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OBJECTIVE: Cardiac CT (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, using trans-oesophageal echocardiography (TEE) as the reference standard. DESIGN: Case-control study. SETTING: Patient data were collected from a tertiary hospital in China between 2017 and 2022. PARTICIPANTS: The study enrolled 726 patients (male: 60.2%, age: 61±11 years) who had both TEE and CCT before catheter ablation of atrial fibrillation. MEASURES: The CCT protocol consisted of one angiographic phase and one delayed scan 30 s 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. RESULTS: Of 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 >0.35 m/s and maximum diameters <10 mm were more prone to have CCT false-negative results. CONCLUSION: For patients undergoing catheter ablation for atrial fibrillation, CCT with a 30 s delay scan is less sensitive to LAA thrombi than TEE, especially for LAA-ostium thrombi with smaller sizes and higher LAA flow velocity.

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Objectives: Angiotensin II (Ang II) plays a key role in the regulation of myocardial hypertrophy via downstream cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1). However, it is still unclear whether Crim1 is involved in ionic channel remodeling. The study aimed to explore the effects of Crim1 on transient outward potassium current (Ito) and Kv4.2 (the main subunit of Ito channel) expression in hypertrophic ventricular cardiomyocytes. Materials and Methods: The ventricular cardiomyocytes were isolated from the neonatal rats. Hypertrophy was induced by Ang II. Crim1 expression was modulated by using adenovirus transfection. The expression of myosin heavy chain beta (ß-MHC), Crim1, and Kv4.2 was determined by RT-qPCR and western blot. The cellular surface area was assessed using Image J software. Ito was recorded by the whole-cell patch clamp technique. Results: Ang II-induced hypertrophy in cardiomyocytes was identified by their larger cellular surface area and higher mRNA expression of ß-MHC. Ang II significantly decreased the expression of Crim1 and Kv4.2 and reduced Ito current density. However, Crim1 overexpression abolished the Ang II-induced hypertrophy and preserved the expression of Kv4.2 and Ito current density. Conclusion: Crim1 overexpression inhibits Ang II-induced hypertrophy and preserves Ito current density via up-regulating Kv4.2 in ventricular cardiomyocytes from neonatal rats. Crim1 could have a role in the development of ventricular arrhythmia in hypertrophic hearts.

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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 Aß (CnAß) 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 CnAß protein expression, downregulation of Kv4.2 mRNA and protein expression, a decrease in I to current density, and prolongation of APD. CnAß gene knockdown significantly inhibited the effects of phenylephrine stimulation. Our data indicate that CnAß 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.

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BACKGROUND: The complexity of left atrial appendage (LAA) in patients with nonvalvular atrial fibrillation (NVAF) is closely related to LAA thrombosis and stroke incidence. But the classification of LAA morphology is not uniform and controversial. HYPOTHESIS: This study divided the LAA into two categories according to the LAA morphology to investigate the risk of thrombosis related to the LAA structural complexity in NVAF patients. METHODS: A total of 336 NVAF patients were enrolled continuously in this study. The patients were divided into thrombosis group and non-thrombosis group according to whether the thrombus presence in LAA. Through computer LAA three-dimensional reconstruction, LAA morphology was divided into the complex type and simple type according to with or without the clearly lobulated structure judged by imaging experts. The relationship between LAA thrombosis and various potential risk factors was analyzed. RESULTS: A total of 19 potential risk factors for LAA thrombosis in NVAF patients were enrolled into statistical analysis. The coincidence rate of LAA morphology classification was 96.4% (324/336) between two imaging experts. Multivariate logistic regression analysis showed that complex LAA morphology (OR 4.168, 95% CI 1.871-9.288, P < .001) was associated with the presence of LAA thrombus, independently of other enrolled risks. CONCLUSIONS: It is a concise and reliable method to divide the LAA morphology into complex type and simple type according to whether with the clearly lobulated structure. The complex LAA is an independent risk factor for LAA thrombosis in NVAF patients.

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[This corrects the article DOI: 10.3892/br.2019.1214.].

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OBJECTIVE: To explore the value of three-dimensional speckle-tracking imaging (3DSTI) in detecting left ventricular systolic function in patients with dilated cardiomyopathy (DCM). METHODS: Totally 31 DCM patients were enrolled in this study. Left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF) were measured using the 3DSTI, two-dimensional echocardiography (2DE), and magnetic resonance imaging (MRI). Left ventricular end-diastolic mass (EDmass) and left ventricular end-diastolic mass index (LVEDmass I) were also detected by 3DSTI and MRI. The differences in these measurements were analyzed and compared. RESULTS: The values of LVESV, LVEDV, and LVEF showed significantly positive correlations among 2DE group, 3DSTI group, and MRI group. The LVEF value showed significant difference among these three groups [(33.3 ± 11.1)%, (30.3 ± 10.6)%, and (26.2 ± 10.7)%; P = 0.04], whereas LVEDV and LVESV values were not significantly different (P > 0.05; respectively). Inter-group comparison showed the mean of LVEF was significantly lower in MRI group than in 2DE group (P = 0.031), whereas there was no significant difference between 2DE group and 3DSTI group and between 3DSTI group and MRI group (P > 0.05; respectively). The EDmass and EDmassI detected by 3DSTI and MRI were (143.2 ± 40.2) g vs (190.0 ± 58.3) g and (83.2 ± 21.1) g/m2 vs (110.1 ± 29.7) g/m2 (P < 0.001; respectively). CONCLUSIONS: The LVEF value detected by 3DSTI is closer to that detected by MRI in DCM patients.

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Left ventricular hypertrophy is a leading cause of heart failure and sudden death. Cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1) is expressed at a high level in the heart and has a regulatory role in heart development. The present study aimed to test the hypothesis that Crim1 can have an inhibitory function on ventricular hypertrophy. Rat primary ventricular myocytes were stretched to induce myocyte hypertrophy, and treated with telmisartan or infected with Crim1-expressing recombinant adenovirus (Ad-Crim1). Rat ventricular hypertrophy was induced by abdominal aortic coarctation (AAC), and treated either with telmisartan or myocardial injection of Ad-Crim1 or empty adenovirus vector. The results showed that the expression of Crim1 decreased in the hypertrophic ventricle. The inhibition of angiotensin receptor type 1 (AT1R) by telmisartan in vitro and in vivo significantly increased the expression of Crim1 in the left ventricle. The overexpression of Crim1 by infection with Ad-Crim1 significantly inhibited stretch-induced ventricular myocyte hypertrophy in vitro. The overexpression of Crim1 by gavage with AT1R inhibitor telmisartan or myocardial injection of Ad-Crim1 markedly suppressed AAC-induced left ventricular hypertrophy in vivo. These results suggest that Crim1 has a suppressive function on ventricular hypertrophy and provides a novel therapeutic target for the treatment of cardiac hypertrophy.

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Previous studies have shown that the activation of angiotensin II receptor type I (AT1 ) is attributed to cardiac remodeling stimulated by increased heart load, and that it is followed by the activation of the calcineurin-nuclear factor of activated T-cells (NFAT) signaling pathway. Additionally, AT1 has been found to be a regulator of cardiocyte ionic channel remodeling, and calcineurin-NFAT signals participate in the regulation of cardiocyte ionic channel expression. A hypothesis therefore follows that stretch stimulation may regulate cardiocyte ionic channel remodeling by activating the AT1 -calcineurin-NFAT pathway. Here, we investigated the role of the AT1 -calcineurin-NFAT pathway in the remodeling of inward rectifier potassium (Ik1 ) channel, in addition to its role in changing action potential, in stretch-induced hypertrophic atrial myocytes of neonatal rats. Our results showed that increased stretch significantly led to atrial myocytes hypertrophy; it also increased the activity of calcineurin enzymatic activity, which was subsequently attenuated by telmisartan or cyclosporine-A. The level of NFAT3 protein in nuclear extracts, the mRNA and protein expression of Kir2.1 in whole cell extracts, and the density of Ik1 were noticeably increased in stretched samples. Stretch stimulation significantly shortened the action potential duration (APD) of repolarization at the 50% and 90% level. Telmisartan, cyclosporine-A, and 11R-VIVIT attenuated stretch-induced alterations in the levels of NFAT3 , mRNA and protein expression of Kir2.1, the density of Ik1 , and the APD. Our findings suggest that the AT1 -calcineurin-NFAT signaling pathway played an important role in regulating Ik1 channel remodeling and APD change in stretch-induced hypertrophic atrial myocytes of neonatal rats.

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A persistent left superior vena cava (PLSVC) is formed by the remains of the oblique vein of the left atrium, which is not completely degenerated during embryonic development. The incidence is approximately 0.3% in the general population. Approximately 80-92% of PLSVCs drain into the right atrium through the coronary sinus. This report describes a rare case of PLSVC in which the coronary sinus (CS) did not open into the right atrium, but rather drained into the left subclavian vein through the PLSVC.

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We have investigated whether VEGF (vascular endothelial growth factor) regulates the proliferative capacity and eNOS (endothelial nitric oxide synthase)/NO (nitric oxide) pathway of EPCs (endothelial progenitor cells) by activating CaN (calcineurin)/NFAT (nuclear factor of activated T-cells) signalling. EPCs were obtained from cultured mononuclear cells isolated from the peripheral blood of healthy adults. Treatment with VEGF (50 ng/ml) potently promoted CaN enzymatic activity, activation of NFAT2, cell proliferation, eNOS protein expression and NO production. Pretreatment with cyclosporin A (10 µg/ml), a pharmacological inhibitor of CaN or 11R-VIVIT, a special inhibitor of NFAT, completely abrogated the aforementioned effects of VEGF treatment and increased apoptosis. The results indicate that VEGF treatment promotes the proliferative capacity of human EPCs by activating CaN/NFAT signalling leading to increased eNOS protein expression and NO production.

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