Cardiovascular diagnosis and therapy最新文献

Background: The correlation between the gamma-glutamyl transferase-to-albumin ratio (GAR) and the risk of bleeding in patients with non-valvular atrial fibrillation (NVAF) undergoing treatment with the dabigatran anticoagulant is poorly understood. This study aims to explore whether GAR is associated with bleeding events among patients with NVAF receiving dabigatran anticoagulant therapy.

Methods: We conducted a multicenter, observational cohort study in 12 Chinese hospitals from six provinces, including Beijing, Shanghai and Guangzhou, to evaluate the effectiveness and safety of dabigatran (110 mg) treatment in NVAF patients who were consecutively enrolled during February 2015 and December 2017. All patients had completed a 3-month follow-up period. The baseline variable of interest was the GAR, and the outcome variable was the occurrence of bleeding events. Both univariate and multivariate Cox proportional hazard models were used to evaluate the relationship between GAR and bleeding outcome.

Results: This prospective cohort study included a total of 834 patients (mean age 65.6±11.1 years; 56.8% male). Overall, 82 subjects experienced bleeding. The patients were categorized based on the tertiles of the GAR. Participants in tertile 2 (0.59-1.03) [hazard ratio (HR): 0.28; 95% confidence interval (CI): 0.14-0.55; P<0.001] and tertile 3 (≥1.04) (HR: 0.47; 95% CI: 0.25-0.89; P=0.02) exhibited a lower rate of bleeding compared to the reference group (T1: ≤0.58). Multivariable models with restricted cubic splines demonstrated a nonlinear relationship between GAR and bleeding outcome, with a GAR inflection point of 0.68. The HR (95% CI) was 0.05 (0.01-0.31) (P=0.002) for GAR values <0.68 and 0.96 (0.70-1.31) (P=0.78) for GAR values ≥0.68. Moreover, the correlation between decreased GAR and an increase in bleeding events remained consistent across various subgroups.

Conclusions: GAR is a prevalent, independent predictor of dabigatran-related bleeding in NVAF patients. Moreover, a significant L-shaped association between GAR and bleeding events has been observed.

Background and objective: The most common valvular heart disease in the US is moderate to severe mitral regurgitation (MR). Function MR or secondary MR comprises many of these cases. Moderate and severe secondary MR are independently associated with increased all-cause mortality and rehospitalization for heart failure. Both ischemic and nonischemic cardiomyopathy can cause secondary MR via similar pathophysiology that leads to inadequate valve leaflets coaptation. The management of secondary MR is complex. The optimal treatment strategy for secondary MR remains controversial, reflected in the vast array of treatment options and the complexity of therapeutic decision-making. Several surgical mitral valve repair techniques have been described in the literature. Many of these aims to facilitate adequate valve leaflet coaptation. In this review, the pathophysiology of MR is described with a focus on evaluating and managing secondary MR.

Methods: A literature review was performed using PubMed and Google Scholar. Clinical trials, meta-analyses, randomized controlled trials, reviews, and systematic reviews were considered from January 1, 1995 through December 31, 2022. Articles published in languages other than English with limited text availability were excluded.

Key content and findings: Optimal therapeutic approach in severe secondary MR is complex and several patient factor should be considered. We provide a framework for the surgical management of secondary MR based on echocardiographic parameters, the presence of ischemia, and myocardial viability.

Conclusions: Further study is needed to guide the selection of patients most likely to benefit from mitral valve repair or replacement in the setting of secondary MR.

The number of adults with congenital heart defects (ACHDs) is steadily increasing and is about 360,000 in Germany. Congenital heart defect (CHD) is often associated with pulmonary hypertension (PH), which sometimes develops early in untreated CHD. Despite timely treatment of CHD, PH not infrequently persists, redevelops in older age, and is associated with significant morbidity and mortality. The revised European Society of Cardiology (ESC)/European Respiratory Society (ERS) 2022 guidelines for the diagnosis and treatment of PH represent a significant contribution to the optimized care of those affected. However, the topic of "adults with congenital heart defects" is treated only relatively superficially in this context. After the first part commenting on a broad range of topics like definition, epidemiology, classification, diagnostics, genetics, risk stratification and follow-up, and gender aspects, the second part focuses on supportive therapy, special situations (pregnancy, contraception, non-cardiac surgery), targeted pharmacotherapy, organ transplantation, special management [shunt lesion, left ventricular (LV) disease, univentricular hearts], interventions, intensive care, ACHD follow-up, and future perspective. In the present article, therefore, this topic is commented on from the perspective of congenital cardiology. By examining these aspects in detail, this article aims to fill the gaps in the existing guidelines and provide a more thorough understanding from the perspective of congenital cardiology.

Background: Left ventricular end-diastolic pressure (LVEDP) is a key indicator of cardiac health. The gold-standard method of measuring LVEDP is invasive intra-cardiac catheterization. Echocardiography is used for non-invasive estimation of left ventricular (LV) filling pressures; however, correlation with invasive LVEDP is variable. We sought to use machine learning (ML) algorithms to predict elevated LVEDP (>20 mmHg) using clinical, echocardiographic, and biomarker parameters.

Methods: We identified a cohort of 460 consecutive patients from the Cleveland Clinic, without atrial fibrillation or significant mitral valve disease who underwent transthoracic echocardiography within 24 hours of elective heart catheterization between January 2008 and October 2010. We included patients' clinical (e.g., heart rate), echocardiographic (e.g., E/e'), and biomarker [e.g., N-terminal brain natriuretic peptide (NT-proBNP)] profiles. We fit logistic regression (LR), random forest (RF), gradient boosting (GB), support vector machine (SVM), and K-nearest neighbors (KNN) algorithms in a 20-iteration train-validate-test workflow and measured performance using average area under the receiver operating characteristic curve (AUROC). We also predicted elevated tau (>45 ms), the gold-standard parameter for LV diastolic dysfunction, and performed multi-class classification of the patients' cardiac conditions. For each outcome, LR weights were used to identify clinically relevant variables.

Results: ML algorithms predicted elevated LVEDP (>20 mmHg) with good performance [AUROC =0.761, 95% confidence interval (CI): 0.725-0.796]. ML models showed excellent performance predicting elevated tau (>45 ms) (AUROC =0.832, 95% CI: 0.700-0.964) and classifying cardiac conditions (AUROC =0.757-0.975). We identified several clinical variables [e.g., diastolic blood pressure, body mass index (BMI), heart rate, left atrial volume, mitral valve deceleration time, and NT-proBNP] relevant for LVEDP prediction.

Conclusions: Our study shows ML approaches can robustly predict elevated LVEDP and tau. ML may assist in the clinical interpretation of echocardiographic data.

Background: Numerous studies have documented the effects of daytime napping, sleep duration, and depression on cardiovascular diseases (CVDs). However, the evidence has been gleaned from observational studies that might be riddled with confounding variables and the possibility of reverse causation bias. Therefore, the present study employed a Mendelian randomization (MR) methodology to meticulously explore the relationships between daytime napping, sleep duration, and depression, and the risk profiles of CVDs.

Methods: Genome-wide significant genetic variants associated with daytime napping, sleep duration, and depression were used as the instrumental variables (IVs). Data on the genetic correlations between these IVs and 15 CVDs were derived from the United Kingdom (UK) Biobank, Finnish Genome Studies, and other large-scale collaborations. We conducted both univariate and multivariate MR analyses to assess the overall effects and mediated relationships after adjusting for potential confounders, including body mass index (BMI), smoking status, and type 2 diabetes. The effect sizes were estimated using inverse variance-weighted (IVW) regression.

Results: The MR analysis revealed that an increased risk of heart failure (HF) [odds ratio (OR): 1.366; 95% confidence interval (CI): 1.013-1.842; P=0.04], coronary atherosclerosis (OR: 1.918; 95% CI: 1.257-2.927; P=0.003), myocardial infarction (MI) (OR: 1.505; 95% CI: 1.025-2.211; P=0.04), and coronary artery disease (CAD) (OR: 1.519; 95% CI: 1.130-2.043; P=0.006) was significantly associated with genetically predicted daytime napping. Prolonged sleep duration was found to be related to a reduced risk of HF (OR: 0.995; 95% CI: 0.993-0.998; P=2.69E-04), peripheral vascular disease (PVD) (OR: 0.984; 95% CI: 0.971-0.997; P=0.02), and CAD (OR: 0.997; 95% CI: 0.994-0.999; P=0.006). Additionally, a statistically significant positive relationship was observed between depressive disorders and the occurrence of atrial fibrillation (AF) (OR: 1.298, 95% CI: 1.065-1.583, P=0.01), indicating a heightened susceptibility. The multivariable MR analyses substantiated the reliability of the observed associations between daytime napping and the incidence of HF and CAD, following adjustments for genetically predicted BMI and smoking. The sensitivity analysis did not reveal any evidence of horizontal pleiotropy or heterogeneity, thus supporting the validity of the study's results.

Conclusions: This MR investigation posits a potential causal nexus between daytime napping, sleep duration, and depression, and the genesis of CVDs, offering new perspectives on the prevention and management of CVDs.

The number of adults with congenital heart defects (ACHDs) is steadily increasing and is about 360,000 in Germany. Congenital heart defect (CHD) is often associated with pulmonary hypertension (PH), which sometimes develops early in untreated CHD. Despite timely treatment of CHD, PH not infrequently persists, redevelops in older age, and is associated with significant morbidity and lethality. The revised European Society of Cardiology (ESC)/European Respiratory Society (ERS) 2022 guidelines for the diagnosis and treatment of PH represent a significant contribution to the optimized care of those affected. However, the topic of "adults with congenital heart defects" is treated only relatively superficially in this context. In the present article, part I, therefore, this topic is commented on in detail from the perspective of congenital cardiology with a special focus on definition, epidemiology, classification, diagnostics, genetics, risk stratification and follow-up and gender aspects of PH in ACHDs. This paper consists of two parts. Part II will provide comments on the topics of supportive therapy, special situations like pregnancy, contraception, and non-cardiac surgery, targeted pharmacotherapy, organ transplantation, special management like shunt lesion, left ventricular disease, and univentricular hearts, interventions, intensive care, ACHDs follow-up and future perspective on PH in ACHDs. By examining these aspects in detail, this article aims to fill the gaps in the existing guidelines and provide a more thorough understanding from the perspective of congenital cardiology.

Background: Myocardial fibrosis is a key pathological feature of many cardiovascular diseases, leading to cardiac dysfunction. Transforming growth factor β1 (TGF-β1) induces the proliferation and activation of cardiac fibroblasts (CFs), key contributors to myocardial fibrosis. To explore the mechanism underlying myocardial fibrosis, we aimed to determine whether serine/threonine kinase 38 like (STK38L) contributes to the development of myocardial fibrosis by regulating the proliferation and activation of CFs triggered by TGF-β1.

Methods: In this study, atrial tissue samples from atrial fibrillation (AF) patients with features of myocardial fibrosis (a category of atrial cardiomyopathy) and sinus rhythm (SR) patients without myocardial fibrosis were collected for RNA sequencing (RNA-seq). The specific molecule STK38L was identified. Primary mouse CFs were activated with TGF-β1 and subsequently transfected with STK38L-small interfering RNA (siRNA). The effect of STK38L-siRNA on fibroblast activation and proliferation was assessed using scratch and Cell Counting Kit-8 (CCK-8) assays. Furthermore, a mouse model of myocardial fibrosis induced by continuous subcutaneous injection of isoprenaline (ISO) was established to assess STK38L expression levels. Molecular experiments confirmed the expression of STK38L in fibrotic atrial tissues, ventricular tissues of ISO mouse, and primary CFs of neonatal mice.

Results: We identified 1,870 genes exhibiting differential expression in the RNA-seq data between the AF and SR groups. Masson's trichrome staining revealed increased fibrosis in the heart tissues of the AF group. Elevated levels of STK38L were observed in the atrial tissues of the AF group and in the TGF-β1-stimulated primary mouse CFs. In vitro, STK38L knockdown suppressed mouse CFs activation and proliferation. Additionally, in vivo experiments showed that elevated mRNA levels of STK38L, periostin (POSTN), and collagen type I alpha 1 chain (COL1A1) in ISO-treated mouse hearts correlated with greater myocardial fibrosis, suggesting that STK38L plays an important role in the development of fibrosis.

Conclusions: This study revealed a significant correlation between increased STK38L expression and AF characterized by atrial fibrosis as well as between STK38L expression and the TGF-β1-related induction of myocardial fibrosis. Additionally, STK38L knockdown was shown to suppress CFs activation and proliferation under TGF-β1 stimulation. These findings suggest an important role of STK38L in the development of fibrosis, and help screen for new strategies to treat this complex disease.

Percutaneous coronary intervention (PCI) for coronary bifurcation disease remains one of the most challenging situations in interventional cardiology in terms of procedural success rates and long-term cardiac events. Optical coherence tomography (OCT), with a higher signal-to-noise ratio and the ability to distinguish plaque components, can display the true condition of bifurcation lesions without overlapping or shortening and achieve detailed visualization of vascular structures, which is superior to those of other imaging modalities. Three-dimensional (3D) reconstruction of OCT images (3D-OCT) helps to gain a more informed understanding of the geometry and morphology of bifurcation lesions and provide additive information on plaque distribution. Following stent implantation, 3D-OCT can also guide the re-crossing of guide wires through stent struts jailing the side branch (SB) ostium and more clearly display the jailing strut configuration, as well as the ideal position of the guidewire recrossing point and stent struct link connection, to confirm the optimal guidewire position and understand interactions between stents and vessel walls, which may improve clinical results after PCI. The present review provides an up-to-date overview of the clinical use of 3D-OCT for accurate assessment of bifurcation anatomy, guiding the optimal guidewire rewiring into SB during bifurcation stenting, and evaluation of post-PCI results, offering novel information about atherosclerotic disease or stenting process.