The crystal structure of zinc diethyldithiophosphate, Zn[S2P(OC2Hs)2]2 has been determined. The final R value obtained by the anisotropic least-squares method was 7"9%. The crystal is monoclinic, space group P21/a, with a= 12-084 (0-003), b= 19.840 (0.006), c=8.463 (0.005)/~, .8= 113.99 (0.03) °, Z--4.One dithiophosphate group is coordinated to a single zinc atom by its two sulphur ends, while the other, also by its two sulphur ends, bridges two different zinc atoms related by a-glide. Thus the fcrmula unit does not exist as a monomer in the crystal, but infinite linear zigzag chains (polymers) are formed along the a axis. These chains are stacked laterally with methyl-sulphur, methyl-methyl and methyloxygen van der Waals contacts. The coordination of the four sulphur atoms about each zinc atom is distorted tetrahedral, the Zn-S distances ranging from 2.337 to 2.401 A.

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...

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.

Background Recent clinical trials have demonstrated the possible pleiotropic effects of SGLT2 (sodium–glucose cotransporter 2) inhibitors in clinical cardiovascular diseases. Atrial electrical and structural remodeling is important as an atrial fibrillation (AF) substrate. Methods and Results The present study assessed the effect of canagliflozin (CAN), an SGLT2 inhibitor, on atrial remodeling in a canine AF model. The study included 12 beagle dogs, with 10 receiving continuous rapid atrial pacing and 2 acting as the nonpacing group. The 10 dogs that received continuous rapid atrial pacing for 3 weeks were subdivided as follows: pacing control group (n=5) and pacing+CAN (3 mg/kg per day) group (n=5). The atrial effective refractory period, conduction velocity, and AF inducibility were evaluated weekly through atrial epicardial wires. After the protocol, atrial tissues were sampled for histological examination. The degree of reactive oxygen species expression was evaluated by dihydroethidium staining. The atrial effective refractory period reduction was smaller ( P =0.06) and the degree of conduction velocity decrease was smaller in the pacing+CAN group compared with the pacing control group ( P =0.009). The AF inducibility gradually increased in the pacing control group, but such an increase was suppressed in the pacing+CAN group ( P =0.011). The pacing control group exhibited interstitial fibrosis and enhanced oxidative stress, which were suppressed in the pacing+CAN group. Conclusions CAN and possibly other SGLT2 inhibitors might be useful for preventing AF and suppressing the promotion of atrial remodeling as an AF substrate.

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BackgroundCardiac troponin T (cTnT) has been reported to be associated with cardiac mortality.In the present study, we evaluated the role of routine assessment of cTnT as a predictor of future cardiac death in patients with left ventricular (LV) dysfunction.MethodsPatients who were eligible for prophylactic implantable cardioverter defibrillator (ICD) were included from cardiac catheterization database. Inclusion criteria were patients with LV ejection fraction of ≤ 35% and with New York Heart Association (NYHA) ≥class II. Exclusion criteria were patients with acute coronary syndrome, ICD for secondary prevention, NYHA class IV, and lack of data. The final study patients were divided into the following three groups in accordance with two quartile points of serum cTnT levels: low cTnT, intermediate cTnT, and high cTnT groups. The primary endpoint of this study was cardiac death.ResultsA total of 70 patients were included (mean age, 62±13 years; male individuals, 56; ischemic, 36; and non-ischemic, 34). During the observation period of 2.2 years, cardiac death was observed in 17 patients (fatal arrhythmic event, 9; heart failure, 7; myocardial infarction, 1). In the Kaplan–Meier analysis, the high cTnT group showed the highest risk among all the groups (p<0.001). Even in sub-analyses for ischemic and non-ischemic patients, the results were the same, and the high cTnT group showed the highest event rate (p<0.05). In contrast, no cardiac death was observed in the low cTnT group.ConclusionThe cTnT levels in a stable state were associated with cardiac death in patients with LV dysfunction, even in those with non-ischemic diseases.

Dipeptidyl peptidase 4 (DPP-4) inhibitors have recently been reported to exhibit additional cardioprotective effects; however, their effect in atrial remodeling, such as in atrial fibrillation (AF), remains unclear. In this study, the effect of linagliptin on atrial electrical and structural remodeling was evaluated in a canine AF model. Sixteen beagle dogs with 3-week atrial rapid stimulation were divided into the linagliptin group (9 mg/kg/day, n = 8) and pacing control group (n = 8). Three additional dogs without rapid pacing were assigned into non-pacing group, which was used as sham in this study. In the dogs with rapid pacing, the atrial effective refractory period (AERP), conduction velocity (CV), and AF inducibility were evaluated and blood was sampled every week. After the entire protocol, atrial tissue was sampled for histological examinations using HE, Azan, and dihydroethidium (DHE) staining to evaluate any tissue damage or oxidative stress. The pacing control group exhibited a gradual AERP shortening and CV decrease along the time course as previously reported. In the linagliptin group, the AERP shortening was not affected, but the CV decrease was suppressed in comparison to the control group (p < 0.05). The AF inducibility was increased in the control group and suppressed in the linagliptin group (p < 0.05). The control group exhibited tissue fibrosis, the degree of which was suppressed in the linagliptin group. DHE staining exhibited suppression of the reactive oxygen species expression in the linagliptin group in comparison to the pacing control group. Linagliptin, a DPP-4-inhibitor, suppressed the AF inducibility, CV decrease, and overexpression of oxidative stress in the canine AF model. Such suppressive effects of linagliptin on AF in the canine model may possibly be related to the anti-oxidative effect.

In a canine rapid atrial stimulation model of atrial fibrillation (AF), we have demonstrated an increased production of reactive oxygen species (ROS) along with electrical and structural remodeling. In the present study, we hypothesized that antioxidants can suppress atrial remodeling canines with AF. We therefore evaluated the effect of febuxostat, a xanthine oxidase (XO) inhibitor and a pure antioxidant, on atrial remodeling.AF was produced by performing a 3-week rapid atrial pacing (400 bpm) in 13 dogs divided into three groups: pacing + febuxostat group (n = 5; atrial pacing with 50 mg/day of febuxostat (administration); pacing control group (n = 5; atrial pacing without any drug administration); and non-pacing group (n = 3). Electrophysiological studies were conducted in the first 2 groups every week. Atrial tissue fibrosis was evaluated by Azan and immunofluorescent staining of fibronectin. Oxidative stress was evaluated by DHE and FCF-DA staining.Shortening of the refractory period and increase in AF inducibility appeared gradually in the pacing control group, but such changes were suppressed in the pacing + febuxostat group (P = 0.05). The pacing control group showed increase in fibrosis, which was suppressed in the febuxostat group. In DHE and DCF-DA staining, the pacing control group showed an increase in oxidative stress, which was suppressed in the pacing + febuxostat group. The pacing control group exhibited fibronectin expression, which was suppressed in the pacing + febuxostat group.The antioxidant effect of febuxostat may achieve an inhibition of new-onset AF in canines.