BACKGROUND:Cardiorenal biomarkers are increasingly recognized as valuable tools for risk stratification in individuals with dysglycemia. However, their comparative prognostic value for long-term all-cause and cardio-cerebrovascular disease (CCD) mortality remains unclear. METHODS:We analyzed data from 4087 adults with prediabetes or diabetes from NHANES 1999-2004, with mortality follow-up through 2019. Nine biomarkers were assessed: NT-proBNP, hs-cTnT, hs-cTnI, CRP, UACR, BUN/Cr ratio, uric acid, cystatin C, and β2-microglobulin. Survey-weighted Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and CCD mortality. Time-dependent receiver operating characteristic (ROC) analysis evaluated discriminative performance. Weighted quantile sum (WQS) regression was applied to assess the collective impact of biomarkers. RESULTS:During a median follow-up of 16.5 years, 1855 all-cause deaths and 630 CCD deaths were recorded. In fully adjusted models, NT-proBNP (HR = 2.19; 95% CI, 1.73-2.78), hs-cTnT (HR = 2.30; 1.63-3.24), hs-cTnI (HR = 1.80; 1.44-2.24), cystatin C (HR = 1.76; 1.36-2.28), β2-microglobulin (HR = 1.72; 1.36-2.16), and UACR (HR = 1.50; 1.23-1.81) were significantly associated with all-cause mortality, with similar findings for CCD mortality. NT-proBNP and hs-cTnT demonstrated the strongest discrimination for 10-year all-cause (AUCs: 0.80 and 0.81) and CCD mortality (AUCs: both 0.85). Adding NT-proBNP or hs-cTnT to the base model significantly improved predictive accuracy. WQS regression confirmed a significant positive association with all-cause (HR = 1.56; 95% CI, 1.32-1.84) and CCD mortality (HR = 1.39; 95% CI, 1.14-1.70), with NT-proBNP, hs-cTnT, and cystatin C contributing most strongly. CONCLUSIONS:Among nine evaluated cardiorenal biomarkers, NT-proBNP, hs-cTnT, and cystatin C demonstrated the strongest and most consistent associations with all-cause and CCD mortality among adults with prediabetes and diabetes, as well as the highest incremental predictive value. These biomarkers may serve as key components in future risk stratification models for individuals with prediabetes or diabetes.

BACKGROUND:This study aims to investigate the mediation effects of the systemic inflammation on the association between urinary polycyclic aromatic hydrocarbons (PAHs) metabolites and hypertension in general US population. METHODS:This cross-sectional study analyzed 9 urinary PAHs metabolites from the 2003-2012 National Health and Nutrition Examination Survey (NHANES). Quantile g-computation (QG-C) were applied to assess the association between PAHs mixture exposure and hypertension prevalence. The associations among PAHs (exposure), hypertension (outcome), and inflammatory markers (C-reactive protein, alkaline phosphatase, white blood cell count, neutrophil count, and monocyte count; mediators) were investigated using mediation analysis. RESULTS:Among the 6846 participants, 2473 (36.1%) were diagnosed with hypertension. The mean of systolic and diastolic BP were 138.6 (20.4) and 72.7 (16.0) mmHg in the hypertensive group, and 115.8 (10.9) mmHg and 69.0 (10.0) mmHg in the non-hypertensive group. The mixture of urinary PAHs metabolites was significantly associated with increased prevalence of hypertension, with β = 0.124 (95% CI: 0.04, 0.20) for every quantile increase. Urinary 1-PHE (36.48%), 2-FLU (27.64%) and 1-PYR (26.64%) had the greatest positive contribution to the overall effect. Mediation analysis revealed that inflammatory markers play a mediating role in the associations between PAHs metabolites (2-FLU, 3-PHE, 1-PHE, 2-PHE, 1-PYR, and 9-FLU) and hypertensive adults. CONCLUSIONS:Our study demonstrated that mixture exposure to PAHs is associated with the prevalence of hypertension in US adult population, which might be primarily driven by 1-PHE, 2-FLU and 1-PYR. Furthermore, we have observed that systemic inflammation plays a significant mediating role in this associations.

BACKGROUND:The American Heart Association (AHA) PREVENT equations provide contemporary estimates of 10-year cardiovascular disease (CVD) risk. Although PREVENT was developed to estimate incident CVD risk, its relation to subsequent mortality in nationally representative US adults has not been well characterised. It also remains unclear whether social determinants of health (SDOH) modify these associations and improve discrimination beyond PREVENT. METHODS:Adults aged 40-75 years in NHANES 2003-2018 were linked to the National Death Index through December 31, 2019. SDOH burden was derived by summing 8 unfavourable SDOH components and categorised as 0, 1-2, 3-4 or ≥ 5. Survey-weighted Cox models were used to evaluate associations with all-cause and cardio-cerebrovascular disease (CCD) mortality, defined as a composite of cardiovascular and cerebrovascular mortality. Effect modification was assessed using multiplicative interaction terms. Incremental discrimination after adding SDOH to PREVENT was evaluated using time-dependent receiver operating characteristic (ROC) curves. RESULTS:Among 18 694 adults (mean age, 54.3 years; 52.6% women), 1646 all-cause deaths and 392 CCD deaths occurred over a median follow-up of 8.2 years (IQR, 4.3-12.3). In multivariable models, each 5-percentage-point higher PREVENT-estimated risk was associated with higher all-cause mortality (HR = 1.55; 95% CI, 1.47-1.64) and CCD mortality (HR = 1.62; 95% CI, 1.52-1.74). Heterogeneity by SDOH burden was demonstrated (p for interaction < 0.001 for both outcomes), with stronger associations in the 0-unfavourable group (all-cause: HR = 2.01; 95% CI, 1.79-2.25; CCD: HR = 2.35; 95% CI, 1.91-2.88) and attenuated associations in the ≥ 5-unfavourable group (all-cause: HR = 1.38; 95% CI, 1.26-1.50; CCD: HR = 1.46; 95% CI, 1.31-1.62). At 10 years, discrimination improved after adding SDOH to PREVENT (all-cause AUC: 0.747 to 0.778; p < 0.001; CCD AUC: 0.790 to 0.812; p = 0.042). CONCLUSIONS:SDOH burden was associated with graded mortality and modified the strength of the association between PREVENT-estimated 10-year CVD risk and mortality. Adding SDOH modestly improved mortality discrimination beyond PREVENT alone, supporting incorporation of social risk in risk stratification.

AIMS:Phospholamban (PLN) is a key regulator of sarco-endoplasmic reticulum calcium ATPase (SERCA) activity and myocardial contractility, but its expression control remains incompletely understood. This study seeks to clarify the molecular mechanism of PLN regulation and its functional relevance in cardiac physiology. METHODS AND RESULTS:Using cardiomyocyte-specific ZBTB20 knockout (CZB20KO) mice and primary cardiomyocytes, we demonstrated that ZBTB20 deficiency significantly reduced PLN protein at a higher magnitude than its mRNA levels, accompanied by a marked increase in the expression levels of miR-221 and miR-222 derived from the same gene cluster. Cardiomyocyte-specific deletion of miR-221/222 alone did not affect cardiac PLN expression in the mice, but fully restored the expression of PLN protein and the basal cardiac contractility in the context of ZBTB20 deficiency, as evidenced by normal left ventricular ejection fraction and fractional shortening compared to control mice. Through luciferase reporter assays with 3'UTR binding site mutagenesis and gain/loss-of-function experiments, we identified miR-221 but not its paralog miR-222 as a direct regulator of PLN by targeting its 3'UTR of mRNA. Moreover, cardiomyocyte-specific overexpression of miR-221 in mice led to a reduction in cardiac PLN protein levels. ChIP assay did not reveal significant binding of ZBTB20 to the miR-221/222 gene cluster. CONCLUSIONS:Our study identifies miR-221 as a novel regulator of cardiac PLN expression and a mediator of the regulation of PLN by ZBTB20. Thus this work provides insights into the regulation of basal contractility and functional reserve of the heart.

The American Heart Association recommends sex-specific thresholds for defining exaggerated systolic blood pressure response to exercise (ESBPR), primarily based on data from young healthy populations. However, their applicability and the sex differences in systolic blood pressure (SBP) response to exercise in real-world clinical settings remain unclear. We conducted a cross-sectional study of 44 418 adults (40.6

Clonal hematopoiesis of indeterminate potential (CHIP) increases with age and has been linked to cardiovascular disease. Apparent treatment-resistant hypertension (aTRH) is a severe, age-associated form of hypertension with poor response to therapy. Here we show that CHIP is enriched in patients with aTRH and is independently associated with poorer treatment response and adverse cardiac remodeling. In a multicenter discovery cohort and two community-based validation cohorts, CHIP was detected in 23

Objective This study was to investigate the correlation between urine volatile organic compound (VOC) metabolites and obesity-related outcomes, including BMI, waist circumference, obesity, and abdominal obesity. Methods Data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2011 and 2016 were utilized for this analysis. Linear regression and logistic regression models were employed to estimate β-coefficients or odds ratios (ORs) along with their corresponding 95% confidence intervals (CIs). Quantile g-computation (Qgcomp) regression, a method designed to evaluate the combined effects of multiple correlated chemical exposures, was used to assess the mixed influence of VOC metabolites on obesity-related outcomes. Results A total of 4,950 adults were included in this analysis. The median age of the participants was 47 (33, 60) years, with 49.3% being male. The median BMI was 27.7 (24.2, 32.4) kg/m2, and the median waist circumference was 98.0 (87.3, 109.0) cm. The prevalence of obesity and abdominal obesity was 36.8% and 56.5%, respectively. After adjusting for all covariates, urine VOC metabolites (including AAMA, AMCC, BMA, CYMA, DHBMA, 3HPMA, 2HPMA, MA, 2MHA, 3MHA+4MHA, MHBMA3, PGA, and HPMMA) exhibited a negative association with obesity. With the exception of BMA and DHBMA, similar results were observed regarding the association between urine VOC metabolites and the prevalence of abdominal obesity. Additionally, Qgcomp regression analysis revealed a significant negative correlation between the mixture of urine VOC metabolites and all obesity-related outcomes, with 2HPMA demonstrating the strongest influence on this negative association. Conclusion Our findings suggest a negative relationship between exposure to VOCs, as measured by urine VOC metabolite levels, and obesity in adults.

Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease, often caused by sarcomere gene mutations, though many sporadic cases remain genetically unexplained. Here we show that the somatic variant NAP1L1 p.D349E was involved in cardiac hypertrophy in sporadic HCM patients. Through next generation sequencing, we found that somatic variant NAP1L1 p.D349E was recurrent in the cardiomyocytes of gene-elusive sporadic HCM patients. Subsequent in vivo and in vitro functional analysis confirmed that NAP1L1 p.D349E contributes to HCM by triggering an innate immunity response. This mutation destabilizes nucleosome formation, causing DNA to leak into the cytoplasm. This leakage activates a key immune pathway, cGAS-STING, which leads to the release of inflammatory molecules and promotes heart muscle thickening. Our findings reveal a new mechanism driving HCM and suggest that somatic variants could be important in understanding and management of HCM.

Metabolic syndrome combines major risk factors for cardiovascular disease, making deeper insight into its pathogenesis important. We here explore the mechanistic basis of metabolic syndrome by recruiting an essential patient cohort and performing extensive gene expression profiling. The mitochondrial fatty acid metabolism enzyme acyl-CoA synthetase medium-chain family member 3 (ACSM3 ) was identified to be significantly lower expressed in the peripheral blood of metabolic syndrome patients. In line, hepatic ACSM3 expression was decreased in mice with metabolic syndrome. Furthermore, Acsm3 knockout mice showed glucose and lipid metabolic abnormalities, and hepatic accumulation of the ACSM3 fatty acid substrate lauric acid. Acsm3 depletion markedly decreased mitochondrial function and stimulated signaling via the p38 MAPK pathway cascade. Consistently, Acsm3 knockout mouse exhibited abnormal mitochondrial morphology, decreased ATP contents, and enhanced ROS levels in their livers. Mechanistically, Acsm3 deficiency, and lauric acid accumulation activated nuclear receptor Hnf4α-p38 MAPK signaling. In line, the p38 inhibitor Adezmapimod effectively rescued the Acsm3 depletion phenotype. Together, these findings show that disease-associated loss of ACSM3 facilitates mitochondrial dysfunction via a lauric acid-HNF4a-p38 MAPK axis, suggesting a novel therapeutic vulnerability in systemic metabolic dysfunction.

BackgroundThe public health burden of cardiomyopathies and competency in their management by health agencies in China are not well understood.MethodsThis study adopted a multi-stage sampling method for hospital selection. In the first stage, nationwide tertiary hospital recruitment was performed. As a result, 88 hospitals with the consent of the director of cardiology and access to an established electronic medical records system, were recruited. In the second stage, we sampled 66 hospitals within each geographic-economic stratification through a random sampling process. Data on (1) the outpatient and inpatient visits for cardiomyopathies between 2017 and 2021 and (2) the competency in the management of patients with cardiomyopathies, were collected. The competency of a hospital to provide cardiomyopathy care was evaluated using a specifically devised scale.FindingsThe outpatient and inpatient visits for cardiomyopathies increased between 2017 and 2021 by 38.6% and 33.0%, respectively. Most hospitals had basic facilities for cardiomyopathy assessment. However, access to more complex procedures was limited, and the integrated management pathway needs improvement. Only 4 (6.1%) of the 66 participating hospitals met the criteria for being designated as a comprehensive cardiomyopathy center, and only 29 (43.9%) could be classified as a primary cardiomyopathy center. There were significant variations in competency between hospitals with different administrative and economic levels.InterpretationThe health burden of cardiomyopathies has increased significantly between 2017 and 2021 in China. Although most tertiary hospitals in China can offer basic cardiomyopathy care, more advanced facilities are not yet universally available. Moreover, inconsistencies in the management of cardiomyopathies across hospitals due to differing administrative and economic levels warrants a review of the nation allocation of medical resources.FundingThis work was supported by the Chinese Academy of Medical Sciences (CAMS) Innovation Fund for Medical Sciences (2023-I2M-1-001) and the National High Level Hospital Clinical Research Funding (2022-GSP-GG-17).

This study was to estimate the associations of volatile organic compounds (VOCs) exposure with the prevalence of total and specific cardiovascular disease (CVD) among the general adult population. This cross-sectional study analyzed 15 urinary VOC metabolites in the general population using the 2011-2016 National Health and Nutrition Examination Survey (n = 5,213). The weighted study population with 47.0 years median age, was primarily female (51.2%). The prevalence of total CVD in the overall population was 7.9%. The single-exposure analyzes of AAMA, ATCA, CEMA, CYMA, DHBMA, 3HPMA, and 3MHA +4MHA were significantly associated with increased prevalence of total CVD. Qgcomp regression consistently showed that urinary VOCs-mixed exposure was positively correlated with the prevalence of total and specific CVDs (chronic heart failure, angina, and stroke), and highlighted each VOCs metabolite weights and direction. The similar results were observed for the WQS regression using mixed analysis methods. In conclusion, exposure to VOCs increases CVD prevalence and advances the identification of risk factors for CVD for environmental study.

BACKGROUND AND AIMS:Flavonoids are widely distributed polyphenolic compounds in the diet that possess various health-promoting effects. This study aimed to investigate the association between dietary flavonoid intake and all-cause and cardiovascular mortality in adults. METHODS AND RESULTS:The data on the six main subclasses of flavonoids, including isoflavones, anthocyanidins, flavan-3-ols, flavanones, flavones, and flavonols, were obtained from the 2007-2010 National Health and Nutrition Examination Survey (NHANES) dataset of adults. The participants were followed up until December 30, 2019. Cox regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for dietary flavonoid intake and mortality. The study included a total of 8758 adults (mean age 44.00 years; 47.40% men). A median follow-up of 10.7 years yielded 1113 all-cause deaths and 261 cardiovascular deaths were recorded. In comparison to category 1, category 4 of flavan-3-ols, flavonols, and total flavonoids were associated with lower risks of all-cause mortality, with multivariable-adjusted HRs of 0.71 (95% CI: 0.55-0.92, Ptrend = 0.021), 0.58 (95% CI: 0.45-0.74, Ptrend<0.001), and 0.63 (95% CI: 0.50-0.80, Ptrend = 0.010), respectively. Similarly, higher intake of category 4 flavonoids was associated with a reduced risk of cardiovascular mortality, with HRs of 0.68 (95% CI: 0.29-0.89, Ptrend = 0.035) for flavones, 0.41 (95% CI: 0.22-0.78, Ptrend = 0.001) for flavonols, and 0.54 (95% CI: 0.36-0.80, Ptrend = 0.021) for total flavonoids. CONCLUSION:Dietary flavonoid intake is associated with all-cause and cardiovascular mortality. Increasing dietary flavonoid intake may reduce the risk of death in adults.

Recent research has explored the potential of the demethylating drug 5-azacytidine (Aza) as therapy for a range of diseases. However, the therapeutic efficacy of Aza for patients of atherosclerosis remains unclear. This study investigates the therapeutic application of Aza to atherosclerosis in order to elucidate the underlying mechanisms. We generated induced Tregs (iTregs) from CD4+ T cells by using Aza in vitro, and this was followed by the intravenous infusion of iTregs for the treatment of atherosclerosis. The adoptive transfer of Aza-iTreg significantly increased peripheral blood Treg cells, suppressed inflammation, and attenuated atherosclerosis in ApoE-/- mice. Furthermore, we observed a notable demethylation of the Forkhead box P3 (Foxp3)-regulatory T cell-specific demethylated region (TSDR) and an upregulation of Foxp3 expression in the CD4+ T cells in the spleen of the ApoE-/- mice following the transfer of Aza- iTregs. We also demonstrated that Aza converted naive CD4+ T cells into Tregs by DNA methyltransferase 1 (Dnmt1)-mediated Foxp3-TSDR demethylation and the upregulation of Foxp3 expression. Conversely, the overexpression of Dnmt1 in the CD4+ T cells attenuated the Aza-induced Foxp3-TSDR demethylation and upregulation of Foxp3 expression. Our results reveal that Aza converts naive CD4+ T cells into functional Tregs by inhibiting Dnmt1, and the transfer of Aza-iTregs suppresses atherosclerosis in mice.

Abstract Aims Risk assessment for triple-vessel disease (TVD) remain challenging. Stress hyperglycemia represents the regulation of glucose metabolism in response to stress, and stress hyperglycemia ratio (SHR) is recently found to reflect true acute hyperglycemic status. This study aimed to evaluate the prognostic value of SHR and its role in risk stratification in TVD patients with acute coronary syndrome (ACS). Methods A total of 3812 TVD patients with ACS with available baseline SHR measurement were enrolled from two independent centers. The endpoint was cardiovascular mortality. Cox regression was used to evaluate the association between SHR and cardiovascular mortality. The SYNTAX (Synergy Between Percutaneous Coronary Intervention With Taxus and Cardiac Surgery) II (SSII) was used as the reference model in the model improvement analysis. Results During a median follow-up of 5.1 years, 219 (5.8%) TVD patients with ACS suffered cardiovascular mortality. TVD patients with ACS with high SHR had an increased risk of cardiovascular mortality after robust adjustment for confounding (high vs. median SHR: adjusted hazard ratio 1.809, 95% confidence interval 1.160–2.822, P = 0.009), which was fitted as a J-shaped pattern. The prognostic value of the SHR was found exclusively among patients with diabetes instead of those without diabetes. Moreover, addition of SHR improved the reclassification abilities of the SSII model for predicting cardiovascular mortality in TVD patients with ACS. Conclusions The high level of SHR is associated with the long-term risk of cardiovascular mortality in TVD patients with ACS, and is confirmed to have incremental prediction value beyond standard SSII. Assessment of SHR may help to improve the risk stratification strategy in TVD patients who are under acute stress.

Fulminant myocarditis is an acute diffuse inflammatory disease of myocardium. It is characterized by acute onset, rapid progress and high risk of death. Its pathogenesis involves excessive immune activation of the innate immune system and formation of inflammatory storm. According to China's practical experience, the adoption of the "life support-based comprehensive treatment regimen" (with mechanical circulation support and immunomodulation therapy as the core) can significantly improve the survival rate and long-term prognosis. Special emphasis is placed on very early identification,very early diagnosis,very early prediction and very early treatment.

Background Coronary artery calcification (CAC) is a highly specific marker of atherosclerosis. Niemann-Pick C1-like 1 (NPC1L1) and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are the therapeutic targets of ezetimibe and statins, respectively, which are important for the progression of atherosclerosis. However, CAC’s genetic susceptibility with above targets is still unknown. We aimed to investigate the association of NPC1L1 and HMGCR gene polymorphisms with CAC in patients with premature triple-vessel disease (PTVD). Methods Four single nucleotide polymorphisms (SNPs) (rs11763759, rs4720470, rs2072183, rs2073547) of NPC1L1 , and three SNPs (rs12916, rs2303151, rs4629571) of HMGCR were genotyped in 872 PTVD patients. According to the coronary angiography results, patients were divided into low-degree CAC group and high-degree CAC group. Results A total of 872 PTVD patients (mean age, 47.71 ± 6.12; male, 72.8%) were finally included for analysis. Multivariate logistic regression analysis showed no significant association between the SNPs of NPC1L1 and HMGCR genes and high-degree CAC in the total population ( P > 0.05). Subgroup analysis by gender revealed that the variant genotype (TT/CT) of rs4720470 on NPC1L1 gene was associated with increased risk for high-degree CAC in male patients only (OR = 1.505, 95% CI: 1.008–2.249, P = 0.046) in dominant model, but no significant association was found in female population, other SNPs of NPC1L1 and HMGCR genes (all P > 0.05). Conclusions We reported for the first time that the rs4720470 on NPC1L1 gene was associated with high-degree CAC in male patients with PTVD. In the future, whether therapies related to this target could reduce CAC and cardiovascular events deserves further investigation.

AIM:Our study aimed to investigate the correlation between glycated hemoglobin (HbA1c) and adverse prognostic events in patients with diabetes and triple-vessel coronary disease (TVD). METHODS:This study ultimately included 2051 patients with TVD and diabetes. Patients were categorized into five groups based on their HbA1c levels: < 6.0 %, 6.0-6.4 %, 6.5-6.9 %, 7.0-7.9 %, and ≥ 8.0 %. The primary endpoint was all-cause death, and the secondary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE). RESULTS:The median follow-up time was 5.88 years. During this period, a total of 323 (15.7 %) all-cause deaths and 537 (26.2 %) MACCEs were recorded. The relationship between HbA1c and the risk of endpoint events showed a J-shaped pattern, with the lowest risk observed between 6.0 % and 6.4 %. Further analysis revealed a significant interaction between HbA1c and age. In the subgroup with age < 70 years, as HbA1c increased, the risk of endpoint events gradually rose. While in the subgroup with age ≥70 years, there was an L-shaped relationship between HbA1c and endpoint events, with the highest risk observed in patients with HbA1c < 6.0 %. CONCLUSION:Our study revealed variations in the relationship between HbA1c levels and endpoint events among patients with TVD and diabetes of different ages. In younger patients, elevated HbA1c levels were associated with a higher risk of death and MACCE, while in older patients, excessively low HbA1c levels (HbA1c < 6 %) were linked to a higher risk of death and MACCE.

暴发性心肌炎是致病源感染或免疫检测点抑制剂所致的严重的心脏炎症性疾病, 起病急、进展快, 死亡风险极高。至今为止, 西方国家除了使用机械循环支持外, 没有其他有效的治疗措施, 患者在住院期间病死率高达50%[1]。我国学者在实践和研究的基础上于2017年提出了"以生命支持为依托"的综合救治方案, 即"中国方案", 其核心内容包括机械循环支持替代强心和升血压药物;用足够剂量的糖皮质激素和免疫球蛋白进行免疫调节治疗, 而非免疫抑制治疗, 并且采取一切可行措施减轻心脏负担[2]。6年多来, "中国方案"在全国推广和应用, 提高了医务人员对暴发性心肌炎的认识和诊断水平, 同时也验证了"中国方案"救治暴发性心肌炎的安全性和有效性[3, 4, 5], 将我国暴发性心肌炎病死率由过去的50%以上降低到5%左右[5, 6], 领先于国际水平, 患者长期预后明显优于西方国家[7, 8]。随着我国临床研究和救治经验的累积, 特别是一些多中心临床研究及原创性基础研究成果的发表, 证据链已充分建立, 中华医学会心血管病学分会决定将2017年成人暴发性心肌炎诊断与治疗中国专家共识升级为指南——《中国成人暴发性心肌炎诊断和治疗指南》, 并于2024年1月在《中华心血管病杂志》发表[9]。该指南提出了明确的暴发性心肌炎诊断标准和行之有效的治疗方案, 也获准英文全文发表[10]。指南的推广应用将能帮助挽救更多患者的生命。指南秉承了2017年专家共识, 也有非常明确的创新和亮点, 主要包括以下几个方面。