Frontiers in Cardiovascular Medicine最新文献

Introduction: Complex Percutaneous coronary intervention (PCI) for the treatment of ischemic heart disease has increased significantly. We aimed to evaluate sex-related differences in patients undergoing complex PCI.

Methods: single-center prospective observational study including patients undergoing complex PCI between 2017 and 2023. Baseline and procedural features, and mid-term outcomes were compared according to the gender distribution. The combined primary endpoint included stroke, myocardial infarction, need for a new coronary revascularization, and all-cause mortality. Propensity score (PS) matching with an inverse probability of treatment weight (IPW) approach was used to adjust for differences in baseline characteristics.

Results: 1,283 patients were included, 983 (76.6%) male and 300 (23.4%) female. Median follow-up was 2.4 (IQR: 1-3.8) years. There was a higher rate of no-reflow phenomenon (4% vs. 1.8%, p = 0.03) among female patients. In the overall cohort, female patients had a greater risk for the combined primary endpoint (HR 1.28, 95% CI: 1.02-1.59). In the matched cohort, female patients exhibited a higher risk for the combined primary endpoint (HR 1.23, 95% CI: 1.06-1.42), as well as for myocardial infarction (HR 1.34, 95% CI 1.03-1.75), and all-cause mortality (HR 1.21, 95% CI 1.02-1.45), and a trend towards a higher risk for the need of a new coronary revascularization (HR 1.22, 95% CI 0.92-1.61).

Conclusions: in a contemporary cohort of patients undergoing complex PCI procedures, female patients are associated with a higher risk of early complications.

Background: Previous studies have shown an association between lipid-lowering drugs, circulating inflammatory factors, and atrial fibrillation (AF), but the specific effects of lipid-lowering drugs on AF and whether they can be mediated by circulating inflammatory factors remain unclear.

Methods: We collected 10 genetic variants encoding lipid-lowering drug targets (LDLR, HMGCR, PCSK9, NPC1L1, APOB, APOB, ABCG5, ABCG8, LPL, APOC3, and PPARA) and AF based on genome-wide association study (GWAS) summary statistics. Drug target Mendelian randomization (MR) was used to explore the causal relationship between lipid-lowering drugs and AF. In addition, we performed a mediation analysis of 91 circulating inflammatory factors to explore potential mediators. Sensitivity analyses were performed to verify the reliability of the MR Results by MR-Egger intercept test, Cochran's Q test and leave-one-out test.

Results: The results of IVW method showed that LPL agonist had a protective effect on AF(OR = 0. 854, 95%CI: 0.816-0.894, P = 1.844E-11). However, the other nine lipid-lowering drug targets had no significant effect on AF. Notably, we found a mediator role of Fibroblast Growth Factor 5 (FGF5) in the protective effect of LPL agonist on AF with a mediator ratio of 9.22%. Sensitivity analyses supported the robustness of our findings, indicating a possible mediating pathway by which LPL agonists affect the risk of AF.

Conclusion: Our study provides new insights into the complex interactions among lipid-lowering agents, circulating inflammatory factors and AF, and also identified a potential mediating role of FGF5 in the pathogenesis of AF. Our findings highlight the potential of LPL agonists and targeting specific inflammatory factors for therapeutic intervention in AF, providing promising avenues for future research and clinical strategies for the management and prevention of AF.

Background: In hypoplastic left heart syndrome (HLHS) patients, neo-aortic valve regurgitation can negatively impact right ventricular (RV) function. We assessed neo-aortic valve function and RV volumetric parameters by analysing serial cardiovascular magnetic resonance (CMR) studies in HLHS patients after completion of total cavopulmonary connection (TCPC).

Methods: Consecutive CMR examinations of 80 patients (female: 22) with two (n = 80) or three (n = 45) examinations each were retrospectively analysed. RV volumetry was performed using short-axis cine images. RV end-diastolic and end-systolic volumes normalised to body surface area (BSA, RVEDVi, RVESVi), ejection fraction (RVEF) and stroke volume (RVSV) were measured. Neo-aortic flow, regurgitant fraction (RF) and peak velocity were quantified from phase-contrast cine images.

Results: Median neo-aortic regurgitation was mild at all three examinations (RF <20%) and there was no significant increase in RF over time (p > 0.05). None of the patients had significant neo-aortic valve stenosis (peak velocity >3 m/s). RF correlated with RVESVi and RVEF at the second examination. At the third examination, RF correlated with RVESVi and RVEDVi even in patients with RF <15% (RVESVi: r = 0.40, p = 0.001; RVEDVi: r = 0.34, p = 0.031).

Conclusion: Assessment of serial CMR studies in HLHS patients after TCPC completion demonstrates a preserved neo-aortic valve function. Nevertheless, thorough follow-up is mandatory as even mild neo-aortic dysfunction might impact RV size and function over a longer term.

Introduction: To assess the prevailing trends in the incidence of ischemic heart disease (IHD) across 204 countries and territories from 1990 to 2019, and to elucidate their correlations with age, period, and birth cohort, a comprehensive analysis was conducted.

Methods: From 1990 to 2019, we employed the Global Burden of Disease Study (GBD) Results Tool in conjunction with an age-period-cohort model. This approach facilitated the estimation of annual percentage changes in incidence, referred to as net drifts, encompassing the overall population. Additionally, we calculated annual percentage changes spanning ages 15 - 19 to 95 + years, denoted as local drifts. Furthermore, our analysis involved determining period and cohort relative risks, elucidating the effects associated with distinct periods and birth cohorts.

Results: Globally, 21,203,479 [95% uncertainty interval (UI): 18,799,322 - 23,704,124] cases of IHD occurred in 2019. There were 33 countries with at least 100000 cases. Between 1990 and 2019, the net drift of IHD incidence exhibited a range from -1.7% per year [95% confidence interval (CI): -1.79, -1.61] in countries with a high socio-demographic index (SDI) to 0.08% per year (95% CI: 0.05, 0.11) in countries with a low SDI. Age effects across all countries and genders demonstrated an increasing trend over time, indicating age as a significant risk factor for IHD. Moreover, period and cohort effects in higher SDI countries exhibited a more rapid decline in both genders compared to lower SDI countries. The findings indicated that nations with a higher SDI manifested overall favorable trends in the relative risk of IHD incidence, both across time and in successive younger birth cohorts.

Discussion: The incidence of IHD serves as a valuable and accessible indicator for assessing trends in IHD provision, spanning from early youth through later life. Enhancements in IHD prevention have the potential to mitigate risks for successively younger cohorts and, over time, redistribute the risk across all age groups. Despite global declines in IHD incidence over the last three decades, decreasing trends in incidence have slowed and, in some countries, flattened. Many countries have experienced unfavorable period and cohort effects.

Background: Accurately assessing the postoperative mortality and rehospitalization for heart failure risks in patients undergoing mitral valve repair surgery is of significant importance for individualized medical strategies.

Objective: We sought to develop and validate a risk assessment system for the prediction of mortality and rehospitalization for heart failure.

Methods: Personalized risk prediction system of mortality and rehospitalization for heart failure was developed. For developing a prediction system with death as the outcome, there were 965 patients (70%) and 413 patients (30%) were included in the the derivation cohort and the validation cohort. For developing a prediction system with rehospitalization for heart failure as the outcome, there were 927 patients (70%) and 398 patients (30%) were included in the derivation cohort and the validation cohort. There were 42 routine clinical variables used to develop the models. The performance evaluation of the model is based on the area under the curve (AUC). Evaluate the improvement with Euro Score II according to NRI and IDI net reclassification improvement (NRI) and integrated discrimination improvement (IDI).

Results: The median follow-up time was 685 days, the incidence of death was 3.85% (n = 53), and the incidence of rehospitalization for heart failure was 10.01% (n = 138). The AUC values of the mortality prediction model in the derivation and validation cohorts were 0.825 (0.764-0.886) and 0.808 (0.699-0.917), respectively. The AUC values of the rehospitalization for heart failure prediction model in the derivation and validation cohorts were 0.794 (0.756-0.832) and 0.812 (0.758-0.866), respectively. NRI and IDI showed that the mortality prediction model exhibited superior performance than the Euro Score II. The mortality and rehospitalization for heart failure risk prediction models effectively stratified patients into different risk subgroups.

Conclusion: The developed and validated models exhibit satisfactory performance in prediction of all-cause mortality and rehospitalization for heart failure after mitral valve repair surgery.

Clinical trial registration: http://www.clinicaltrials.gov, Unique identifier: (NCT05141292).

Background: Atherosclerosis is a leading cause of cardiovascular disease worldwide, while carotid atherosclerosis (CAS) is more likely to cause ischemic cerebrovascular events. Emerging evidence suggests that cuproptosis may be associated with an increased risk of atherosclerotic cardiovascular disease. This study aims to explore the potential mechanisms linking cuproptosis and CAS.

Methods: The GSE100927 and GSE43292 datasets were merged to screen for CAS differentially expressed genes (DEGs) and intersected with cuproptosis-related genes to obtain CAS cuproptosis-related genes (CASCRGs). Unsupervised cluster analysis was performed on CAS samples to identify cuproptosis molecular clusters. Weighted gene co-expression network analysis was performed on all samples and cuproptosis molecule clusters to identify common module genes. CAS-specific DEGs were identified in the GSE100927 dataset and intersected with common module genes to obtain candidate hub genes. Finally, 83 machine learning models were constructed to screen hub genes and construct a nomogram to predict the incidence of CAS.

Results: Four ASCRGs (NLRP3, SLC31A2, CDKN2A, and GLS) were identified as regulators of the immune infiltration microenvironment in CAS. CAS samples were identified with two cuproptosis-related molecular clusters with significant biological function differences based on ASCRGs. 220 common module hub genes and 1,518 CAS-specific DEGs were intersected to obtain 58 candidate hub genes, and the machine learning model showed that the Lasso + XGBoost model exhibited the best discriminative performance. Further external validation of single gene differential analysis and nomogram identified SGCE, PCDH7, RAB23, and RIMKLB as hub genes; SGCE and PCDH7 were also used as biomarkers to characterize CAS plaque stability. Finally, a nomogram was developed to assess the incidence of CAS and exhibited satisfactory predictive performance.

Conclusions: Cuproptosis alters the CAS immune infiltration microenvironment and may regulate actin cytoskeleton formation.

Myocardial infarction (MI), a widespread cardiovascular issue, mainly occurs due to blood clot formation in the coronary arteries, which reduces blood flow to the heart muscle and leads to cell death. Incorporating exercise into a lifestyle can significantly benefit recovery and reduce the risk of future cardiac events for MI patients. Non-coding RNAs (ncRNAs) play various roles in the effects of exercise on myocardial infarction (MI). ncRNAs regulate gene expression, influence cardiac remodeling, angiogenesis, inflammation, oxidative stress, apoptosis, cardioprotection, and cardiac electrophysiology. The expression of specific ncRNAs is altered by exercise, leading to beneficial changes in heart structure, function, and recovery after MI. These ncRNAs modulate molecular pathways that contribute to improved cardiac health, including reducing inflammation, enhancing angiogenesis, promoting cell survival, and mitigating oxidative stress. Furthermore, they are involved in regulating changes in cardiac remodeling, such as hypertrophy and fibrosis, and can influence the electrical properties of the heart, thereby decreasing the risk of arrhythmias. Knowledge on MI has entered a new phase, with investigations of ncRNAs in physical exercise yielding invaluable insights into the impact of this therapeutic modality. This review compiled research on ncRNAs in MI, with an emphasis on their applicability to physical activity.

Background: The complex relationship between insulin-like growth factor 1 (IGF-1) levels and heart failure (HF) is not fully understood, particularly across different populations and conditions. This meta-analysis aims to elucidate the dual perspectives of IGF-1 levels in the general population, HF patients, and individuals with treatment-naïve acromegaly, highlighting IGF-1 as a biomarker and potential therapeutic target in HF management.

Methods: Studies were searched across multiple electronic databases up to January 2024 and independently identified by reviewers. The outcomes were analyzed using RevMan 5.4 and STATA 15.

Results: A total of 25 articles were ultimately included in the analysis. Six studies compared IGF-1 levels between HF patients and non-HF controls, revealing significantly lower IGF-1 levels in HF patients (mean difference -20.93; 95% CI -37.88 to -3.97; p = 0.02). This reduction was consistent across various HF subtypes and severities. In addition, individuals with intermediate IGF-1 levels had a lower risk of developing HF [risk ratio (RR) 0.78; 95% CI 0.74-0.83; p < 0.01] and HF-related mortality (RR 0.98; 95% CI 0.97, 0.99; p < 0.01) compared to those with low IGF-1 levels, suggesting a protective role for maintaining adequate IGF-1 levels. Conversely, treatment-naïve acromegaly patients, characterized by excessively high IGF-1 levels, showed a significantly higher incidence of both diastolic HF [odds ratio (OR) 9.08; 95% CI 6.20-13.29; p < 0.01] and systolic HF (OR 13.1; 95% CI 6.64-25.84; p < 0.01), implicating supraphysiological IGF-1 levels in adverse cardiac outcomes.

Conclusions: Our meta-analysis highlights the complex interplay between IGF-1 levels and HF. We found that reduced IGF-1 levels are commonly observed in HF patients and are associated with an increased risk of HF and higher HF-related mortality. Conversely, excessively high levels, as observed in acromegaly, are linked to a higher incidence of HF. Based on these results, it is recommended that cardiac function be closely monitored in patients with reduced IGF-1 levels and in those with acromegaly. These findings suggest that IGF-1 could hold potential prognostic value for risk stratification in HF.