This comprehensive meta-analysis reveals that GLP-1 and dual GLP-1/GIP receptor agonists are associated with reduced risk of composite cardiovascular endpoints and worsening heart failure events. However, no statistically significant differences were observed regarding all-cause or cardiovascular mortality.
Dual antiplatelet therapy with aspirin and a P2Y₁₂ inhibitor is standard for patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention. While ticagrelor offers superior efficacy in reducing ischemic events compared to clopidogrel, its use is limited by a higher incidence of dyspnea, an adverse reaction whose underlying predictors remain incompletely understood. Genetic variations in CYP3A4/5, the principal enzymes responsible for ticagrelor metabolism, may influence interindividual susceptibility to this side effect.
In a prospective cohort of 385 ACS patients on ticagrelor, we genotyped CYP3A4 rs2242480 and CYP3A5 rs776746. Outcomes (dyspnea per CTCAE v5.0, bleeding per BARC criteria) were assessed over 1 year. Associations were analyzed using logistic regression and GMDR modeling.
The CYP3A5 rs776746 genotype strongly predicted dyspnea risk. Compared to the CC genotype, CT and TT genotypes were associated with a 55% and 91% reduced risk, respectively. Carriers of the combined CT/TT genotypes had a 63% lower risk. CC genotype carriers (poor metabolizers) exhibited a 2.3-fold higher dyspnea incidence. No significant associations were found for CYP3A4 rs2242480 or for bleeding outcomes.
The CYP3A5 rs776746 CC genotype is a significant genetic biomarker for ticagrelor-induced dyspnea. Pre-emptive genotyping could enable personalized antiplatelet therapy, such as alternative P2Y₁₂ inhibitors for high-risk CC carriers, to improve patient safety.
We read with great interest the article titled “Epicardial Fat Thickness as a Marker of Coronary Artery Disease in Diabetics: A Single Center Study” [1]. The authors highlight significant findings regarding epicardial fat thickness (EFT) as an effective marker of coronary artery disease (CAD) severity in diabetic patients. However, several methodological and analytical aspects warrant further clarification and discussion.
Firstly, the exclusion criteria used in the study notably omit consideration of chronic kidney disease (CKD), frequently comorbid with diabetes mellitus and potentially impactful on both CAD prevalence and EFT [2]. Additionally, the retrospective design of this study raises critical questions regarding the practicality and reliability of assessing CAD presence and severity in a substantial patient cohort (n = 2340). The authors describe employing invasive and noninvasive tests retrospectively based on clinical indications, but the specifics of these indications and the process for systematically retrieving and validating past clinical data remain unclear. This approach might introduce substantial bias related to clinician-dependent test selection.
Moreover, despite collecting detailed lipid profiles, the study did not address statin therapy usage, an essential consideration given its widespread use and known influence on CAD progression and potentially EFT itself. Future investigations would benefit from clarifying the role of statins or other pharmacotherapies that may influence EFT and CAD outcomes.
In summary, while this study provides insightful findings that underscore EFT's potential as a noninvasive cardiovascular marker, addressing these methodological and analytical concerns would considerably enhance the study's robustness and clinical applicability.
Sincerely,
Data sharing is not applicable for this article.
As marijuana use increases globally, understanding its cardiovascular impact is crucial. This study investigates the relationship between marijuana use patterns and coronary heart disease (CHD) risk.
Using 2023 Behavioral Risk Factor Surveillance System data, we conducted cross-sectional analysis examining marijuana consumption methods (smoking, vaping, eating, dabbing) and CHD risk. Multivariable logistic regression assessed associations while controlling for demographic variables and established cardiovascular risk factors.
Significant associations emerged between various marijuana consumption methods and increased CHD risk. Individuals engaging in both smoking and vaping showed significantly higher CHD risk. Combined consumption methods, particularly smoking and eating, further compounded risk among those with pre-existing cardiovascular risk factors. Traditional risk factors including hypertension, diabetes, and obesity remained critical CHD predictors.
This study reveals complex relationships between marijuana use patterns and CHD risk, emphasizing the need for comprehensive public health strategies addressing cardiovascular implications of marijuana consumption. As usage rises, particularly among younger populations, healthcare providers and policymakers must educate individuals about potential cardiovascular risks associated with different consumption methods. Further research is needed to elucidate mechanisms and inform future guidelines for CHD risk reduction.
Evaluation of percutaneous coronary intervention (PCI) effectiveness typically focuses on overall coronary events, often overlooking the specific location of these events within the coronary vasculature. This study aimed to evaluate the incidence of coronary events in patients treated with PCI and to investigate the correlation between these events, the location of the event within the treated site, and the type of stent used.
This study determined the proportion of coronary events occurring after percutaneous coronary intervention (PCI) and investigated the association between these events and the location of the previous treatment site. A retrospective cohort analysis was conducted on patients with stable coronary artery disease (CAD) who underwent PCI using either conventional or drug-eluting stents. Data was obtained from the MASS Clinical Research Unit database. The location of the coronary event was determined by angiography.
Five hundred and sixty two patients were included, with 232 (41.3%) experiencing coronary events. 55.8% of the events occurred at the treated site, while the remaining 44.2% were unrelated to the treated site. Of the events related to the treated site, 54.1% occurred in the conventional stent group and 61.1% in the drug-eluting stent group. No statistically significant association was found between the event in the treated site and the type of stent used (p = 0.363).
A significant proportion of coronary events occurred in untreated sites. Our results suggest that isolated evaluation of the treated site may provide a more accurate estimate of the effectiveness of stents.
To assess left atrial (LA) structure and function in marathon runners using two-dimensional speckle tracking echocardiography (2D-STE) and real-time three-dimensional echocardiography (RT-3DE).
This study enrolled 50 healthy volunteers (control group) and 132 marathon runners, and collected their general information. 2D-STE and RT-3DE were performed to obtain LA structural and functional parameters and left ventricular mass index (LVMI). According to the LVMI criteria for diagnosing left ventricular hypertrophy (LVH), all marathon runners were divided into an LVMI normal group and an LVH group. A comparative analysis was performed among the three groups. Multivariate logistic regression was used to analyze the association, and curve fitting was used to show the change trends.
Compared with the control group, LA total ejection fraction (LATEF) and LA passive ejection fraction (LAPEF) were higher in the LVMI normal group (p < 0.05). Compared with the control group and the LVMI normal group, LA maximal volume index (LAVImax), LA presystolic volume index (LAVIpre), and LA stiffness index (LASI) were higher in the LVH group, whereas LA reservoir strain (LASr), LA conduit strain (LAScd), and LA contraction strain (LASct) were lower (p < 0.05). Multivariate logistic regression analysis showed that LAVImax, LAScd, and LASct were significantly associated with LVH in marathon runners. Curve fitting showed that LAVImax increased with the increase of LVMI, whereas LAScd and LASct decreased.
2D-STE and RT-3DE can effectively assess LA structure and function in marathon runners. Marathon runners with normal LVMI exhibit normal LA structure and function, and even some functional enhancement, while those with LVH exhibit increased LA volume and decreased LA strain function.
The prognostic impact of catheter ablation in patients with atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF) remains controversial. Using a nationwide database, the authors demonstrated that catheter ablation was associated with cardiovascular and cerebral benefits, as well as a reduction in all-cause mortality, in patients with AF and HFpEF [1]. Several concerns arise from these findings.
The authors assessed all-cause mortality in the HFpEF cohort, although the prescription rates of guideline-directed medical therapy—including sodium–glucose cotransporter-2 inhibitors—were extremely low [1]. This may limit the interpretation of mortality reduction attributable to catheter ablation itself.
The major causes of death in HFpEF are generally noncardiac [2]. The mechanism by which catheter ablation would reduce all-cause mortality in this population therefore remains unclear. Catheter ablation helps prevent thrombus formation and stroke, and may reduce worsening heart failure by preserving atrial contraction. However, it is unlikely to directly decrease noncardiac events, which represent a substantial proportion of deaths in HFpEF.
The authors excluded patients who underwent valve replacement [1]. Yet, one of the most advanced clinical scenarios of HFpEF with AF involves significant valvular disease—particularly mitral regurgitation—that requires intervention [3]. Including such patients would improve the generalizability of the findings to a more representative HFpEF population. Moreover, individuals with severe valvular disease often have markedly remodeled atria and are seldom considered for catheter ablation.
Another important issue not evaluated in this study is bleeding related to anticoagulant therapy [1]. Patients with HFpEF may be at higher risk of bleeding complications than those with reduced ejection fraction [4]. In this regard, we strongly recommend considering left atrial appendage closure at the time of catheter ablation to mitigate anticoagulant-related bleeding risk, if applicable.
The authors have nothing to report.
The authors have nothing to report.
The authors declare no conflicts of interest.
The authors have nothing to report.
Insomnia is a prevalent sleep disorder increasingly recognized as a risk factor for cardiovascular diseases (CVDs). However, its causal relationship with myocardial infarction (MI) and its impact on coronary plaque vulnerability remain poorly understood.
We performed Mendelian randomization (MR) analysis using genome-wide association study (GWAS) summary data for insomnia (n = 462,341) and MI (n = 484,598) in populations of European descent. Additionally, 340 patients with coronary artery disease (CAD) underwent coronary angiography and optical coherence tomography (OCT) imaging. Insomnia was assessed by the Insomnia Severity Index (ISI), and OCT was used to evaluate plaque features including thin-cap fibroatheroma (TCFA), fibrous cap thickness, lipid arc, macrophage infiltration, and plaque rupture.
MR analysis showed a potential causal effect of genetically predicted insomnia on MI risk (OR = 1.015; 95% CI: 1.004–1.027; p = 0.007), with no evidence of pleiotropy or heterogeneity. Clinically patients with insomnia (ISI ≥ 8) had higher rates of hypertension (54.3% vs. 39.6%) and MI (32.4% vs. 21.7%), elevated CRP levels, and exhibited greater plaque vulnerability on OCT, including increased incidence of TCFA (29.5% vs. 17.0%), thinner fibrous caps, larger lipid arcs, and more frequent macrophage infiltration and plaque rupture. Logistic regression identified both insomnia (OR = 1.806; p = 0.037) and CRP (OR = 1.384; p = 0.034) as independent predictors of TCFA.
This study provides genetic and clinical evidence that insomnia contributes to MI risk and coronary plaque vulnerability, underscoring the importance of addressing sleep disturbances in CAD management.
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