Introduction The CLOSE protocol combines ablation index (AI) and ≤6 mm interlesion distance using standard power settings for the treatment of atrial fibrillation (AF). The purpose was to compare the safety and efficacy of a conventional CLOSE and a higher power shorter duration (HPSD)‐CLOSE pulmonary vein isolation (PVI) strategy. Methods and Results All consecutive patients referred for PVI were included after informed consent was obtained from them. Group 1 was treated with a standard CLOSE protocol and group 2 with a HPSD‐CLOSE protocol (45 W anterior and 35 W posterior). Procedural parameters and 6‐month follow‐up were analyzed. In total, 174 patients (group 1: n = 94 [paroxysmal: n = 74]; group 2: n = 80 [paroxysmal: n = 65], similar baseline characteristics) were included. PVI was reached in all, but procedure duration (82 ± 18 minutes vs 100 ± 22 minutes; P < .0001) and radiofrequency (RF) time (23 ± 5 minutes vs 36 ± 11 minutes; P < .0001) was shorter in group 2. First pass isolation was similar in groups 2 and 1 (left veins: 94% vs 90%; P = .42 and right veins: 83% vs 84%; P = .79, respectively). Six‐month off‐ antiarrhythmic drugs freedom of AF/AT was similar in groups 2 and 1 (82% [paroxysmal: 86%] vs 83% [paroxysmal: 88%]; P = .93, respectively). Major complications were similar (group 2: 1% vs group 1: 3%; P = .39). Conclusion A higher‐power short duration approach can shorten a CLOSE procedure and reduce ablation time without having a negative impact on safety or efficiency.

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Acute MI stimulates a spectrum of changes in remote vessels, including up-regulation of endothelial inflammatory adhesion molecules and platelet-endothelial adhesion from endothelial-associated VWF multimers. These remote arterial alterations persist longer in the presence of hyperlipidemia, are associated with accelerated plaque growth and inflammation, and are attenuated by Nox inhibition.

The third-generation tyrosine kinase inhibitor (TKI) ponatinib has been associated with high rates of acute ischemic events. The pathophysiology responsible for these events is unknown. We hypothesized that ponatinib produces an endothelial angiopathy involving excessive endothelial-associated von Willebrand factor (VWF) and secondary platelet adhesion. In wild-type mice and ApoE−/− mice on a Western diet, ultrasound molecular imaging of the thoracic aorta for VWF A1-domain and glycoprotein-Ibα was performed to quantify endothelial-associated VWF and platelet adhesion. After treatment of wild-type mice for 7 days, aortic molecular signal for endothelial-associated VWF and platelet adhesion were five- to sixfold higher in ponatinib vs sham therapy (P &lt; .001), whereas dasatinib had no effect. In ApoE−/− mice, aortic VWF and platelet signals were two- to fourfold higher for ponatinib-treated compared with sham-treated mice (P &lt; .05) and were significantly higher than in treated wild-type mice (P &lt; .05). Platelet and VWF signals in ponatinib-treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinant ADAMTS13. Ponatinib produced segmental left ventricular wall motion abnormalities in 33% of wild-type and 45% of ApoE−/− mice and corresponding patchy perfusion defects, yet coronary arteries were normal on angiography. Instead, a global microvascular angiopathy was detected by immunohistochemistry and by intravital microscopy observation of platelet aggregates and nets associated with endothelial cells and leukocytes. Our findings reveal a new form of vascular toxicity for the TKI ponatinib that involves VWF-mediated platelet adhesion and a secondary microvascular angiopathy that produces ischemic wall motion abnormalities. These processes can be mitigated by interventions known to reduce VWF multimer size.

Objectives To study safety and performance of the MANTA Vascular closure device (VCD) under real world conditions in 10 centers. Background The MANTA is a novel plug‐based device for large bore arteriotomy closure. Methods We included all eligible patients who underwent transfemoral large bore percutaneous procedures. Exclusion criteria were per operator's discretion and included severe calcification or marked tortuosity of the access vessel, presence of marked obesity/cachexia or a systolic blood pressure above 180 mmHg. The primary performance endpoint was time to hemostasis. Primary and secondary safety endpoints were major and minor access site related vascular complications up to 30 days, respectively. Vascular complications were adjudicated by an independent clinical event committee according to VARC‐2 criteria. We performed multivariable logistic regression to estimate the effect of baseline and procedural characteristics on any and major vascular complications. Results Between February 2018 and July 2019 500 patients were enrolled undergoing Transcatheter aortic valve replacement (TAVR, N = 496), Balloon aortic valvuloplasty (BAV, N = 2), Mechanical circulatory support (MCS, N = 1) or Endovascular aneurysm repair (EVAR, N = 1). Mean age was 80.8 ± 6.6 years with a median STS‐score of 2.7 [IQR 2.0–4.3] %. MANTA access site complications were major in 20 (4%) and minor in 28 patients (5.6%). Median time to hemostasis was 50 [IQR 20–120] sec. Severe femoral artery calcification, scar presence in groin, longer procedure duration, female gender and history of hypertension were independent predictors for vascular complications. Conclusion In this study, MANTA appeared to be a safe and effective device for large bore access closure under real‐world conditions.