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Aims Facial features were associated with increased risk of coronary artery disease (CAD). We developed and validated a deep learning algorithm for detecting CAD based on facial photos. Methods and results We conducted a multicentre cross-sectional study of patients undergoing coronary angiography or computed tomography angiography at nine Chinese sites to train and validate a deep convolutional neural network for the detection of CAD (at least one ≥50% stenosis) from patient facial photos. Between July 2017 and March 2019, 5796 patients from eight sites were consecutively enrolled and randomly divided into training (90%, n = 5216) and validation (10%, n = 580) groups for algorithm development. Between April 2019 and July 2019, 1013 patients from nine sites were enrolled in test group for algorithm test. Sensitivity, specificity, and area under the receiver operating characteristic curve (AUC) were calculated using radiologist diagnosis as the reference standard. Using an operating cut point with high sensitivity, the CAD detection algorithm had sensitivity of 0.80 and specificity of 0.54 in the test group; the AUC was 0.730 (95% confidence interval, 0.699–0.761). The AUC for the algorithm was higher than that for the Diamond–Forrester model (0.730 vs. 0.623, P Conclusion Our results suggested that a deep learning algorithm based on facial photos can assist in CAD detection in this Chinese cohort. This technique may hold promise for pre-test CAD probability assessment in outpatient clinics or CAD screening in community. Further studies to develop a clinical available tool are warranted.

Smooth muscle cells (SMCs), which form the walls of blood vessels, play an important role in vascular development and the pathogenic process of vascular remodeling. However, the molecular mechanisms governing SMC differentiation remain poorly understood. Glycoprotein M6B (GPM6B) is a four‐transmembrane protein that belongs to the proteolipid protein family and is widely expressed in neurons, oligodendrocytes, and astrocytes. Previous studies have revealed that GPM6B plays a role in neuronal differentiation, myelination, and osteoblast differentiation. In the present study, we found that the GPM6B gene and protein expression levels were significantly upregulated during transforming growth factor‐β1 (TGF‐β1)‐induced SMC differentiation. The knockdown of GPM6B resulted in the downregulation of SMC‐specific marker expression and repressed the activation of Smad2/3 signaling. Moreover, GPM6B regulates SMC Differentiation by Controlling TGF‐β‐Smad2/3 Signaling. Furthermore, we demonstrated that similar to p‐Smad2/3, GPM6B was profoundly expressed and coexpressed with SMC differentiation markers in embryonic SMCs. Moreover, GPM6B can regulate the tightness between TβRI, TβRII, or Smad2/3 by directly binding to TβRI to activate Smad2/3 signaling during SMC differentiation, and activation of TGF‐β‐Smad2/3 signaling also facilitate the expression of GPM6B. Taken together, these findings demonstrate that GPM6B plays a crucial role in SMC differentiation and regulates SMC differentiation through the activation of TGF‐β‐Smad2/3 signaling via direct interactions with TβRI. This finding indicates that GPM6B is a potential target for deriving SMCs from stem cells in cardiovascular regenerative medicine. stem cells 2018 Stem Cells 2019;37:190–201, In summary, the present study revealed that GPM6B play a crucial role in SMC differentiation. GPM6B promotes SMC differentiation through the activation of TGF‐β‐Smad2/3 signaling via regulating the tightness between TβRI and TβRII or Smad2/3 by directly binding to TβRI to activate Smad2/3 signaling, and activation of TGF‐β‐Smad2/3 signaling also facilitate the expression of GPM6B.

Background Esophageal injury caused by cryoballoon-based PVI is common. Cryoablation guided by transoesophageal echocardiography (TEE) for occlusion of the pulmonary vein (PV) is safe and effective. Objective To investigate the protective effect of mechanical displacement of the esophagus by TEE probe in cryoablation of atiral fibrillation. Methods Fifty patients with paroxysmal AF (PAF) were enrolled in the present study. 25 patients underwent cryoablation without TEE (non-TEE group) and the other 25 underwent with TEE (TEE group) for PV occlusion guidance and displacement of the esophagus. In the TEE group during the procedure, TEE was used to guide the movement of the balloon to achieve PV occlusion. And before freezing, the probe of the TEE was moved to displace the esophagus away from the PV being freezed in order to reduce the risk of cryoinjury. All patients underwent esophagogastroscopy within 2 days of the procedure. The patients were followed up in our center at regularly scheduled visits every 2 months. Results There was no significant difference between the TEE group and non-TEE group in regard to the procedure time. The fluoroscopy time in the TEE group was less compared to the non-TEE group (4.1±3.3 min vs. 16.6±6.9 min, P Conclusion Cryoablation of AF with TEE for protecting the esophagus from cryoinjury is safe and effective. Lower risk of esophageal injury can be achieved with the help of TEE probe movement for mechanical displacement of the esophagus during freezing. Funding Acknowledgement Type of funding source: None

Background There is increasing evidence that inflammatory biomarkers growth differentiation factor 15 (GDF-15) and neutrophil-lymphocyte ratio (NLR) appear to be associated with stroke and adverse cardiovascular events in patients with atrial fibrillation (AF). However, long-term impact of catheter ablation (CA) on GDF-15 and NLR is still unknown. Objective To evaluate the long-term change in GDF-15 and NLR after CA in paroxysmal AF patients. Methods A total of 58 paroxysmal AF patients were consecutively enrolled to perform CA. The inflammatory biomarkers GDF-15 and NLR were measured at baseline and 6-months postablation. Results All patients except one could complete 6-Months follow up. Fifty (87.7%) patients maintained sinus rhythm (SR group) and seven (12.3%) patients sustained AF recurrence (AFR group). No significant difference was noted in clinical and procedural characteristics between two groups (p>0.05), except mean fluoroscopy time (minutes 22±11.7 vs. 13±5.3, p=0.001) significantly longer in AFR than SR group. The GDF-15 (pg/ml 195±57 vs. 216±88, p=0.398), and NLR (% 1.8 (1.3–3) vs. 2.6 (1.4–3.4), p=0.395) were comparable at baseline in both SR and AFR groups respectively. At 6-months postablation, GDF-15 (pg/ml 133±41 vs. 195±57, p0.05) Conclusion Inflammatory biomarkers; GDF-15 and NLR significantly decreased at long-term on successful maintenance of sinus rhythm by CA in paroxysmal AF patients. Acknowledgement/Funding None

Background Baicalein, a specific lipoxygenase (LOX) inhibitor, has anti-inflammatory and antioxidant effects. However, the functional role of baicalein in angiotensin II (Ang II)-induced hypertension and cardiac remodeling remains unclear. Here we investigated the effect of baicalein on cardiac hypertrophy and fibrosis and the underlying mechanism. Methods Wild-type (WT) mice were injected with Ang II (1,200ng/kg/min) alone or together with 12/15-LOX inhibitor baicalein (25mg/kg) for 14 days. Histological examinations were performed on heart sections with hematoxylin and eosin, Masson's trichrome, wheat germ agglutinin staining, and immunohistochemistry. The messenger RNA (mRNA) expression of cytokines and protein levels were detected by real-time polymerase chain reaction (PCR) and western blot analysis respectively. Results Ang II infusion significantly increased blood pressure but decreased cardiac contractile function reflected by fractional shortening% and ejection fraction% compared with saline-treated mice. Moreover, Ang II infusion resulted in marked cardiac hypertrophy and fibrosis, promoted accumulation of macrophages and T cells, the expression of proinflammatory cytokines and malondialdehyde (MDA) production. However, these actions were markedly reversed by administration of baicalein in mice. Mechanistically, the protective effects of baicalein were associated with the inhibition of inflammation, oxidative stress, and multiple signaling pathways (AKT/mTOR, ERK1/2, nuclear factor-κB (NF-κB), and calcineurin) in the Ang II-treated mice. Conclusions This study demonstrates that baicalein can significantly ameliorate Ang II-induced hypertension and cardiac remodeling, and may be a novel therapeutic drug for prevention of hypertensive heart diseases.