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Objective To investigate the transcriptomic changes in atherosclerosis after cetp knockout of zebrafish. Methods The gene editing technology CRISPR/Cas9 was used to knock out cetp of zebrafish to construct a homozygous mutant model. Total RNA of livers from wild type and cetp-/- model was extracted by the Trizol method, and gene expression profiles of cetp knockout were observed by transcriptomics. KEGG enrichment analysis was performed on significantly different expressed genes to explore the signal pathways it may affect. Results Homozygous mutant zebrafish that has a frameshift mutation of adding 5 base pairs was created through CRISPR/Cas9 technology. Transcriptomics analysis showed that the gene expression profile of zebrafish liver changed significantly after cetp knockout. A total of 3 808 different expressed genes were screened (P＜0.05), of which 1 918 genes were up-regulated and 1 890 genes were down-regulated. Genes related to lipid metabolism such as abca1 and abcg2a were significantly up-regulated and lipg were significantly down-regulated. Genes related to autophagy signaling pathways such as atg13 were significantly up-regulated, and down-regulated genes were enriched in related pathways such as DNA and RNA synthesis and the tricarboxylic acid cycle. Conclusions A zebrafish model with cetp knockout is established to study the mechanism of cholesteryl ester transfer protein (CETP) in atherosclerotic diseases. Although increased high-density lipoprotein cholesterol due to the inhibition of CETP prevents atherosclero-sis, inflammation is activated after cetp knockout in zebrafish and causes atherosclerosis. It suggests that CETP has a dual regulation mechanism in the development of atherosclerosis.

Background: Obesity is highly prevalent in patients with hypertrophic cardiomyopathy (HCM) and believed to influence its phenotype. Purpose: To explore the effects of obesity on left ventricular (LV) remodeling and long‐term clinical course in Chinese patients with HCM. Study Type: Longitudinal. Population: A total of 247 patients with HCM classified according to body mass index (BMI) (normal weight: BMI = 18.0–22.9 kg/m2 [N = 90]; overweight: BMI = 23.0–24.9 kg/m2 [N = 58]; and obese: BMI ≥ 25 kg/m2 [N = 99]). Field Strength/Sequence: 3.0 T/Balanced steady‐state free precession sequence and phase‐sensitive inversion recovery late gadolinium enhancement (LGE) sequence. Assessment: LV function and geometry were measured. LV peak strain analysis was performed. The presence and percentage of LGE in the LV were recorded. The endpoints including heart failure, sudden cardiac death, and overall composite outcome were assessed during a median follow‐up of 4.1 years (interquartile range, 3.0–6.2 years). Statistical Tests: One‐way analysis of variance, Kruskal–Wallis test, or chi‐square test; Pearson correlation coefficient (r); multivariable linear regression analysis; Kaplan–Meier survival analysis; and Cox proportional hazards model analysis were conducted. A two‐tailed P‐value < 0.05 was considered statistically significant. Results: Obese patients exhibited a significant progressive increase in LV mass compared with normal‐weight patients. The magnitude of all LV strain indices gradually and significantly decreased as BMI increased, whereas LV ejection fraction was not significantly different among BMI groups (P = 0.364). Multivariable linear regression analysis showed that obesity had a significant association with impaired strain indices as well as with indexed LV mass. Multivariable Cox model analysis retained obesity as an independent marker for future endpoints, and conveyed a > 3‐fold increase in risk compared with patients with normal weight (hazard ratio, 3.04; 95% confidence interval, 1.07–6.57). Data Conclusion: Obesity is an important environmental modifier that is associated with adverse LV remodeling and is independently associated with future clinical outcomes in Chinese patients with HCM. Level of Evidence: 3 Technical Efficacy: Stage 2 [ABSTRACT FROM AUTHOR]

The safety profiles when performing stress oxygenation‐sensitive magnetic resonance imaging (OS‐MRI) have raised concerns in clinical practice. Adenosine infusion can cause side effects such as chest pain, dyspnea, arrhythmia, and even cardiac death. The aim of this study was to investigate the feasibility of breathing maneuvers‐induced OS‐MRI in acute myocardial infarction (MI). This was a prospective study, which included 14 healthy rabbits and nine MI rabbit models. This study used 3 T MRI/modified Look‐Locker inversion recovery sequence for native T1 mapping, balanced steady‐state free precession sequence for OS imaging, and phase‐sensitive inversion recovery sequence for late gadolinium enhancement. The changes in myocardial oxygenation (ΔSI) were assessed under two breathing maneuvers protocols in healthy rabbits: a series of extended breath‐holding (BH), and a combined maneuver of hyperventilation followed by the extended BH (HVBH). Subsequently, OS‐MRI with HVBH in acute MI rabbits was performed, and the ΔSI was compared with that of adenosine stress protocol. Student's t‐test, Wilcoxon rank test, and Friedman test were used to compare ΔSI in different subgroups. Pearson and Spearman correlation was used to obtain the association of ΔSI between breathing maneuvers and adenosine stress. Bland–Altman analysis was used to assess the bias of ΔSI between HVBH and adenosine stress. In healthy rabbits, BH maneuvers from 30 to 50 s induced significant increase in SI compared with the baseline (all p < 0.05). By contrast, hyperventilation for 60 s followed by 10 s‐BH (HVBH 10 s) exhibited a comparable ΔSI to that of stress test (p = 0.07). In acute MI rabbits, HVBH 10 s‐induced ΔSIs among infarcted, salvaged, and the remote myocardial area were no less effectiveness than adenosine stress when performing OS‐MRI (r = 0.84; p < 0.05). Combined breathing maneuvers with OS‐MRI have the potential to be used as a nonpharmacological alternative for assessing myocardial oxygenation in patients with acute MI. Level of Evidence: 2 Technical Efficacy Stage: 2 [ABSTRACT FROM AUTHOR]

Background: Both acute and chronic myocardial infarction (AMI and CMI, respectively) exhibit delayed enhancement; however, clinical decision-making processes frequently require the differentiation of these two types of myocardial injury.Purpose: To investigate the reliability of AMI and CMI characterization using native T1 mapping and its feasibility for discriminating AMI from CMI.Study Type: Case-control.Animal Model: The study cohort comprised 12 AMI (mean post-MI, 3.75 ± 1.29 days) and 15 CMI (mean post-MI, 39.53 ± 6.10 days) Bama mini-pigs.Field Strength/sequence: Balanced steady-state free precession (bSSFP), segmented-turbo-FLASH-PSIR, and modified Look-Locker inversion recovery (MOLLI) sequences at 3.0T.Assessment: The infarct sizes were compared on matching short-axis slices of late-gadolinium-enhanced (LGE) images and T1 maps by two experienced radiologists.Statistical Tests: The infarct sizes were compared on matching short-axis slices of LGE images and T1 maps, and agreement was determined using linear regression and Bland-Altman analyses. The native T1 values were compared between AMI and CMI models (independent sample t-test). The intraclass correlation coefficient was used to assess inter- and intraobserver variability.Results: Measured infarct sizes did not differ between native T1 mapping and LGE images (AMI: P = 0.913; CMI: P = 0.233), and good agreement was observed between the two techniques (AMI: bias, -3.38 ± 19.38%; R2  = 0.96; CMI: bias, -10.55 ± 10.90%; R2  = 0.90). However, the native infarction myocardium T1 values and the T1 signal intensity ratio of infarct and remote myocardium (T1 SI ratio) did not differ significantly between AMI and CMI (P = 0.173).Data Conclusion: Noncontrast native T1 mapping can accurately determine acute and chronic infarct areas as well as conventional LGE imaging; however, it cannot distinguish acute from chronic MI.Level Of Evidence: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:1406-1414. [ABSTRACT FROM AUTHOR]

Background: Both acute and chronic myocardial infarction (AMI and CMI, respectively) exhibit delayed enhancement; however, clinical decision-making processes frequently require the differentiation of these two types of myocardial injury., Purpose: To investigate the reliability of AMI and CMI characterization using native T 1 mapping and its feasibility for discriminating AMI from CMI., Study Type: Case-control., Animal Model: The study cohort comprised 12 AMI (mean post-MI, 3.75 ± 1.29 days) and 15 CMI (mean post-MI, 39.53 ± 6.10 days) Bama mini-pigs., Field Strength/sequence: Balanced steady-state free precession (bSSFP), segmented-turbo-FLASH-PSIR, and modified Look-Locker inversion recovery (MOLLI) sequences at 3.0T., Assessment: The infarct sizes were compared on matching short-axis slices of late-gadolinium-enhanced (LGE) images and T 1 maps by two experienced radiologists., Statistical Tests: The infarct sizes were compared on matching short-axis slices of LGE images and T 1 maps, and agreement was determined using linear regression and Bland-Altman analyses. The native T 1 values were compared between AMI and CMI models (independent sample t-test). The intraclass correlation coefficient was used to assess inter- and intraobserver variability., Results: Measured infarct sizes did not differ between native T 1 mapping and LGE images (AMI: P = 0.913; CMI: P = 0.233), and good agreement was observed between the two techniques (AMI: bias, -3.38 ± 19.38%; R 2  = 0.96; CMI: bias, -10.55 ± 10.90%; R 2  = 0.90). However, the native infarction myocardium T 1 values and the T 1 signal intensity ratio of infarct and remote myocardium (T 1 SI ratio) did not differ significantly between AMI and CMI (P = 0.173)., Data Conclusion: Noncontrast native T 1 mapping can accurately determine acute and chronic infarct areas as well as conventional LGE imaging; however, it cannot distinguish acute from chronic MI., Level of Evidence: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:1406-1414., (© 2017 International Society for Magnetic Resonance in Medicine.)