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Introduction: The aim of the current study was to elucidated the reliable atrial fibrillation (AF) drivers identified by CARTOFINDER using OctaRay catheter. Methods and Results: The reliability of focal and rotational activations identified by CARTOFINDER using OctaRay catheter was assessed by the sequential recordings in each site of both atrium before and after pulmonary vein isolation (PVI) in 10 persistent AF patients. The outcome measures were the reproducibility rate during the sequential recordings and the stability rate between pre‐ and post‐PVI as reliable focal and rotational activations. The study results were compared with those under use of PentaRay catheter (N = 18). Total 68928 points of 360 sites in OctaRay group and 24 177 points of 311 sites in PentaRay were assessed. More focal activation sites were identified in OctaRay group than PentaRay group (7.9% vs. 5.7%, p <.001), although the reproducibility rate and the stability rate were significantly lower in OctaRay group (45.3% vs. 58.9%, p <.001; 11.2% vs. 28.4%, p <.001). Meanwhile, the prevalence of reproducible focal activation sites among overall points was comparable (3.6% vs. 3.3%, p =.08). Regarding rotational activation, more rotational activation sites were identified in OctaRay group (5.1% vs. 0.2%, p <.001), and the reproducibility rate and the stability rate were significantly higher in OctaRay group (45.2% and 12.5% vs. 0.0%, p <.001). Both reliable focal and rotational activation sites were characterized by significantly shorter AF‐cycle length (CL) and higher repetition of focal and rotational activations during the recordings compared with the sites of non or unreliable focal and rotational activations. Conclusion: In CARTOFINDER, OctaRay catheter could identify reliable focal activation with high resolution and reliable rotational activation compared with PentaRay catheter. The repetitive focal and rotational activations with short AF‐CL could be the potential target during ablation. [ABSTRACT FROM AUTHOR]

BACKGROUND:Despite its recommendation by the current guidelines, the role of long-term oral beta-blocker therapy has never been evaluated by randomized trials in uncomplicated ST-segment elevation myocardial infarction (STEMI) patients without heart failure, left ventricular dysfunction or ventricular arrhythmia who underwent primary percutaneous coronary intervention (PCI). METHODS AND RESULTS:In a multi-center, open-label, randomized controlled trial, STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06). CONCLUSION:Long-term carvedilol therapy added on the contemporary evidence-based medications did not seem beneficial in selected STEMI patients treated with primary PCI. TRIAL REGISTRATION:CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) ClinicalTrials.gov.number, NCT 01155635.

Aims: The mechanisms underlying the acute decompensation of heart failure (HF) remain unclear. The present study examined intracardiac dynamics during decompensated HF using echo-vector flow mapping., Methods and Results: Fifty patients admitted for decompensated HF were prospectively enrolled, and intracardiac energy loss (EL) was assessed by echo-vector flow mapping at admission (decompensated HF) and discharge (compensated HF). Outcome measures were average EL in the left ventricle (LV) in decompensated and compensated HF and were compared with those in 40 stable non-HF patients with cardiovascular diseases. The mean age of HF patients was 80.8 ± 12.4 years. The prevalence of both females and atrial fibrillation was 48.0%. The prevalence of HF with a reduced ejection fraction (<40%) (HFrEF) was 34.0%. The prevalence of decompensated HF classified into clinical scenario 1 was 33.3%. Blood pressure and NT-proBNP were significantly higher in decompensated HF than in compensated HF, while the ejection fraction (EF) was significantly lower. Average EL was significantly higher in compensated HF patients than in non-HF patients (40 mW/m·L vs. 26 mW/m·L, P = 0.047). A multivariable analysis identified age, systolic blood pressure, LVEF, and the absence of chronic obstructive pulmonary disease as independent risk factors for high LV-EL regardless of the presence of HF. Furthermore, average EL in HF patients was significantly higher under acute decompensated conditions than under compensated conditions (55 mE/m·L vs. 40 mE/m·L, [+18 mE/m·L, P = 0.03]). Higher EL under decompensated HF conditions was significant in non-HFrEF (+19 mW/m·L, P = 0.009) and clinical scenario 1 (+23 mW/m·L, P = 0.008). The multivariable analysis identified eGFR as an independent risk factor for a decrease in average LV-EL under decompensated conditions., Conclusions: Energy inefficiency in LV was apparent even in stable HF patients and significant under acute decompensated conditions, particularly in HF with preserved EF and clinical scenario 1., (© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: Pericardiocentesis under echocardiography guidance is a common procedure, but still poses a risk of injury to surrounding tissues. Nowadays, pericardiocentesis is being performed in patients with normal pericardium, for epicardial ablation or atrial appendage exclusion. Access to the normal pericardial space with the conventional needle procedure is very difficult. Thus, development of a novel method enabling safer pericardiocentesis is necessary. The present study aimed to assess the feasibility of using an originally developed ultrathin endoscopy-guided pericardiocentesis device in a swine model., Methods and Results: We developed a novel ultrathin endoscopy-guided pericardiocentesis device. The device comprised a 1.2 mm ultrathin endoscope, a 20 G needle, and a grasping forceps. Pericardiocentesis was conducted as follows. A 12 Fr introducer sheath was inserted between the pericardium and the diaphragm under fluoroscopy. The pericardium was grasped with the originally developed forceps under endoscopy guidance to create a space in the pericardial sac. The 20 G needle was then inserted and a coiled-tip guidewire was placed into the pericardial sac. Five independent operators performed pericardiocentesis twice using this technique in a healthy pig with a body weight of approximately 25 kg. Procedural success rate and procedure time were assessed as the primary endpoints. The procedural success rate was 100% in all operators. The average procedure time was 65 ± 40 seconds (median, 46 seconds; interquartile range, 40-85 seconds). No procedure-related complications were noted., Conclusions: The study results indicate that ultrathin endoscopy-guided pericardiocentesis for normal pericardial space is feasible and safe.

Percutaneous coronary intervention (PCI) for anomalous coronary arteries is often difficult because the support provided by the guide catheter is insufficient. We encountered a patient with severe three-vessel coronary disease including a totally occluded anomalous right coronary artery (RCA) originating from the left sinus of Valsalva. Initial PCI for the anomalous RCA via the transradial approach failed. Therefore, we constructed a three-dimensional (3D) aortocoronary model and conducted an in vitro simulation to plan the second PCI and found that a Judkins left (JL) 3.5 guide catheter in the power position yielded maximum backup support for the anomalous RCA. Thus, the second PCI was conducted using an 8 Fr JL 3.5 guide catheter in the power position via the transfemoral approach. The procedure was smooth and successful, without any adverse events. Our experience suggests that case-specific 3D models are useful for strategic planning of complex PCIs.

Background: Myocardial fractional flow reserve (FFR) is a reliable index in coronary intervention. A simple FFR measurement does not predict the true functional severity of an individual stenosis in multiple sequential coronary stenoses because of complex interaction between the stenoses. Application of the theoretical equations to predict the true FFR of individual stenosis is limited in a tandem lesion. Two novel equations applicable to a multiple sequential coronary stenoses are mathematically derived. One predicts the true FFR of each stenosis (equation A), and the other predicts the true FFR after releasing a given stenosis (equation B). The present study aimed to validate the two derived equations in an in vitro model of coronary circulation., Methods and Results: Predictive FFR was compared with true FFR in an in vitro model of three sequential stenoses using linear regression analysis. The difference between apparent FFR and true FFR was compared with the difference between predictive FFR and true FFR. The legitimacy of equation A was first assessed. A close correlation was found between predictive FFR and true FFR (r² = 0.92). The difference between predictive FFR and true FFR was significantly lower compared to the difference between apparent FFR and true FFR (0.18 ± 0.10 vs 0.05 ± 0.05; P<.001). The legitimacy of equation B was also assessed, and a close correlation was found (r² = 0.97). The difference was significantly lower when we applied equation B (0.13 ± 0.06 vs 0.04 ± 0.02; P<.001)., Conclusions: Equations A and B strongly predict the true value of FFR in the experimental model of coronary circulation.