BackgroundCardiac computed tomography (CCT) is an emerging non-invasive modality for assessing left atrial appendage (LAA) thrombus, but the results were conflicting. Our study aims to evaluate the accuracy of CCT for detecting LAA thrombus in patients undergoing catheter ablation of atrial fibrillation (AF), using transesophageal echocardiography (TEE) as the reference standard.MethodsFrom May 2017 to December 2022, 726 patients (male: 60.2%, age: 61±11 years) who had both TEE and CCT before catheter ablation of AF were retrospectively included. The CCT protocol consisted of one angiographic phase and one delayed scan 30 seconds later. LAA thrombi were defined as solid masses on TEE or persistent defects on CCT. The thrombus dimension and location, the LAA filling and emptying flow velocity were assessed by TEE.ResultsOf the 57(7.9%) patients with LAA thrombi identified by TEE, 29(50.9%) were located at the LAA ostium, and 28(49.1%) were in the LAA. The former showed higher motility following blood flow and heartbeats than the latter. The CCT detected 14(48.3%) of the LAA-ostium thrombi but 25(89.3%) of those in the LAA (p= 0.001). The LAA-ostium thrombi with the LAA mean flow velocity higher than 0.35m/s and maximum diameters shorter than 10mm were more prone to have CCT false-negative results.ConclusionFor patients undergoing catheter ablation for AF, CCT with a 30s delay scan is less sensitive to LAA thrombi than TEE, especially LAA-ostium thrombi with smaller sizes and higher LAA flow velocity.Clinical perspective sectionWhat are new?Over half of the LAA thrombi were located at the LAA ostium.The CCT was less sensitive to the LAA-ostium thrombi with smaller sizes and higher LAA flow velocity.What is the clinical implication?1. The CCT using a 30s delay scan did not reliably exclude the LAA thrombi for the patients scheduled for pulmonary vein isolation, especially those located at the LAA ostium.

It has been shown that the activation of calcineurin is involved in regulating ion channel remodeling in hypertrophic cardiomyocytes. But the precise role of calcineurin in the regulation of transient outward potassium current (I to), an ion channel associated with fatal arrhythmia, remains controversial. This study aimed to examine the effects of calcineurin Aβ (CnAβ) gene knockdown on I to channel remodeling and action potential duration (APD) in the hypertrophic ventricular myocytes of neonatal rats. Results showed that phenylephrine stimulation caused hypertrophy of ventricular myocytes, upregulation of CnAβ protein expression, downregulation of Kv4.2 mRNA and protein expression, a decrease in I to current density, and prolongation of APD. CnAβ gene knockdown significantly inhibited the effects of phenylephrine stimulation. Our data indicate that CnAβ gene knockdown can inhibit I to channel remodeling and APD prolongation in hypertrophic neonatal rat ventricular myocytes. This finding suggests that calcineurin may be a potential target for the prevention of malignant ventricular arrhythmia in a hypertrophic heart.