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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for the diagnosis of brief episodes of arrhythmia, including paroxysmal AF, which are recorded as atrial high-rate episodes (AHREs), particularly in patients without ECGdocumented AF. 6 Using this technique, new-onset atrial tachyarrhythmia (AT)/AF can be diagnosed earlier in patients with CIEDs than in patients without CIEDs. AHREs detected using CIEDs are reportedly associated with an increased risk of stroke and systemic embolism, even in patients without any evidence of AF. 7 Furthermore, AHREs lasting longer (>5.5 h during a 30-day period) are associated with a double risk of embolic events. 8,9 Although Healey et al reported no association between subclinical AF and hospitalization for HF, 9 more recent studies have indicated that AHREs detected using CIEDs are associated with an increased risk of worsening HF. 10,11 Therefore, the correlation between AHREs detected using CIEDs and A trial fibrillation (AF) is a common cardiac tachyarrhythmia that is associated with an increased risk of stroke, heart failure (HF), and death. The presence of AF is reportedly associated with an increased risk of HF, regardless of its clinical pattern. 1,2 Changes in clinical AF (i.e., progression to permanent/persistent AF from paroxysmal AF, prolongation of AF duration, and/or increase in the left atrial size, etc.) are clinical predictors of HF. 1-5 However, clinically detecting AF in the early phase is not always easy, particularly in cases of asymptomatic AF. Although repeat ECG recording or 24-h ambulatory ECG monitoring are considered useful in detecting AF in the early phase, their sensitivities as detection tools are totally limited. 4 Continuous rhythm monitoring using cardiac implantable electronic devices (CIEDs) has recently been attempted

Optimal antithrombotic strategy for atrial fibrillation (AF) patients with a history of percutaneous coronary intervention (PCI) has been under debate. The actual prescription trend of antithrombotic therapy for these patients remains unclear, especially in chronic phase. Patients with AF having at least a 1-year history of PCI were retrospectively evaluated in 2010, 2012, 2014, and 2016. A total of 266 patients were finally enrolled in this study. The proportion of patients prescribed with oral anticoagulants (OACs) gradually increased over the study period (56%, 67%, 73%, and 74% in 2010, 2012, 2014, and 2016, respectively). According to the type of OACs, the proportion of direct oral anticoagulant (DOAC), launched in 2011, increased compared with warfarin (DOAC versus warfarin = 3% versus 64% in 2012, 24% versus 49% in 2014, and 32% versus 42% in 2016). Single antiplatelet therapy (SAPT) with OAC was the most popular prescription every year, and its proportion increased over the study period (41%, 44%, 55%, and 59%, respectively). The proportion of OAC monotherapy gradually increased (2%, 3%, 8%, and 9%, respectively), whereas that of triple therapy, i.e., dual antiplatelet therapy with OAC, gradually decreased (14%,

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A 57‐year‐old man was admitted to our hospital due to syncopal attack. He was diagnosed with Brugada syndrome due to which a subcutaneous implantable cardiac defibrillator (S‐ICD) was inserted using the standard technique. Two hours after the implantation, he experienced inappropriate shock while conscious. Device interrogation revealed a contentious baseline shift and frequent oversensing of low‐amplitude signals, which was followed by a shock. Lateral chest X‐ray revealed subcutaneous air surrounding the proximal electrode. Another inappropriate shock could be avoided by changing the sensing vector. The subcutaneous air was completely resolved 7 days after implantation.

Background Although the lesion size index (LSI) has been well established, it is sometimes difficult to achieve first‐pass pulmonary vein isolation (PVI) and to avoid acute pulmonary vein reconnections, even with LSI‐guided procedures. The purpose of this study was to assess the predictive accuracy of a novel parameter, the optimized lesion size index (o‐LSI), to perform PVI. Methods The voltage maps created by the Advisor™ high‐density (HD) grid catheter before PVI in 35 atrial fibrillation (AF) patients were examined for an association between the voltage amplitude and insufficient ablation sites (IAS), which were defined as either (i) spontaneous reconnection sites, (ii) dormant PV conduction sites unmasked with 20 mg of adenosine triphosphate disodium hydrate (ATP) injection, or (iii) PV‐LA gap sites after the initial PVI. Results IAS was observed in 25/1417 of the total ablation sites. IAS was significantly associated with higher bipolar voltage areas (4.20 ± 2.68 vs 2.43 ± 1.93 mV, P < .0001) but not with LSI. A novel index, o‐LSI (defined as LSI/bipolar voltage), was significantly lower in IAS than in others (1.14 [0.82, 1.81] vs 2.35 [1.31, 4.80] LSI/mV). By receiver operating characteristic analysis, an o‐LSI of 2.04 was the best cutoff value for the prediction of IAS (88% sensitivity and 55% specificity, P < .0001, areas under the curve: 0.742). Conclusion Low o‐LSI was strongly associated with IAS, potentially providing a novel index to improve first‐pass PV isolation.

previously healthy 7-year-old boy, who was diagnosed with B-cell precursor acute lymphoblastic leukemia without central nervous system infiltration, was being treated with the standard risk protocol of the Japanese Pediatric Leukemia/Lymphoma Study Group B12. He had already completed induction therapy, early intensification, and intensification without any severe adverse effects, and had just started the first reinduction therapy. After he had received oral dexamethasone 10 mg/m 2 daily from day 1, vincristine 1.5 mg/m 2 and pirarubicin 25 mg/m 2 on day 1, and L-asparaginase 10 000 U/m 2 on days 1 and 4, thunderclap headaches developed on days 6 and 7 without high blood pressure or abnormal electrolytes. Although the headaches improved with loperamide, cerebral magnetic resonance angiography on day 7 revealed vasoconstriction (Figure, A). Cerebrospinal fluid examination on the following day was normal. He continued with chemotherapy along with nifedipine and did not develop a headache until after finishing the entire chemotherapy regimen. Antithrombin III was replaced when its activity was <70%. The irregular narrowing arteries disappeared in 5 months without any parenchymal abnormalities (Figure, B), and we diagnosed it as reversible cerebral vasoconstriction syndrome (RCVS). 1 RCVS is characterized by thunderclap headaches with or without additional neurologic symptoms and vasoconstriction of the cerebral arteries. It spontaneously resolves in 1-3 months. 2 Although anticancer drugs are not generally considered to be putative precipitants, a few cases of RCVS complicated with cerebral infarction in pediatric patients with leukemia have been recently reported. 3-5 Tibussek et al 5 suspected that intrathecal cytarabine was associated with the vasoconstriction. However, our patient had not received intrathecal cytarabine for >3 weeks; the other drugs could have induced the condition. L-asparaginase is well known to cause thrombosis during chemotherapy induction, but that disorder is venous in general and does not appear similar to the arterial findings in our patient. 6 As cerebral infarction usually occurs after the first thunderclap headache, 2 appropriate intervention in RCVS may prevent the complications, such as infarction and hemorrhage. Nimodipine is usually given for the treatment and prevention of RCVS. 2 ■