Ruijuan Han

Background: Insulin resistance is closely associated with pericardial fat. In this prospective study, we aimed to compare the utility of six surrogate insulin resistance indices, including the triglyceride glucose (TyG) index, TyG-waist circumference (TyG-WC), TyG-waist-to-height ratio (TyG-WHtR), lipid accumulation production (LAP), visceral adiposity index (VAI), and Chinese VAI (CVAI) in predicting pericardial fat accumulation on noncontrast computed tomography. Methods: The six surrogate insulin resistance indices (TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI) were calculated using their respective formulae. The pericardial fat volume (PFV) was obtained from noncontrast computed tomography scans and categorized into PFV-low (PFV-L) and PFV-high (PFV-H) via the Youden statistic according to the risk for atherosclerotic cardiovascular disease (ASCVD). A logistic regression model, receiver operating characteristic (ROC) curves, and generalized additive model were used for statistical analyses. Results: Overall, 2,735 adults were analyzed. The TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI were significantly higher in the PFV-H group than in the PFV-L group. All six insulin resistance surrogates showed significant positive correlations with PFV. The CVAI demonstrated the highest predictive value for assessing PFV, followed by TyG-WC, TyG-WHtR, LAP, TyG, and VAI. The CVAI was associated with the largest increase in PFV based on the original model [age, sex, diabetes, hypertension, hyperlipidemia, and estimated glomerular filtration rate (eGFR)] as compared to the other insulin resistance indices. Conclusions: The TyG, TyG-WC, TyG-WHtR, LAP, VAI, and CVAI were positively associated with PFV in patients without overt cardiovascular diseases. The CVAI may effectively reflect PFV accumulation.

Background Endothelial cells (ECs) can confer neuroprotection by secreting molecules. This study aimed to investigate whether DNA methylation contributes to the neuroprotective gene expression induced by hypoxia preconditioning (HPC) in ECs and to clarify that the secretion of molecules from HPC ECs may be one of the molecular mechanisms of neuroprotection. Methods Human microvascular endothelial cell-1 (HMEC-1) was cultured under normal conditions (C), hypoxia(H), and hypoxia preconditioning (HPC), followed by the isolation of culture medium (CM). SY5Y cell incubated with the isolated CM from HMEC-1 was exposed to oxygen-glucose deprivation (OGD). The DNA methyltransferases (DNMTs), global methylation level, miR-126 and its promotor DNA methylation level in HMEC-1 were measured. The cell viability and cell injury in SY5Y were detected. Results HPC decreased DNMTs level and global methylation level as well as increased miR-126 expression in HMEC-1. CM from HPC treated HMEC-1 also relieved SY5Y cell damage, while CM from HMEC-1 which over-expression of miR-126 can reduce injury in SY5Y under OGD condition. Conclusions These findings indicate EC may secrete molecules, such as miR-126, to execute neuroprotection induced by HPC through regulating the expression of DNMTs.

Circular RNA (circRNA) has been reported to be involved in the pathogenesis of cardiovascular disease; however, it is unclear whether circRNA carried by exosomes (exos) can be used as biomarkers for chronic coronary syndrome (CCS). High-throughput sequencing was carried out in the plasma exosomal RNA of 15 CCS patients and 15 non-cardiac chest pain patients (NCCP, control group) to screen for differentially expressed circRNAs. Selected differentially expressed exo-circRNAs were further verified by real-time polymerase chain reaction in a small-sample cohort and a large-sample cohort. A total of 276 circRNAs were differentially expressed in the plasma exosomes of CCS patients, with 103 up-regulated and 173 down-regulated. Among the 103 up-regulated circRNAs, 5 circRNAs with high expression levels were selected for validation. Real time quantitative PCR of the first and second validation cohort demonstrated that exo-hsa_circ_0075269 and exo-hsa_circ_0000284 were significantly up-regulated in patients with CCS. Circulating exo-hsa_circ_0075269 and exo-hsa_circ_0000284 yielded the area under the curve values of 0.761 (p < 0.001, 95%CI = 0.669, 0.852) and 0.623 (p = 0.015, 95%CI = 0.522, 0.724) for CCS, respectively, by ROC curve analysis. In conclusion, the expression profile of circRNA in plasma exosomes of patients with CCS was significantly different from that of the control group. Plasma exo-hsa_circ_0075269 and exo-hsa_circ_0000284 have the potential to be new biomarkers for CCS.

Purpose: This study aims to develop a low-radiation dose, one-step integrated coronary–carotid–cerebral computed tomography angiography (ICCC-CTA) technique to analyze the relationship between cardiovascular and cerebrovascular atherosclerosis and evaluate the risk factors of plaque to provide an early-stage treatment to patients and reduce vascular events. Methods: A total of 300 consecutive asymptomatic patients with cardiovascular risk factors who underwent ICCC-CTA were enrolled in this prospective study. The association between coronary and carotid-cerebrovascular atherosclerosis was assessed. The primary cardiovascular risk factors for various plaque types in cardiovascular or cerebrovascular disease were evaluated using multivariate analysis. Results: Among 300 patients, 189 (63%) had plaques in their coronary and cerebral arteries. The presence of calcified and mixed plaques in the carotid-cerebral and coronary arteries was strongly correlated (χ² = 20.71, P = 0.001; χ² = 8.96, P = 0.003, respectively). Multivariate logistic regression analysis revealed that abnormal blood glucose [OR = 1.44, 95% CI 0.12–0.62, P = 0.01] and abnormal total cholesterol [OR = 1.28, 95% CI 0.07–0.46, P = 0.01] are risk factors in all the models in the coronary artery, non-calcified plaque group. Abnormal blood glucose [OR = 1.43, 95% CI 0.11–0.61, P = 0.01] and abnormal systolic blood pressure [OR = 1.02, 95% CI 0.01–0.04, P = 0.02] are risk factors in all the models in the coronary artery calcified plaque group. Abnormal blood glucose level [OR = 1.44, 95% CI = 0.12–0.62, P = 0.01] was only a risk factor in the non-calcified plaque carotid–cerebral artery group. Conclusions: We confirm that elevated blood glucose and total cholesterol levels are associated with coronary and carotid-cerebrovascular plaques using the novel one-step low dose cerebral-carotid-cardiac CTA technique. These findings will provide insights for further studies focusing on developing low-radiation dose one-step ICCC-CTA to screen cardiovascular/cerebrovascular plaques in general population with cardiovascular risk factors. Advances in knowledge: We developed a low–radiation dose, one-step ICCC-CTA technique to detect cardiovascular and cerebrovascular atherosclerosis. We evaluated the risk factors for plaque burden for the early treatment and reduction of vascular events. These findings supported the development of low–radiation dose one-step ICCC-CTA to screen for cardiovascular/cerebrovascular disease in general population with cardiovascular risk factors.

Objectives To evaluate myocardial viability in patients with myocardial ischemia reperfusion injury (MIRI) via dual-energy computed tomography myocardial blood pool imaging (DECT MBPI). Methods Between September 2017 and January 2019, we prospectively recruited 59 patients with acute myocardial infarction (AMI) who developed MIRI after revascularization during invasive coronary angiography (ICA). Then, they received DECT MBPI, SPECT, and PET sequentially within 1 week after the onset of MIRI. A total of 1003 myocardial segments of 59 patients were recruited for this study. The iodine reduction areas and delayed enhancement areas were calculated by cardiac iodine map with SPECT rest myocardial perfusion imaging (MPI) + PET myocardial metabolism imaging (MMI) as reference criteria. The paired sample t-test was used to measure the difference of the myocardial iodine value. Cohen’s Kappa analysis was used to test the consistency among different observers. ROC analysis was used to calculate the myocardial viability of DECT MBPI. Results ROC showed the AUCs of DECT MBPI iodine value to identify a normal myocardium, an ischemic myocardium, and an infarcted myocardium were 0.957, 0.900, and 0.906 (p < 0.001). The sensitivity, specificity, and accuracy of DECT MBPI in identifying an ischemic myocardium were 87.6%, 89.3%, and 97.9% (p < 0.001). The sensitivity, specificity, and accuracy of DECT MBPI in identifying an infarcted myocardium were 88.9%, 92.2%, and 98.6% (p < 0.001). The cutoff value for DECT MBPI to differentiate between an ischemic and a normal myocardium was 0.84 mg I/mL. The cutoff value for DECT MBPI to differentiate between an infarct and a normal myocardium was 2.01 mg I/mL. Conclusion DECT MBPI can be used to assess myocardial viability in patients with MIRI with high sensitivity and specificity. Key Points • Dual-energy computed tomography myocardial blood pool imaging (DECT MBPI) can evaluate myocardial viability of myocardial ischemia-reperfusion injury (MIRI). • DECT MBPI is a non-invasive and timesaving method for evaluation on myocardial ischemia-reperfusion injury in patients with acute myocardial infarction after coronary intervention

Background. It has been reported that ischemia and ischemic preconditioning (IPC) have different effects on the expression of tuberous sclerosis complex 1 (TSC1), which may contribute to the tolerance to ischemia/hypoxia with the increase of autophagy. The mechanisms of TSC1 differential expression are still unclear under ischemia/IPC conditions in hippocampal Cornu Ammon 1 (CA1) and Cornu Ammon 3 (CA3) area neuronal cells. While we have shown that 5‐Aza‐CdR, a DNA methyltransferase inhibitor, can upregulate TSC1 and increase hypoxic tolerance by autophagy in vivo and in vitro, in this study, we examined whether DNA methylation was involved in the differential expression of TSC1 in the CA1 and CA3 regions induced by hypoxic preconditioning (HPC). Methods. Level of rapamycin (mTOR) autophagy, a downstream molecular pathway of TSC1/TSC2 complex, was detected in HPC mouse hippocampal CA1 and CA3 areas as well as in the HPC model of mouse hippocampal HT22 cells. DNA methylation level of TSC1 promoter (‐720 bp~ ‐360 bp) was determined in CA1 and CA3 areas by bisulfite‐modified DNA sequencing (BMDS). At the same time, autophagy was detected in HT22 cells transfected with GFP‐LC3 plasmid. The role of TSC1 in neuroprotection was measured by cell viability and apoptosis, and the role of TSC1 in metabolism was checked by ATP assay and ROS assay in HT22 cells that overexpressed/knocked down TSC1. Results. HPC upregulated the expression of TSC1, downregulated the level of P‐mTOR (Ser2448) and P‐p70S6K (Thr389), and enhanced the activity of autophagy in both in vivo and in vitro. The increased expression of TSC1 in HPC may depend on its DNA hypomethylation in the promoter region in vivo. HPC also could reduce energy consumption in HT22 cells. Overexpression and knockdown of TSC1 can affect cell viability, cell apoptosis, and metabolism in HT22 cells exposed to hypoxia. Conclusion. TSC1 expression induced by HPC may relate to the downregulation of its DNA methylation level with the increase of autophagy and the decrease of energy demand.

At present, artificial intelligence (AI) has already been applied in cardiovascular imaging (e.g., image segmentation, automated measurements, and eventually, automated diagnosis) and it has been propelled to the forefront of cardiovascular medical imaging research. In this review, we presented the current status of artificial intelligence applied to image analysis of coronary atherosclerotic plaques, covering multiple areas from plaque component analysis (e.g., identification of plaque properties, identification of vulnerable plaque, detection of myocardial function, and risk prediction) to risk prediction. Additionally, we discuss the current evidence, strengths, limitations, and future directions for AI in cardiac imaging of atherosclerotic plaques, as well as lessons that can be learned from other areas. The continuous development of computer science and technology may further promote the development of this field.

Objective:We assessed the diagnostic value of “one-step” dual-energy computed tomography (DECT) in combination with coronary CT angiography and iodine mapping within the myocardial blood pool in detecting AMI.Methods:Five minipigs were subjected to transcatheter embolization of coronary artery with a gelatin sponge to induce AMI. Arterial-phase myocardial DECT imaging was carried out 1 h before and 24 h after embolism of the coronary. Color-coded iodine maps were used to evaluate myocardial blood pool deficits in the 17-segment model. Myocardial DECT imaging 24 h after MI induction was used for final comparison with post-mortem histology. Results:We found a sensitivity of 95.55% and a specificity of 95%, respectively, for AMI detection by DECT-based iodine mapping within the myocardial blood pool. The DLP values were 219.4 ± 60.9 mGy.cm (172 ~ 321 mGy.cm) and the effective radiation dose was 5.7 ± 1.5 mSv (4.4 ~ 8.3 mSv).Conclusion:This experimental study demonstrated that DECT-based iodine mapping shows ...