Minerva cardiology and angiology最新文献

Background: Early diagnosis of hypertension (HT) is crucial for preventing end-organ damage. This study aims to identify the risk factors for future HT in young individuals through the application of machine learning (ML) models.

Methods: The study included individuals aged 18-40 years who had not been diagnosed with HT through ambulatory blood pressure monitoring (ABPM). These participants were monitored for hypertension diagnosis from the date of ABPM application until the date of data collection. Hypertension prediction was carried out using three distinct ML methods: Support Vector Machine, Random Forest, and Least Absolute Shrinkage and Selection Operator. The identification of variables significant for future HT was based on the outcomes of these models.

Results: This study comprised 516 patients, with a mean follow-up duration of 793.4±58.6 days. Following the integration of demographic data, laboratory results, and ABPM findings into the ML models, age, high-density lipoprotein cholesterol, triglycerides, and the standard deviation of systolic blood pressure (SDsis) were identified as predictors for future HT. A logistic regression with the selected variables (age, diabetes mellitus history, HDL, triglycerides, white blood cell count, and SDsis) using the full data set gave the following log odds 0.0737 (P<0.001), 0.7146 (P<0.001), -0.0160 (P=0.071), 0.0026 (P=0.002), 0.0857 (P=0.069), and 0.0850 (P=0.005), respectively. The corresponding probability values of age, diabetes mellitus history, HDL, triglycerides, white blood cell count, and SDsis were 0.5184, 0.6714, 0.4960, 0.5006, 0.5214, and 0.5212, respectively. This indicates a unit increase in all factors, except diabetes mellitus history, increases the probability of future HT by 50%. A history of diabetes, however, increases the probability of future HT by more than two thirds. The history of diabetes mellitus emerged as the most crucial predictor of future HT across all applied methods.

Conclusions: ML methods appear to be valuable tools for predicting future HT. The widespread adoption of these methods and the refinement of more comprehensive models will lay the groundwork for future studies.

Anticoagulation is indicated for treatment and prevention of arterial and venous thrombosis. Targeting different steps of the coagulation process, currently available anticoagulants entail an increased risk of bleeding, which detrimentally impacts on prognosis and hinders the administration of an effective antithrombotic regimen. Factor XI (FXI) inhibition has emerged as a strategy to uncouple prevention of thrombosis from bleeding. Indeed, while FXI is crucial for the amplification phase in pathological thrombosis, it is ancillary in physiological hemostasis. A comprehensive search in several scientific databases has been performed to identify relevant studies in the field. In addition, ongoing trials have been searched for in proper datasets to provide an updated and comprehensive assessment of the current state of investigations on FXI inhibition. Many compounds have been tested to inhibit FXI at different stages (i.e., synthesis, activation, or interactions with target molecules and coagulation factors). These include antisense oligonucleotides, monoclonal antibodies, small molecules, natural peptides and aptamers. In phase 2 studies, FXI inhibitors reduced thrombotic complications without any corresponding increase in bleeding. FXI inhibitors were noninferior and potentially superior to low-molecular-weight heparin in orthopedic surgery and reduced bleeding compared to apixaban in patients with atrial fibrillation. FXI inhibition is also under testing in other conditions, including end-stage renal disease, cancer, or noncardioembolic stroke. FXI inhibition represents a promising and rapidly emerging approach for a number of clinical indications. This article reviews the rationale, evidence, pharmacology, and future applications of FXI inhibition.

Background: We aimed to explore the impact of aspirin use on the risk of readmission and mortality in patients with myocardial infarction and pneumonia.

Methods: This was a cohort study including 703 participants with severe pneumonia and myocardial infarction included in the Medical Information Mart for Intensive Care (MIMIC)-III and the MIMIC-IV. Kaplan-Meier survival analysis was used to show the readmission and survival probability of patients with or without aspirin. In addition, univariate and multivariable models were used to investigate the impact of aspirin on the risk of readmission or mortality of patients. Subgroup analyses were conducted in terms of age, gender, antibiotic use, vancomycin and ampicillin use.

Results: Average follow-up was one year, 22% of patients experienced readmission, and 72% patients survived. After the confounders were adjusted for, a 0.46-fold decreased risk of readmission (hazard ratio [HR]=0.46, 95% confidence interval [CI]: 0.27-0.78) and a 0.58-fold decreased risk of one-year mortality (HR=0.56, 95%CI: 0.42-0.82) were observed favoring aspirin use. Subgroup analyses revealed that aspirin was, however, associated with an increased risk of mortality in patients not receiving vancomycin treatment (HR=1.79, 95%CI: 1.08-2.97).

Conclusions: Our findings suggest that clinicians should consider using aspirin in patients with severe myocardial infarction and pneumonia was recommended.

Background: Doxorubicin (DOX) is a potent anti-cancer medication that is associated with numerous adverse effects, particularly concerning damage to the heart.

Methods: This study aimed to investigate the impact of sophocarpine (SOP) on DOX-induced heart injury through both in vivo and in vitro experiments. The experimental techniques employed encompassed echocardiography, hematoxylin/eosin (H&E) staining, Masson staining, immunohistochemical staining, western blotting, and so on.

Results: Echocardiography showed that SOP alleviated DOX-induced cardiac dysfunction, as evidenced by the improvements in both left ventricle ejection fraction and left ventricle fractional shortening. DOX caused upregulations of creatine kinase-MB and lactate dehydrogenase, while SOP decreased these indices. Staining methods such as H&E and Masson showed that SOP reversed the pathological changes induced by DOX. DOX elevated the expression levels of fibrosis-associated proteins such as Collagen I, Collagen III, α-SMA, Fibronectin, MMP-2, and MMP-9. However, SOP reversed these changes. Moreover, the study further revealed that SOP inhibited the TGF-β1/Smad3 signaling pathway.

Conclusions: These findings imply that SOP has the potential to mitigate DOX-induced heart injury by suppressing fibrosis. The underlying molecular mechanism may involve the inhibition of the TGF-β1/Smad3 signaling pathway.

Background: Heart failure with preserved ejection fraction (HFpEF) with renal dysfunction (RD) is considered to be a specific phenotype of HFpEF. This study aimed to compare the clinical characteristics and prognostic factors for in-hospital mortality between HFpEF-diagnosed patients with and without RD.

Methods: This multicenter retrospective study included 5867 consecutive patients with acute HFpEF. RD was defined by an estimated glomerular filtration rate (eGFR) of <60 mL/min per 1.73 m². Kaplan-Meier survival curves and log-rank tests were used to compare the in-hospital mortality between the groups. Univariable and multivariable Cox regression analyses were performed to identify significant prognostic factors.

Results: Across the study cohort, 68% of patients had RD. In-hospital mortality was significantly higher in HFpEF patients with RD than in those without RD. The comorbidities and laboratory data differed significantly between the groups. Independent prognostic factors for in-hospital mortality in the HFpEF patients with RD were age (hazard ratio [HR], 1.039), systolic blood pressure (HR, 0.991), eGFR (HR, 0.981), C-reactive protein (CRP; HR, 1.028), diuretics (HR, 0.374), angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers (ACE-I/ARBs; HR, 0.680), and beta-blockers (HR, 0.662). In HFpEF patients without RD, age (HR, 1.039), systolic blood pressure (HR, 0.979), and ACE-I/ARBs (HR, 0.373) were independent prognostic factors.

Conclusions: Significant differences in the clinical characteristics and prognostic factors, such as CRP and beta-blockers, were observed between the HFpEF patients with and without RD. These results have implications for future research and may help guide individualized patient management strategies.

Coronary physiological assessment has garnered extensive application in managing patients with coronary artery disease, encompassing both acute and chronic scenarios. Beyond the historical purpose as tool to define the hemodynamic significance of a given artery lesion, coronary artery physiology allows for a complete investigation of epicardial and microvascular circulation. The longitudinal assessment of the distribution pattern of coronary disease based on pressure wire technology provides crucial information to define the best management and procedural planning. Moreover, post-percutaneous coronary intervention physiology reassessment showed a strong association with clinical outcomes and, more importantly, it can spot residual pressure gradients potentially amenable to further intervention and optimization. Growing evidence about the non-invasive angiography-based indices helps to overcome the limitations of the use of intracoronary physiology. This review aims to provide an overview of different utilizations of coronary physiology offering a historical perspective with a particular focus on current challenges and future potential applications.

Transcatheter aortic valve intervention (TAVI) was introduced in early 2000 to offer treatment to inoperable patients with severe aortic valve stenosis. In a couple of decades, the procedure resulted effective and safe also in patients with intermediate to low risk for surgery; therefore, due to the progressive ageing of the population, the clinical need for TAVI is continuously increasing and is hardly met by the availability of the procedure, the so-called "TAVI capacity". As a result, many patients encounter difficulties in being referred to TAVI centers or face long waiting list times, thus risking severe adverse events (including death) before the procedure is performed. Although contemporary guidelines and consensus documents recommend that TAVI should only be performed in hospitals with active cardiac surgery departments, starting TAVI programs also in interventional cardiac laboratories without on-site cardiac surgery could represent a way to increase TAVI capacity, thus leading to a greater number of patients being treated in less time. On the other side of the coin, such a strategy may jeopardize patient safety in case of periprocedural complications needing bailout surgery and may lead to a suboptimal multidisciplinary Heart Team evaluation. This review aims to assess and discuss available clinical data and implementation of TAVI programs in hospitals without on-site active cardiac surgery departments considering the growing unmet clinical need and technical advancement of TAVI platforms, yet not overlooking the recommendations of international scientific societies.

Background: LncRNAs, miRNAs, and the sponge effect between them exert diverse biological influences on the pathogenesis and progression of coronary artery disease (CAD), thus necessitating an exploration of the lncRNA-miRNA-gene regulatory network in CAD.

Methods: Expression profile GSE98583 was obtained from NCBI, containing the data of 12 CAD patients and 6 controls. Limma package was utilized to determine the differentially expressed genes (DEGs). Functional enrichment analysis was performed by DAVID. The CAD-related miRNA-DEG associations were retrieved via HMDD and miRTarBase, and the CAD-related lncRNA-miRNA associations were retrieved via LncRNADisease and starBase. The CAD-related lncRNA-miRNA-DEG regulatory network was constructed by combining these associations. The dual luciferase test was carried out to validate the connections among lncRNA, miRNA, and gene.

Results: Overall, 534 DEGs were identified between CAD samples and controls, including 243 up-regulated and 291 down-regulated, and were enriched in various gene ontology biological processes and KEGG pathways. The CAD-related miRNAs targeting DEGs included hsa-miR-206, has-miR-320b, has-miR-4513, has-miR-765, and has-miR-92a-3p, and hsa-miR-92a-3p regulated the most DEGs. In the lncRNA-miRNA associations, only CDKN2B-AS1 regulated the CAD-related miRNA, hsa-miR-92a-3p, which was validated using the dual luciferase test.

Conclusions: CDKN2B-AS1 may act as an hsa-miR-92a-3p sponge to regulate the downstream DEGs in CAD. CDKN2B-AS1/ hsa-miR-92a-3p/GATA2 might be a novel mechanism for CAD.

Background: Coronary flow reserve (CFR) has an emerging role to predict outcome in patients with and without flow-limiting stenoses. However, the role of its surrogate pressure bounded-CFR (Pb-CFR) is controversial. We investigated the usefulness of combined use of fractional flow reserve (FFR) and Pb-CFR to predict outcomes.

Methods: This is a sub-study of the PROPHET-FFR Trial, including patients with chronic coronary syndrome and functionally tested coronary lesions. Patients were divided into four groups based on positive or negative FFR (cut-off 0.80) and preserved (lower boundary ≥2) or reduced (upper boundary <2) Pb-CFR: Group1 FFR≤0.80/ Pb-CFR <2; Group 2 FFR≤0.80/Pb-CFR≥2; Group 3 FFR >0.80/Pb-CFR<2; Group 4 FFR>0.80/Pb-CFR≥2. Lesions with positive FFR were treated with PCI. Primary endpoint was the rate of major adverse cardiac events (MACEs), defined as a composite of death from any cause, myocardial infarction, target vessel revascularization, unplanned cardiac hospitalization at 36-months.

Results: A total of 609 patients and 816 lesions were available for the analysis. At Kaplan-Meier analysis MACEs rate was significantly different between groups (36.7% Group 1, 27.4% Group 2, 19.2% Group 3, 22.6% Group 4, P=0.019) and more prevalent in groups with FFR≤0.80 irrespective of Pb-CFR. In case of discrepancy, no difference in MACEs were observed between groups stratified by Pb-CFR. FFR≤0.80 was associated with an increased MACEs rate (30.2% vs. 21.5%, P<0.01) while Pb-CFR<2 was not (24.5% vs. 24.2% Pb-CFR≥2 P=0.67).

Conclusions: FFR confirms its ability to predict outcomes in patients with intermediate coronary stenoses. Pb-CFR does not add any relevant prognostic information.