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Virus-like particles (VLPs) are used as nanocontainers for targeted drug, protein, and vaccine delivery. The phage P22 VLP is an ideal macromolecule delivery vehicle, as it has a large exterior surface area, which facilitates multivalent genetic and chemical modifications for cell recognition and penetration. Arginine-rich cell-penetrating peptides (CPPs) can increase cargo transport efficiency in vivo . However, studies on the tissue distribution and retention of P22 VLPs mediated by TAT and 8R are lacking. This study aimed to analyze the TAT and 8R effects on the P22 VLPs transport efficiency and tissue distribution both in vitro and in vivo . We used a prokaryotic system to prepare P22 VLP self-assembled particles and expressed TAT-or 8R-conjugated mCherry on the VLP capsid protein as model cargoes and revealed that the level of P22 VLP-mCherry penetrating the cell membrane was low. However, both TAT and 8R significantly promoted the cellular uptake efficiency of P22 VLPs in vitro , as well as enhanced the tissue accumulation and retention of P22 VLPs in vivo . At 24 h postinjection, TAT enhanced the tissue distribution and retention in the lung, whereas 8R could be better accumulation in brain. Thus, TAT was superior in terms of cellular uptake and tissue accumulation in the P22 VLPs delivery system. Understanding CPP biocompatibility and tissue retention will expand their potential applications in macromolecular cargo delivery., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Su, Shen, Shi, Li, Chen, Yang, Sun, Tang, Wang, Wang, Cai, Lu, An, Yang and Meng.)

The porcine reproductive and respiratory syndrome virus (PRRSV) is a highly significant infectious disease that poses a substantial threat to the global pig industry. In recent years, the NADC30-like strain has gradually emerged as prevalent in China, causing a profound impact on the country's pig farming industry. Therefore, it is important to conduct an in-depth study on the characteristics and gene functions of the NADC30-like strain. An infectious cDNA clone is an indispensable tool for investigating the functions of viral genes. In this current study, we successfully isolated a NADC30-like strain and constructed its full-length infectious cDNA clone. The utilization of this clone will facilitate our investigation into the viral replication, pathogenesis, and immune response associated with the PRRSV NADC30-like strain., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Qiao, Wang, Lu, Wang, Zhang, Gu, Cai, Xu, Chen and Tang.)

N -glycosylation is a highly conserved glycan modification that plays crucial roles in various physiological processes, including protein folding, trafficking, and signal transduction. Porcine deltacoronavirus (PDCoV) poses a newly emerging threat to the global porcine industry. The spike protein of PDCoV exhibits a high level of N -glycosylation; however, its role in viral infection remains poorly understood. In this study, we applied a lentivirus-based entry reporter system to investigate the role of N -glycosylation on the viral spike protein during PDCoV entry stage. Our findings demonstrate that N -glycosylation at positions 652 and 661 of the viral spike protein significantly reduces the infectivity of PDCoV pseudotyped virus. Overall, our results unveil a novel function of N -glycosylation in PDCoV infection, highlighting its potential for facilitating the development of antiviral strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Wang, Qiao, Liu, Cai, Yang, Lu and Tang.)

Pseudorabies virus (PRV) is an important swine virus that has a significant impact on the global swine industry. PRV is a member of the herpesvirus family, specifically the alphaherpesvirus subfamily, and has been extensively utilized as a prototype herpesvirus. Notably, recent studies have reported that PRV sporadically spills over into humans. The PRV genome is approximately 150 kb in size and is difficult to manipulate at the genomic level. The development of clustered regularly interspaced short palindromic repeat-associated protein (CRISPR/Cas9) technology has revolutionized PRV genome editing. CRISPR/Cas9 has been widely used in the construction of reporter viruses, knock-out/knock-in of genes of interest, single virus tracking and antiviral strategies. Most importantly, for vaccine development, virulence gene knockout PRV vaccine candidates can be obtained within 2 weeks using CRISPR/Cas9. In this mini-review, we provide a concise overview of the application of CRISPR/Cas9 in PRV research and mainly share our experience with methods for efficiently editing the PRV genome. Through this review, we hope to give researchers better insight into the genome editing of pseudorabies virus., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wang, Qiao, Cai, Tan, Na, Wang, Lu and Tang.)

Both autophagy and apoptosis are mechanisms that maintain homeostasis in cells and that play essential roles in viral infections. Previous studies have demonstrated that autophagy and apoptosis pathways occurred with complex relationships in virus-infected cells. However, the regulation between these two processes in Pseudorabies virus (PRV) infection remains unclear. In the present study, we demonstrated that activated autophagy was induced at the early stage of PRV infection and that apoptosis was induced at the late stage of infection. Autophagy induction inhibited apoptosis and decreased viral replication, and autophagy inhibition promoted apoptosis and increased viral replication. We also found that viral infection resulted in an increase in the production of reactive oxygen species (ROS) and activation of apoptosis in autophagy-impaired cells, suggesting that ROS may participate in the cross-talk between autophagy and apoptosis in PRV-infected cells. Our studies provide possible molecular mechanisms for the cross-talk between apoptosis and autophagy induced by PRV infection in porcine cells. This suggests that these two cell death processes should be considered as the same continuum rather than as completely separate processes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Sun, Hou, Song, Lyu, Tang, Qin, Liu, Wang, Meng and Cai.)

Background: Observational studies have shown inconsistent results of the associations between type 2 diabetes mellitus (T2DM) and blood lipid profiles, while there is also a lack of evidence from randomized controlled trials (RCTs) for the causal effects of T2DM on blood lipid profiles and lipoprotein subclasses., Objectives: Our study aimed at investigating the causal effects of T2DM on blood lipid profiles and concentration of particle-size-determined lipoprotein subclasses by using the two-sample Mendelian randomization (MR) method., Methods: We obtained genetic variants for T2DM and blood lipid profiles including high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC) from international genome-wide association studies (GWASs). Two-sample MR method was applied to explore the potential causal effects of genetically predicted T2DM on blood lipid profiles based on different databases, respectively, and results from each MR analysis were further meta-analyzed to obtain the summary results. The causal effects of genetically predicted T2DM on the concentration of different subclasses of lipoproteins that are determined by particle size were also involved in MR analysis., Results: Genetically predicted 1-unit higher log odds of T2DM had a significant causal effect on a higher level of TG (estimated β coefficient: 0.03, 95% confidence interval [CI]: 0.00 to 0.06) and lower level of HDL-C (estimated β coefficient: -0.09, 95% CI: -0.11 to -0.06). The causality of T2DM on the level of TC or LDL-C was not found (estimated β coefficient: -0.01, 95% CI: -0.02 to 0.01 for TC and estimated β coefficient: 0.01, 95% CI: -0.01 to 0.02 for LDL-C). For different sizes of lipoprotein particles, 1-unit higher log odds of T2DM was causally associated with higher level of small LDL particles, and lower level of medium HDL particles, large HDL particles, and very large HDL particles., Conclusion: Evidence from our present study showed causal effects of T2DM on the level of TG, HDL-C, and concentration of different particle sizes of lipoprotein subclasses comprehensively, which might be particularly helpful in illustrating dyslipidemia experienced by patients with T2DM, and further indicate new treatment targets for these patients to prevent subsequent excessive cardiovascular events from a genetic point of view., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Chen, Zheng, Shao, Zhou, Yang, Huang and Tang.)

Background and Aims: Early detection of mortality after percutaneous coronary intervention (PCI) is crucial, whereas most risk prediction models are based on outdated cohorts before the year 2000. This study aimed to establish a nomogram predicting 30-day mortality after PCI., Materials and Methods: In total, 10,444 patients undergoing PCI in National Center for Cardiovascular Diseases in China were enrolled to establish a nomogram to predict 30-day mortality after PCI. The nomogram was generated by incorporating parameters selected by logistic regression with the stepwise backward method., Results: Five features were selected to build the nomogram, including age, male sex, cardiac dysfunction, STEMI, and TIMI 0-2 after PCI. The performance of the nomogram was evaluated, and the area under the curves (AUC) was 0.881 (95% CI: 0.8-0.961). Our nomogram exhibited better performance than a previous risk model (AUC = 0.7, 95% CI: 0.586-0.813) established by Brener et al. The survival curve successfully stratified the patients above and below the median score of 4., Conclusion: A novel nomogram for predicting 30-day mortality was established in unselected patients undergoing PCI, which may help risk stratification in clinical practice., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Song, Liu, Wang, Chen, Yang, Wen, Gao, Shao and Tang.)

In the last decade, the emergence of QYYZ-like porcine reproductive and respiratory syndrome virus (PRRSV) has attracted increasing attention due to the high incidence of PRRSV mutation and recombination. However, the endemic status and genomic characteristics of the QYYZ-like strains are unclear. From 2018 to October 2021, 24 QYYZ-like PRRSV isolates were obtained from 787 PRRSV-positive clinical samples. Only one QYYZ-like positive sample was from a northern province, and the rest were from central and southern provinces. We selected 9 samples for whole-genome sequencing, revealing genome lengths of 15,008-15,316 nt. We retrieved all the available whole-genome sequences of QYYZ-like PRRSVs isolated in China from 2010 to 2021 ( n = 28) from GenBank and analyzed them together with the new whole-genome sequences ( n = 9). Phylogenetic tree analysis based on the ORF5 gene showed that all QYYZ-like PRRSV strains belonged to sublineage 3.5 but were clustered into three lineages (sublineage 1.8, sublineage 3.5, and sublineage 8.7) based on whole-genome sequences. Genomic sequence alignment showed that QYYZ-like strains, have characteristic amino acids insertions or deletions in the Nsp2 region (same as NADC30, JXA1 and QYYZ) and that thirteen strains also had additional amino acid deletions, mostly between 468 and 518 aa. Moreover, QYYZ-like strains (sublineage 3.5) have seven identical characteristic amino acid mutations in ORF5. Recombination analysis revealed that almost all QYYZ-like complete genome sequences (36/37) were products of recombination and mainly provided structural protein fragments (GP2-N) for the recombinant strains. Overall, QYYZ-like strains were mainly prevalent in central and southern China from 2018 to 2021, and these strains provided recombinant fragments in the PRRSV epidemic in China., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Xu, Xiang, Tang, Li, Zhao, Gong, Sun, Leng, Peng, Wang, Zhou, An, Cai, Tian, Zhang and Song.)

Objectives: The aim of this study was to analyze long-term outcomes of Chinese coronary artery disease (CAD) patients with (and without) chronic obstructive pulmonary disease (COPD) after percutaneous coronary intervention (PCI)., Background: Chronic obstructive pulmonary disease is a chronic condition which often develops in conjunction with CAD. PCI is a core therapy for CAD, although we still need to understand CAD-COPD outcomes and to identify factors that influence prognoses, across ethnicities., Methods: This double-cohort study involved 12,343 Chinese CAD patients who received PCI. Baseline characteristics were collected in two independent, specialty centers. Propensity-score matching was performed to control confounding factors, using a nearest neighbor matching method within a 0.02 caliper and on a propensity score scale of 0.1 for each center. Comorbid CAD-COPD cases were compared to non-COPD patients in terms of major adverse cardiac events (MACEs)., Results: Patients with COPD were generally older than those without COPD (65.4 ± 9.2 vs. 58.2 ± 10.3, p < 0.001). There were no significant differences in the end points between COPD and non-COPD groups after PCI (All p > 0.05); however, the incidence of MACEs increased after 450 days. Further subgroup analysis suggests that COPD is approximately four times more prevalent among those aged over 75 years (HR, 3.818; 95%CI, 1.10-13.29; p = 0.027) and those aged below 55 years (HR = 4.254; 95% CI, 1.55-11.72; p = 0.003)., Conclusion: Having COPD does not appear to have a significant impact on CAD outcomes 2 years after PCI, and beyond. However, an increasing number of MACEs was observed after 450 days, which suggests that there may be a double-stage effect of COPD on PCI prognosis. There is a need for focused comorbidity management, specifically for those aged below 55 years and above 75 years., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer ZT declared a shared affiliation with the authors YZ, JY, CL, and XW to the handling editor at the time of review., (Copyright © 2022 Zheng, Qi, Seery, Wang, Zhao, Shen, Zhou, Yang, Li, Wang, Gao, Meng, Dong and Tang.)

Background: Observational studies have shown an association between early age at menarche (AAM) and myocardial infarction (MI) with recorded cases. In this Mendelian randomization (MR) study, we used large amounts of summary data from genome-wide association studies (GWASs) to further estimate the association of genetically predicted AAM with genetically predicated risk of MI and investigate to what extent this association is mediated by genetically determined lifestyles, cardiometabolic factors, and estrogen exposure., Methods: A two-step, two-sample MR study was performed by mediation analysis. Genetic variants identified by GWAS meta-analysis of reproductive genetics consortium ( n = 182,416) were selected for genetically predicted AAM. Genetic variants identified by the Coronary ARtery DIsease Genome-wide Replication and Meta-analysis plus The Coronary Artery Disease Genetics Consortium ( n = 184,305) were selected for genetically predicted risk of MI. Genetic variants from other international GWAS summary data were selected for genetically determined mediators., Results: This MR study showed that increase in genetically predicted AAM was associated with lower risk of genetically predicted MI (odds ratio 0.91, 95% confidence interval 0.84-0.98). Inverse variance weighted (IVW) MR analysis also showed that decrease in genetically predicted AAM was associated with higher genetically predicted alcohol intake frequency, current smoking behavior, higher waist-to-hip ratio, and higher levels of systolic blood pressure (SBP), fasting blood glucose, hemoglobin A1c (HbA1c), and triglycerides (TGs). Furthermore, increase in genetically predicted AAM was associated with genetically predicted longer sleep duration, higher levels of high-density lipoproteins, and older age at which hormone replacement therapy was started. The most essential mediators identified were genetically predicted current smoking behavior and levels of HbA1c, SBP, and TGs, which were estimated to genetically mediate 13.9, 12.2, 10.5, and 9.2%, respectively, with a combined mediation proportion of 37.5% in the association of genetically predicted AAM with genetically predicted increased risk of MI in an MR framework., Conclusion: Our MR analysis showed that increase in genetically predicted AAM was associated with lower genetically predicted risk of MI, which was substantially mediated by genetically determined current smoking behavior and levels of HbA1c, SBP, and TGs. Intervening on the above mediators may reduce the risk of MI., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zheng, Chen, Huang, Shao, Li, Wang, Wang, Zhang, Meng, Gao, Wang, Liu, Song, Dong and Tang.)

Senecavirus A (SVA), an important member of the Picornaviridae family, causes vesicular disease in pigs. Here, we generated an EGFP-expressing recombinant SVA re-SVA-EGFP, which exhibited similar growth kinetics to its parental virus. The reporter SVA was used to study the role of pig ANTXR1 (pANTXR1) in SVA infection in a porcine alveolar macrophage cell line (PAM-Tang cells). Knockdown of the pANTXR1 significantly reduced SVA infection and replication in PAM-Tang cells, while re-expression of the pANTXR1 promoted the cell susceptibility to SVA infection. The results indicated that pANTXR1 is a crucial receptor mediating SVA infection. Subsequently, the viral endocytosis pathways for SVA entry into pig cells were investigated and the results showed that cholesterol played an essential role in receptor-mediated SVA entry. Together, these results demonstrated that SVA entered into host cells through the pANTXR1-mediated cholesterol pathway. Our findings provide potential targets to develop antiviral drugs for the prevention of SVA infection in the pig population., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer TS declared a shared affiliation with the authors to the handling editor at the time of the review., (Copyright © 2022 Jia, Sun, Tang, Zhang, Wang, Cai and Meng.)

Introduction and Objectives: The risk of ventricular arrhythmia and heart failure in patients with hypertrophic obstructive cardiomyopathy (HOCM) is much higher than that in the general population. More and more pieces of evidence showed that HOCM is the leading cause of sudden cardiac death in young people. We reported our experience in a study, comparing surgical myectomy, alcohol septal ablation (ASA), and medical therapy., Methods: The original cohort included 965 consecutive patients with HOCM. The patients were divided into three groups according to treatment strategies: myectomy group ( n = 502), ASA group ( n = 138), and medical treatment group ( n = 325). The median follow-up duration was 42.99 ± 18.32 months, and the primary endpoints were all-cause mortality and heart transplantation., Results: Both in short- and long-term observations, surgical myectomy reduced the left ventricular outflow tract (LVOT) gradients more effectively (7 days, 16.15 ± 12.07 mmHg vs. 42.33 ± 27.76 mmHg, p < 0.05; 1 year, 14.65 ± 13.18 mmHg vs. 41.17 ± 30.76 mmHg, p < 0.05). Among the three groups, the patients in the medical treatment group were at a higher risk of mortality and cardiac transplantation (vs. the myectomy group, p < 0.001 by log-rank test; vs. the alcohol septal ablation group, p = 0.017 by log-rank test), and the myectomy group shows a lower risk of reaching the primary endpoint than the two other groups. In the multivariate Cox regression analysis, previous atrial fibrillation (AF), N terminal pro B type natriuretic peptide (NT-pro-BNP), and surgical myectomy predicted an HOCM prognosis. However, the impact of surgical myectomy on HOCM prognosis seems to be limited to the <56 years group., Conclusions: The patients with medical treatments seemed to suffer from the highest risk of achieving an all-cause mortality and the endpoint of heart transplantation. In the long-term survival and clinical outcome, myectomy seemed better than alcohol septal ablation, especially the younger patients. Due to the less-controllable degree, periprocedural complication frequency after alcohol septal ablation was higher, compared with myectomy. Furthermore, gradients after myectomy are lower at late follow-up. To sum up, when selecting treatment strategies, the patients should be individually evaluated by a multidisciplinary team of cardiologists and surgeons., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Meng, Wang, Gao, Zhang, Zheng, Wang, Liu, Shao and Tang.)

Objective: The objective of this study is to investigate the roles of cardiometabolic factors (including blood pressure, blood lipids, thyroid function, body mass, and insulin sensitivity) in mediating the causal effect of type 2 diabetes (T2DM) on cardiovascular disease (CVD) outcomes., Design: Two-step, two-sample multivariable Mendelian randomization (MVMR) study., Setting: International genome-wide association study (GWAS) consortia data., Exposure: Type 2 diabetes, blood pressure: systolic blood pressure (SBP), diastolic blood pressure (DBP); blood lipids: low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides (TG); thyroid function: hyperthyroidism, hypothyroidism; body mass index (BMI), waist-hip-ratio (WHR), and insulin sensitivity., Main Outcomes: Cardiovascular disease includes coronary heart disease (CHD), myocardial infarction (MI), and stroke., Methods: Summary-level data for exposures and main outcomes were extracted from GWAS consortia. We used two-sample MR to illustrate the causal effect of T2DM on CVD subtypes and regression-based MVMR to quantify the possible mediation effects of cardiometabolic factors on CVD., Results: Each additional unit of log odds of T2DM increased 16% risk of CHD [odds ratio (OR): 1.16, 95% CI: 1.12-1.21], 15% risk of myocardial infarction (MI) (OR: 1.15, 95% CI: 1.10-1.20), and 10% risk of stroke (OR: 1.10, 95% CI: 1.06-1.13). In mediation analysis, SBP, DBP, and TG were found as main mediators, while the mediation effects of other cardiometabolic factors were not significant. The proportion of total effect of T2DM on CHD mediated by SBP, DBP, and TG was 16% (95% CI: 8-24%), 7% (95% CI: 1-13%) and 10% (95% CI: 2-18%), respectively. Mediation effect of SBP and DBP on MI and stroke, TG on MI was also prominent, while mediation effect of TG on stroke was not significant. The combined mediation effect of all the three mediators accounted for 29%, 26%, and 13% of the total effect of T2DM on CHD, MI, and stroke, respectively., Conclusion: Systolic blood pressure, DBP, and TG mediate a substantial proportion of the causal effect of T2DM on CVD and thus interventions on these factors might reduce the considerable excess risk of CVD among patients with T2DM., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer, ZW, declared a shared affiliation with the authors KC, CS, JZ, QZ, and Y-DT to the handling editor at time of review., (Copyright © 2022 Chen, Zhuang, Shao, Zheng, Zhou, Dong, Huang and Tang.)

Trueperella pyogenes causes disease in cattle, sheep, goats and swine, and is involved occasionally in human disease worldwide. Most reports implicating T. pyogenes have been associated with clinical cases, whereas no report has focused on pathogenicity of T. pyogenes in mouse models or precision-cut lung slice (PCLS) cultures from swine. Here, we isolated and identified a virulent, β-hemolytic, multidrug-resistant T. pyogenes strain named 20121, which harbors the virulence marker genes fimA, fimE, nanH, nanP and plo . It was found to be highly resistant to erythromycin, azithromycin and medemycin. Strain 20121 was pathogenic in mouse infection models, displaying pulmonary congestion and inflammatory cell infiltration, partial degeneration in epithelial cells of the tracheal and bronchiolar mucosa, a small amount of inflammatory cell infiltration in the submucosa, and bacteria (>10 4 CFU/g) in the lung. Importantly, we used T. pyogenes 20121 to infect porcine precision-cut lung slices (PCLS) cultures for the first time, where it caused severe bronchoconstriction. Furthermore, dexamethasone showed its ability to relieve bronchoconstriction in PCLS caused by T. pyogenes 20121, highlighting dexamethasone may assist antibiotic treatment for clinical T. pyogenes infection. This is the first report of T. pyogenes used to infect and cause bronchoconstriction in porcine PCLS. Our results suggest that porcine PCLS cultures as a valuable 3D organ model for the study of T. pyogenes infection and treatment in vitro ., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Qin, Meng, He, Yang, Wang, Tang, Sun, Zhang, Cai and Wang.)

Background: The prevalence of familial hypercholesterolemia (FH) in the patients with acute myocardial infarction (AMI) in China is unclear. Materials and Methods: In China Acute Myocardial Infarction (CAMI) Registry, 13,002 patients with age 18-80 were consecutively enrolled with first-onset AMI who were naïve to statin before admission from January 1st, 2013 to October 31st, 2014. According to Dutch Lipid Clinical Network Criteria (DLCNC), the patients were divided to heterozygous familial hypercholesterolemia (HeFH) (definite/probable HeFH, possible HeFH) or non-HeFH group. Results: The number of the patients in the three groups was as following, 62 in definite/probable HeFH group, 484 in possible HeFH group, 12,456 in non-HeFH group. The prevalence of HeFH is 4.2% (including 0.47% of definite/probable HeFH, 3.73% of possible FH). The average age of onset of first-time AMI was 54 ± 12, 56 ± 12, 63 ± 12 years old ( p < 0.0001) in definite/probable HeFH group, possible HeFH group and non-HeFH group, respectively. The percentage of Killip III or above (8.1 vs. 4.3 vs. 6.3%, p = 0.1629), cardiac arrest (1.6 vs. 0.6 vs. 0.9%, p = 0.6990), and TIMI 0-2 grade after primary percutaneous cardiac intervention (PCI) (0 vs. 6.8 vs. 4.3%, p = 0.5866) was not significantly different in definite/probable HeFH group, possible HeFH group and non-HeFH group, respectively. Conclusions: The prevalence of HeFH in Chinese patients with AMI is 4.2%. The patients were significantly younger in HeFH group, when compared with those with non-HeFH. However, no significant differences were found in the severity of clinical manifestations in both HeFH and non-HeFH group., (Copyright © 2020 Shi, Yang, Wang, Li, Guo, Gao, Tang, Li, Wu and Yang.)