Frontiers in Cardiovascular Medicine最新文献

Objective: This study aims to explore the association between risk stratification and total occlusion (TO) of the culprit artery and multivessel disease (MVD) in patients with non-ST-segment-elevation myocardial infarction (NSTEMI) and to obtain more data on clinical decision-making in addition to risk stratification.

Methods: We retrospectively collected data from 835 patients with NSTEMI admitted to our hospital between 1 January 2016 and 1 August 2022. All patients underwent percutaneous coronary intervention (PCI) within 72 h of admission. We excluded patients with a history of cardiac arrest, myocardial infarction, coronary artery bypass grafting, or PCI. Univariate and multivariate regression analyses were performed to determine the predictors of acute TO and MVD.

Results: A total of 349 (41.8%) patients presented with a TO culprit vessel, whereas 486 (58.2%) had a patent culprit vessel. Thrombolysis in myocardial infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) risk stratifications were similar between the two groups of patients (P = 0.712 and 0.991, respectively). The TO infarct vessel was more commonly observed in the left circumflex artery. Patients with TO were more likely to develop MVD (P = 0.004). Univariate and multivariate linear regression analyses were performed to evaluate the role of variables in the presence of TO and MVD in patients with NSTEMI. Regional wall motion abnormalities (RWMAs) [odds ratio (OR) = 4.022; confidence interval (CI): 2.782-5.813; P < 0.001] were significantly linked to TO after adjusting for potentially related variables. Furthermore, age (OR = 1.032; CI: 1.018-1.047; P < 0.001), hypertension (OR = 1.499; CI: 1.048-2.144; P = 0.027), and diabetes mellitus (OR = 3.007; CI: 1.764-5.125; P < 0.001) were independent predictors of MVD in patients with NSTEMI. TIMI and GRACE risk scores were related to MVD prevalence in the multivariate logistic regression model. Patients with a TO culprit vessel had a higher risk of out-of-hospital cardiac death after a 2-year follow-up compared with those without a TO culprit vessel (P = 0.022).

Conclusion: TIMI and GRACE risk scores were not associated with a TO of the culprit artery; however, they correlated with the prevalence of MVD in patients with NSTEMI. RWMA is an independent predictor of acute TO in patients with NSTEMI. Patients with a TO culprit vessel had worse clinical outcomes than those without a TO culprit vessel.

Introduction: Accurate in-hospital mortality prediction following percutaneous coronary intervention (PCI) is crucial for clinical decision-making. Machine Learning (ML) and Data Mining methods have shown promise in improving medical prognosis accuracy.

Methods: We analyzed a dataset of 4,677 patients from the Regional Vascular Center of Primorsky Regional Clinical Hospital No. 1 in Vladivostok, collected between 2015 and 2021. We utilized Extreme Gradient Boosting, Histogram Gradient Boosting, Light Gradient Boosting, and Stochastic Gradient Boosting for mortality risk prediction after primary PCI in patients with acute ST-elevation myocardial infarction. Model selection was performed using Monte Carlo Cross-validation. Feature selection was enhanced through Recursive Feature Elimination (RFE) and Shapley Additive Explanations (SHAP). We further developed hybrid models using Augmented Grey Wolf Optimizer (AGWO), Bald Eagle Search Optimization (BES), Golden Jackal Optimizer (GJO), and Puma Optimizer (PO), integrating features selected by these methods with the traditional GRACE score.

Results: The hybrid models demonstrated superior prediction accuracy. In scenario (1), utilizing GRACE scale features, the Light Gradient Boosting Machine (LGBM) and Extreme Gradient Boosting (XGB) models optimized with BES achieved Recall values of 0.944 and 0.954, respectively. In scenarios (2) and (3), employing SHAP and RFE-selected features, the LGB models attained Recall values of 0.963 and 0.977, while the XGB models achieved 0.978 and 0.99.

Discussion: The study indicates that ML models, particularly the XGB optimized with BES, can outperform the conventional GRACE score in predicting in-hospital mortality. The hybrid models' enhanced accuracy presents a significant step forward in risk assessment for patients post-PCI, offering a potential alternative to existing clinical tools. These findings underscore the potential of ML in optimizing patient care and outcomes in cardiovascular medicine.

Background and aims: Long QT syndrome (LQTS) and coronary artery disease (CAD) are both associated with increased risk of ventricular tachyarrhythmia. However, there are limited data on the incremental risk conferred by CAD in adult patients with congenital LQTS. We aimed to investigate the risk associated with CAD and life threatening events (LTEs) in patients with LQTS after age 40 years.

Methods: The risk of LTEs (comprising aborted cardiac arrest, sudden cardiac death, or appropriate defibrillator shock) from age 40 through 75 years was examined in 1,020 subjects from the Rochester LQTS registry, categorized to CAD (n = 137) or no-CAD (n = 883) subgroups.

Results: Survival analysis showed that patients with CAD had a significantly higher cumulative event rate of LTEs from 40 to 75 years (35%) compared with those without CAD (7%; p < 0.001 for the overall difference during follow-up). Consistently, multivariate analysis showed that the presence of CAD was associated with a 2.5-fold (HR = 2.47; p = 0.02) increased risk of LTEs after age 40 years. Subgroup analyses showed that CAD vs. no CAD was associated with a pronounced >4-fold (p = 0.008) increased risk of LTEs among LQTS patients with a lower-range QTc (<500 ms). The increased risk of LTEs associated with CAD was not significantly different among the 3 main LQTS genotypes. Patient treatment was suboptimal, with only 63% on β-blockers and 44% on non-selective β-blockers.

Conclusions: Our findings suggest that CAD is associated with a higher risk of LTEs in LQTS patients, with the risk being more pronounced in those with QTc <500 ms.

Background: Cytokines play a pivotal role in the progression of heart failure (HF) by modulating inflammatory responses, promoting vasoconstriction, and facilitating endothelial injury. However, it is now difficult to distinguish the causal relationship between HF and cytokines in observational studies. Mendelian randomization (MR) analyses of cytokines probably could enhance our comprehension to the underlying biological processes of HF.

Methods: This study was to explore the correlation between 41 cytokines with HF at the genetic level by MR analysis. We selected a HF dataset from the Heart Failure Molecular Epidemiology for Therapeutic Targets (HERMES) 2018 and a cytokine dataset from a meta-analysis of cytokine levels in Finns. Two-sample, bidirectional MR analyses were performed using Inverse Variance Weighted (IVW), Weighted Median and MR- egger, and the results were tested for heterogeneity and pleiotropy, followed by sensitivity analysis.

Results: Genetic prediction of high levels of circulating Macrophage inflammatory pro-tein-1β(MIP-1β) (P = 0.0389), Interferon gamma induced protein 10(IP-10) (P = 0.0029), and Regu-lated on activation, normal T cell expressed and secreted(RANTES) (P = 0.0120) expression was associated with an elevated risk of HF. HF was associated with the increased levels of circulating Interleukin-2 receptor, alpha subunit(IL-2ra) (P = 0.0296), Beta nerve growth fac-tor(β-NGF) (P = 0.0446), Interleukin-17(IL-17) (P = 0.0360), Basic fibroblast growth factor(FGF-basic) (P = 0.0220), Platelet derived growth factor BB(PDGF-BB) (P = 0.0466), and Interferon-gamma(IFN-γ) (P = 0.0222); and with decreased levels of Eotaxin (P = 0.0133). The heterogeneity and pleiotropy of the cytokines were acceptable, except for minor heterogeneity of FGF-basic and IL-17.

Conclusion: These findings provide compelling evidence for a genetically predictive relationship between cytokines and HF, emphasizing a great potential of targeted modulation of cytokines in slowing the progression of HF. This study draws further conclusions at the genetic level, providing a basis for future large-scale clinical trials.

Introduction: Cardiovascular disease (CVD) is a leading global cause of morbidity and mortality, with high systolic blood pressure (SBP) identified as a major risk factor. Aspirin (Acetylsalicylic acid-ASA) has been considered for CVD prevention, prompting questions about its optimal use in primary and secondary prevention and the ideal dosing time to maximize its impact on circadian blood pressure rhythms. Previous research suggests a potential benefit of bedtime aspirin dosing in reducing blood pressure, attributed to its effects on the renin-angiotensin-aldosterone system and nitric oxide production. This systematic review and meta-analysis aim to further explore the circadian effects of aspirin on blood pressure, focusing on the timing of administration.

Methods: Adhering to PRISMA guidelines, a comprehensive search of PubMed, Cochrane Library, and clinicaltrials.gov was conducted. Randomized controlled trials (RCTs) involving patients aged >18 with cardiovascular history and hypertension were included. The primary objective was to assess the impact of bedtime-dosed and morning-dosed aspirin on systolic and diastolic blood pressure. Low-dose aspirin was administered for primary or secondary prevention. The Cochrane Risk of Bias tool evaluated study quality. Meta-analyses were conducted using RevMan 5.3, with mean deviations and 95% confidence intervals employed for outcomes.

Results: Initial searches yielded 1,181 articles, with six studies meeting the inclusion criteria. These RCTs involved 1,470 patients, with 1,086 completing follow-up. Bedtime aspirin dosing demonstrated a significant reduction in both systolic and diastolic blood pressure compared to morning dosing (p < 0.05). Meta-analysis results for systolic blood pressure revealed a weighted mean difference of approximately 3.65 mmHg in favour of bedtime dosing, with low heterogeneity (I ² = 0%). For diastolic blood pressure, the weighted mean difference was 1.92, again favouring bedtime dosing, with 3% heterogeneity.

Conclusion: This meta-analysis, involving over 1,300 cardiovascular/hypertensive patients, supports the effectiveness of bedtime aspirin in reducing systolic and diastolic blood pressure compared to morning dosing. The results align with previous findings but distinguish themselves by incorporating a more diverse patient population and addressing moderate heterogeneity. While the study's outcomes are promising, further research, including larger sample sizes and longer durations, is warranted for comprehensive clinical implementation. As the study exclusively focused on aspirin timing, future investigations should explore sustained blood pressure effects in patients with clinical indications for aspirin alongside other hypertensive medications.

Myocardial fibrosis is a common pathological feature in various cardiovascular diseases including myocardial infarction, heart failure, and myocarditis. Generally, persistent myocardial fibrosis correlates with poor prognosis and ranks among the leading causes of death globally. Currently, there is no effective treatment for myocardial fibrosis, partly due to its unclear pathogenic mechanism. Increasing studies have shown IL-17 family cytokines are strongly associated with the initiation and propagation of myocardial fibrosis. This review summarizes the expression, action, and signal transduction mechanisms of IL-17, focusing on its role in fibrosis associated with cardiovascular diseases such as myocardial infarction, heart failure, hypertension, diabetes, and myocarditis. It also discusses its potential as a therapeutic target, offering new insights for the clinical treatment of myocardial fibrosis.

Fulminant myocarditis (FM) is characteristically associated with rapid progressive decline in cardiac function and high mortality, with rapid onset of hemodynamic dysfunction and severe arrhythmias. In this report, we describe a case concerning a patient clinically diagnosed with FM, marked by rapid progression leading to intractable ventricular fibrillation and subsequent cardiac arrest. Conventional cardiopulmonary resuscitation (CCPR) was performed 120 min before extracorporeal membrane oxygenation (ECMO) was initiated. This critical situation was effectively addressed through the utilization of extracorporeal cardiopulmonary resuscitation (ECPR). By providing sustained cardiopulmonary support, effective hemodynamics were obtained. Eventually, the patient made a full recovery, and discharged without neurologic complications on hospital day 13.

Objective: This study aimed to explore the relationship between total burden of cerebral small vessel disease (CSVD) and daytime and nighttime heart rate variability (HRV) parameters.

Method: Consecutive patients with nondisabling ischemic cerebrovascular events were recruited from the cerebrovascular disease clinic of Changzhou Second People's Hospital between January 2022 and June 2023. A total of 144 enrolled participants were divided into a mild CSVD group (74 patients) and a moderate-to-severe CSVD group (70 patients) based on total burden of CSVD. Various HRV parameters measured during 24-h, 4-h daytime, and 4-h nighttime periods (including natural log-transformed [ln] root mean square of successive RR interval differences [RMSSD], ln absolute power of the high-frequency band [0.15-0.4 Hz] [HF], ln absolute power of the low-frequency band [0.04-0.15 Hz][LF], and LF-to-HF ratio [LF/HF]) were then assessed in the 2 groups. Spearman correlation analysis was used to assess the correlation between total burden of CSVD and HRV parameters. HRV parameters with P-value < 0.05 in correlation analysis were included in the multivariable logistic regression analysis, and restricted cubic spline analysis was performed to assess dose-response relationships.

Results: Daytime 4-h lnRMSSD (r = -0.221; P = 0.008) and 4-h lnHF (r = -0.232; P = 0.005) were negatively correlated with total burden of CSVD, and daytime 4-h lnLF/HF (r = 0.187; P = 0.025) was positively correlated with total burden of CSVD. There was no correlation between nighttime HRV parameters and total burden of CSVD. After adjustments were made for potential confounders, daytime 4-h lnRMSSD (OR = 0.34; 95% CI: 0.16-0.76), 4-h lnHF (OR = 0.57; 95% CI: 0.39-0.84), and 4-h lnLF/HF (OR = 2.12; 95% CI: 1.18-3.82) were independent predictors of total burden of CSVD (all P < 0.05). S-shaped linear associations with moderate-to-severe total burden of CSVD were seen for daytime 4h-lnRMSSD (P for nonlinearity = 0.543), 4-h lnHF (P for nonlinearity = 0.31), and 4-h lnLF/HF (P for nonlinearity = 0.502).

Conclusion: Daytime parasympathetic HRV parameters are independent influencing factors of total burden of CSVD and may serve as potential therapeutic observation indicators for CSVD.