of bepridil. (Circ J 2008; 72: 318 -326)

We investigated the lipid lowering and anti-atherosclerotic effects of atorvastatin in patients with hypercholesterolemia. Thirty patients were given atorvastatin 10 mg daily, and assessed for serum lipids, intima-media thickness (IMT), and brachial-ankle pulse wave velocity (ba-PWV) at the baseline, 6 months, and 12 months. Remnant-like particle-cholesterol (RLP-C), lipoprotein (a) (Lp(a)), and high-sensitivity C-reactive protein (hs-CRP) were measured in some patients at the baseline and at 6 months. Total cholesterol, triglyceride and low-density lipoprotein cholesterol were significantly decreased by 32%, 23% and 44% at 6 months, respectively, and these effects were sustained at 12 months. There was no change in high-density lipoprotein cholesterol. IMT at the baseline was 0.

rence, 2,3 and thus might yield improved clinical outcomes in terms of ischemic stroke, heart failure, and death. For patients in whom PVI is truly curative, it should be possible to discontinue oral anticoagulants (OACs) without fear that an AF-related clinical event will occur. Despite A trial fibrillation (AF) affects quality of life and increases the risks of stroke, heart failure, and death. 1 Pulmonary vein isolation (PVI) is reported to be more effective than antiarrhythmic drug (AAD) therapy for relief of symptoms and freedom from AF recur

AimsRemodelling of the extracellular matrix (ECM) plays an important role in the production of arrhythmogenic substrate for atrial fibrillation (AF), and is considered to be promoted by the connective tissue growth factor (CTGF). Our objective was to assess the relationship between CTGF and ECM synthesis, and the effect of olmesartan on these processes.Methods and resultsFifteen canine AF models were produced by rapid atrial stimulation. They were divided into three groups: pacing control (n = 5): 6-week pacing, pacing + olmesartan (n = 5): pacing with olmesartan (2 mg/kg/day), and non-pacing group (n = 5). In the pacing control group, messenger ribonucleic acid expressions of CTGF and collagen types 1 and 3 were up-regulated in comparison with the non-pacing group (P < 0.05) while transforming growth factor-β (TGF-β) did not exhibit a significant difference. In the pacing + olmesartan group, these up-regulations were suppressed (P < 0.05). In fluorescent immunostaining, the expression of CTGF was localized in the cytoplasm. The protein level of collagen type 3 was increased in the pacing control and it was suppressed in the pacing + olmesartan group.ConclusionsCTGF and associated genes were up-regulated in the atria with the appearance of fibrosis. Because this up-regulation was independent of TGF-β and suppressed by olmesartan, CTGF up-regulation was considered to be mediated by angiotensin II.

ST-T abnormalities were frequently seen in patients using AEDs. The presence of Brugada-type ST elevation was associated with polytherapy with sodium channel-blocking AEDs.

SummaryIt is unknown whether 12-lead ECG can predict new-onset AF. In the present study, we identified patients with new onset AF from our digitally stored ECG database, and the P wave morphologies were analyzed in their preceding sinus rhythm recordings as the precursor state for AF. The P wave was analyzed in the most recent ECG recording of sinus rhythm preceding new onset AF within 12 months. The duration and amplitude of P waves were analyzed in 12 leads and compared between the 2 groups with the other clinical parameters. The study population consisted of 68 patients with new-onset AF and 68 age and sex-matched controls. Multivariate analysis revealed that the P wave amplitude in leads II and V 1 (0.157 ± 0.056 versus 0.115 ± 0.057 mV, P = 0.032, and 0.146 ± 0.089 versus 0.095 ± 0.036 mV, P = 0.002) and P wave dispersion (56.9 ± 14.8 versus 33.5 ± 12.9 ms, P = 0.001) were significant independent factors for the prediction of new-onset AF. By using these factors, new-onset AF could be predicted with a sensitivity of 69.1% and specificity of 88.2%. P wave analysis is useful for predicting new onset AF. (Int Heart J 2014; 55: 422-427) Key words: P wave dispersion, P wave duration, Atrial remodeling A lthough several experimental studies predicted a preventive effect of upstream therapies for atrial fibrillation (AF) using angiotensin receptor blockades (ARBs), 1,2) recent clinical trials of such upstream therapies have failed to demonstrate their preventive effect in clinical cases. The reason for this discrepancy is unclear; however, it may be partly explained by the heterogeneity of the pathogenic conditions of AF in clinical cases.3,4) Because a meta-analysis of ARB studies 2) has suggested a possible effect of ARB in the prevention of new-onset AF in clinical cases, upstream therapy may possibly exhibit an effect if it could be performed in the precursor state of AF. Even when considering catheter ablation for AF, it is important to detect the early or precursor state of AF in clinical cases because the effect of catheter ablation is higher in patients with earlier-stage AF, even in those with simple circumference ablation of pulmonary veins.5-7) The arrhythmogenic substrate of AF is known to be constructed progressively under various pathological conditions, including AF itself; 7-11) therefore, it could be speculated that the electrophysiological properties of the atrium may be modified in its precursor state. Several studies have attempted to identify the changes in P waves during sinus rhythm in AF patients. 7,8,[12][13][14][15][16] In these reports, prolongation of the P wave duration or expansion of the dispersion of the P wave duration in the surface 12-lead electrocardiogram (ECG) have been focused on as indices for identification of AF patients. [10][11][12][13][14][15] In the present study, we retrospectively identified patients with new-onset AF in the digital ECG profiling system of our hospital, and P waves in the preceding sinus rhythm state were analyzed as the precursor state for new-on...

t has been documented that atrial electrical remodeling characterized by shortening of the atrial effective refractory period (ERP) and a decrease in the conduction velocity plays a role in promoting atrial fibrillation (AF) by shortening the electrophysiological wavelength of the atrial muscle. [1][2][3][4][5][6][7] However, the progression of atrial remodeling does not seems to be homogeneous 8-11 and we have previously reported that both dispersion of the ERP and AF inducibility were increased during several weeks of rapid atrial pacing in a canine model of AF. 9,12 Interestingly, the ERP shortening was always more prominent in the left atrium (LA) than in the sites in the right atrium (RA), and the AF inducibility was always higher in the LA than in the RA. 9,13 Because it has been revealed that premature atrial activation that originates from the pulmonary veins cause AF in many clinical cases, the LA is considered to play a key role, even in clinical cases, 13,14 which might be explained not only by higher arrhythmogenicity of the LA, but also by the origin of the premature atrial contractions (APC). [15][16][17] In the present study, the arrhythmogenicity of both atria was evaluated by comparing a left and right atrial pacing model to reveal the importance of the location of rapid atrial firing in promoting AF in a canine rapid atrial Methods Subjects and Surgical ProcedureIn 14 adult beagle dogs weighing 12.7±1.3 kg, the cardiac surface was exposed via a right thoracotomy under pentobarbital anesthesia (30 mg/kg, iv) and mechanical ventilation (Model SN-480-5, Shinano Manufacturing, Circ J 2007; 71: 1629 -1635 (Received April 4, 2007 revised manuscript received June 6, 2007; accepted June 14, 2007 Background Continuous rapid atrial stimulation causes atrial remodeling, but little is known about the difference in the arrhythmogenicity of the left (LA) and right atria (RA). Methods and ResultsIn 14 beagle dogs, continuous rapid pacing (400 beats/min) was delivered from the right (n=7) or left (n=7) atrial appendage (RAA or LAA) for 2 weeks. The atrial effective refractory period (ERP), ERP dispersion, and inducibility of atrial fibrillation (AF) were evaluated along the time course from 4 atrial sites: (1) RAA, (2) area close to the inferior vena cava (IVC), (3) Bachmann's bundle (BB) and (4) LA. The ERP exhibited progressive shortening at all sites, but the degree of shortening differed among them. In the RA stimulation group, ERP shortening was more prominent in the RAA and LA than in the IVC or BB. In contrast, in the LA stimulation group, ERP shortening was more prominent in the LA than in the other sites. As a result, ERP dispersion was larger in the LA stimulation group than in the RA stimulation group and the AF inducibility was higher in the LA stimulation group than in the RA stimulation group, especially at the LA site (p<0.05). Conclusion LAA stimulation was more arrhythmogenic than RAA stimulation in this model. This result may partly explain the importance of premature contractions occur...