Ventricular arrhythmia (VA) is the major cause of death in patients with left ventricular (LV) hypertrophy and/or acute ischemia. We hypothesized that apamin, a blocker of small-conductance Ca2+-activated K+ (SK) channels, alters Ca2+ handling and exhibits anti-arrhythmic effects in ventricular myocardium. Spontaneous hypertensive rats were used as a model of LV hypertrophy. A dual optical mapping of membrane potential (Vm) and intracellular calcium (Cai) was performed during global hypoxia (GH) on Langendorff perfusion system. The majority of pacing-induced VAs during GH were initiated by triggered activities. Pretreatment of apamin (100 nmol/L) significantly inhibited the VA inducibility. Compared with SK channel blockers (apamin and NS8593), non-SK channel blockers (glibenclamide and 4-AP) did not exhibit anti-arrhythmic effects. Apamin prevented not only action potential duration (APD80) shortening (−18.7 [95% confidence interval, −35.2-−6.05] ms vs −2.75 [95% CI, −10.45-12.65] ms, p = 0.04) but also calcium transient duration (CaTD80) prolongation (14.52 [95% CI, 8.8-20.35] ms vs 3.85 [95% CI, −3.3-12.1] ms, p < 0.01), thereby reducing CaTD80−APD80 which denotes "Cai/Vm uncoupling" (33.22 [95% CI, 22-48.4] ms vs 6.6 [95% CI, 0-14.85] ms, p < 0.01). The reduction of Cai/Vm uncoupling was attributable to less prolonged Ca2+ decay constant and suppression of diastolic Cai increase by apamin. The inhibition of VA inducibility and changes in APs/CaTs parameters caused by apamin were negated by the addition of ouabain, an inhibitor of Na+/K+ pump. Apamin attenuates APD shortening, Ca2+ handling abnormalities and Cai/Vm uncoupling, leading to inhibition of VA occurrence in hypoxic hypertrophied hearts.

This paper deals with a harmonic compensation method using a synchronous machine with resonant field circuits. Recently, harmonics have become one of the major problems in power systems and a lot of methods of harmonic suppression have been studied. The authors have proposed a new method of harmonic suppression using a synchronous machine excited with the 6th harmonic current. This paper shows that armature inductances for the 5th or 7th harmonics decrease when the field circuits are connected to capacitors resonating at the 6th harmonic. The variations of armature impedances are explained theoretically by Park's equations. The optimal capacitances are selected so as to resonate with field inductances for the short-circuited armature. The experiments to suppress the 5th and 7th harmonics using the synchronous machine are successful.96 SM 363-2 EC A paper recommended and approved by the IEEE Electric Machinery Commlttee of the IEEE Power Engineering Society for presentatlon at the 19% IEEBPES Summer

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geneity of HFpEF and are very important not only in the development of HFpEF, but also in the development of subsequent adverse events. 10,11 Despite HFpEF being a heterogeneous syndrome, most previous studies have dealt with all phenotypes of HFpEF in a similar manner. 12 In fact, the prognostic value of AF has been evaluated only in the whole HFpEF cohort, without subgroup analyses in each specific comorbidity. 6,13,14 This delays the characterization of HFpEF patients in whom AF may have a greater H eart failure (HF) with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) are coexisting conditions. The prevalence of HFpEF in AF is high, at around 20%, 1,2 and the prevalence of AF in HFpEF is as high as 32-61.5%. 3-5 AF is also an independent prognostic determinant in patients with HF. 6,7 Notably, the development of AF may have more unfavorable effects on clinical outcomes in patients with HFpEF than in those with HF with reduced ejection fraction (HFrEF). 8,9 Other comorbid conditions in HFpEF, such as hypertension, diabetes, obesity, chronic obstructive pulmonary disease, and coronary artery disease (CAD), result in hetero-Editorial p 374

Diabetic cardiomyopathy has been reported to increase the risk of fatal ventricular arrhythmia. The beneficial effects of the selective sodium-glucose co-transporter 2 inhibitor have not been fully examined in the context of anti-arrhythmic therapy, especially its direct cardioprotective effects despite the negligible SGLT2 expression in cardiomyocytes. We aimed to examine the anti-arrhythmic effects of empagliflozin (EMPA) treatment on diabetic cardiomyocytes, with a special focus on Ca2+ handling. We conducted echocardiography and hemodynamic studies and studied electrophysiology, Ca2+ handling, and protein expression in C57BLKS/J-leprdb/db mice (db/db mice) and their non-diabetic lean heterozygous Leprdb/+ littermates (db/+ mice).　Preserved systolic function with diastolic dysfunction was observed in 16-week-old db/db mice. During arrhythmia induction, db/db mice had significantly increased premature ventricular complexes (PVCs) than controls, which was attenuated by EMPA. In protein expression analyses, calmodulin-dependent protein kinase II (CaMKII) Thr287 autophosphorylation and CaMKII-dependent RyR2 phosphorylation (S2814) were significantly increased in diabetic hearts, which were inhibited by EMPA. Additionally, global O-GlcNAcylation significantly decreased with EMPA treatment. Furthermore, EMPA significantly inhibited ventricular cardiomyocyte glucose uptake. Diabetic cardiomyocytes exhibited increased spontaneous Ca2+ events and decreased sarcoplasmic reticulum (SR) Ca2+ content, along with impaired Ca2+ transient, all of which normalized with EMPA treatment. Notably, most EMPA-induced improvements in Ca2+ handling were abolished by the addition of an O-GlcNAcase (OGA) inhibitor. In conclusion, EMPA attenuated ventricular arrhythmia inducibility by normalizing the intracellular Ca2+ handling, and we speculated that this effect was, at least partly, due to the inhibition of O-GlcNAcylation via the suppression of glucose uptake into cardiomyocytes.

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