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Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine that increased in patients with established type 2 diabetes mellitus (DM). Diabetic cardiomyopathy (DC), defined as left ventricular diastolic dysfunction (LVDD) in patients with type 2 DM in the absence of arterial hypertension, heart disease, or other heart disease, was assessed by GDF-15 levels in type 2 DM patients with and without DC. A total of 213 DM outpatients had blood samples drawn and on the same day (basal) underwent echocardiography and treadmill exercise testing. Plasma GDF-15 concentrations were measured by an enzyme-linked immunosorbent assay (ELISA) at baseline. DC was diagnosed in the presence of LVDD, defined when early mitral valve flow velocity (E) and early diastolic lengthening velocity (E′) ratio was E/E′ ≥15. The prevalence of DC was 21.13%. GDF-15 levels were higher in patients with DC compared with those without DC (5,273 [8,708.4] vs 2,812.66 [7,662.1] pg/ml, respectively, p <0.001). We assessed predictors of DC using multivariate regression analysis. GDF-15 (odds ratio 9.9; 95% confidence interval [3.9 to 24.5], p <0.001) was the unique independent predictor of DC. The results of receiver operating characteristic curve show that the cut-off point of 3,812 pg/ml of GDF-15 was indicative for DC (AUC = 0.83, sensitivity = 82.2% and specificity = 70.2%, p <0.0001). In conclusion, GDF-15 represents a useful and novel tool to screen DC in patients with type 2 DM.

A significant portion of the population is exposed to airborne PM 10 levels exceeding WHO guidelines, particularly during desert dust events, which are increasing due to climate change. Cardiovascular mortality has been linked to PM 10 exposure, but most studies rely on outdoor air quality data that may not reflect indoor exposure. This study, DESERT HEART, examines whether indoor PM 10 exposure during dust events influences airway inflammation and oxidative stress in 40 patients with stable chronic heart failure (HF). Sputum samples were collected weekly for three weeks, and biomarkers (IL-8, MDA, MMP-9, TGF-ß1, CRP) were analyzed. Indoor PM 10 levels were monitored at patients’ homes. Mixed regression models assessed the impact of PM 10  ≥ 90 µg/m 3 on biomarkers. Analysis of 120 sputum samples and 720 days of air quality data showed that exposure significantly increased biomarker levels on the first day: IL-8 (+ 6.9 ng/gwt, p  = 0.032), MDA (+ 1.3 nmol/gwt, p  = 0.014), MMP-9 (+ 222.4 ng/gwt, p  = 0.09), TGF-ß1 (+ 4.1 ng/gwt, p  = 0.058), and CRP (+ 2 ng/gwt, p  = 0.02), followed by a sharp decline. These findings suggest that indoor PM 10 exposure from desert dust events acutely exacerbates airway inflammation and oxidative stress in HF patients, highlighting the need for targeted interventions.

Background: Whether or not inhalation of airborne desert dust has adverse health effects is unknown. The present study, based on a systematic review and meta-analysis, was carried out to assess the influence desert dust on cardiovascular mortality, acute coronary syndrome, and heart failure. Methods: A systematic search was made in PubMed and Embase databases for studies published before March 2020. Studies based on daily measurements of desert dust were identified. The meta-analysis evaluated the impact of desert dust on cardiovascular events the same day (lag 0) of the exposure and during several days after the exposure (lags 1 to 5). The combined impact of several days of exposure was also evaluated. The incidence rate ratio (IRR) with 95% confidence intervals (CI) was calculated using the inverse variance random effects method. Results: Of the 589 identified titles, a total of 15 studies were selected. The impact of desert dust on the incidence of cardiovascular mortality was statistically significant (IRR = 1.018 (95%CI 1.008–1.027); p < 0.001) in lag 0 of the dust episode, in the following day (lag 1) (IRR = 1.005 (95%CI 1.001–1.009); p = 0.022), and during both days combined (lag 0–1) (IRR = 1.015 (95%CI 1.003–1.028); p = 0.014). Conclusions: The inhalation to desert dust results in a 2% increase (for every 10 µg/m3) in cardiovascular mortality risk.

Background/Objectives: Heart failure (HF) is associated with chronic systemic inflammation, resulting in increased mortality. The intestinal microbiota can modulate systemic inflammation, and changes in the microbiota have been observed in patients with HF. Methods: A systematic search was performed in PubMed/MEDLINE up until July 2025 for studies comparing the intestinal microbiota between patients with HF and healthy controls (HCs). The PRISMA (Preferred Reporting Items for Systemic reviews and Meta-Analyses) criteria were used. The risk of bias was evaluated with the Newcastle–Ottawa scale for cross-sectional studies. Results: Fourteen studies with 1167 participants (550 patients with HF and 617 HC) were included. The patients with HF had less alpha and beta diversity compared with HC. In turn, the patients with HF presented an increase in proinflammatory bacteria belonging to the genera Streptococcus and Escherichia-Shigella, and a decrease in bacteria with anti-inflammatory effects, pertaining to the genera Faecalibacterium, Blautia and Lachnospira. Conclusions: Patients with HF present an altered intestinal microbiota, favoring the growth of bacteria that increase systemic inflammation through their metabolic activity. Modulation of the intestinal microbiota through different approaches is seen as a new therapeutic target in HF.

Background/Objectives: Mitral regurgitation (MR) is the most common valvular defect worldwide, with an increasing incidence attributed to the aging population. Transcatheter edge-to-edge repair (TEER) is a viable treatment, but its long-term survival impact, particularly across sexes, remains underexplored. We aimed to assess relative survival (RS) and excess mortality (EM) in patients undergoing TEER for significant MR, with a focus on sex-based differences. Methods: We analyzed 253 patients treated with TEER between October 2015 and August 2024, stratified by sex. Observed survival (OS) was calculated using the actuarial life table method; expected survival (ES) was estimated via the Ederer II method using matched population data. Primary endpoints were RS and EM; secondary endpoints included mortality differences by MR subtype. Results: OS at 1, 2, and 3 years was 88.9%, 87.4%, and 78.9%, respectively. EM peaked in the first year (7.8%) and declined thereafter. RS was lower than in the general population, primarily due to persistently reduced RS and elevated EM in men. Women achieved RS comparable to matched peers from year one. Sex was not an independent predictor of mortality (HR 0.88, 95% CI 0.38–2.03, p = 0.771). Conclusions: In patients with significant MR undergoing TEER, EM was concentrated in the first year. Women reached RS comparable to the general population, while men showed persistent excess mortality. Sex was not independently associated with survival after adjustment.

Background/Objectives: Long QT Syndrome type 2 (LQT2) is a cardiac channelopathy linked to pathogenic variants in the KCNH2 gene, which encodes the Kv11.1 potassium channel, essential for cardiac repolarization. Variants affecting splice sites disrupt potassium ion flow, prolong QT interval, and increase the risk of arrhythmias and sudden cardiac death (SCD). Understanding genotype–phenotype correlations is key, given the variability of clinical manifestations even within families sharing the same variant. We aimed to evaluate new pathogenic variants by analyzing genotype–phenotype correlations in informative families. Methods: Genetic and clinical assessments were performed on index cases and family members carrying KCNH2 pathogenic variants, referred for genetic testing between 2010 and June 2023. The next-generation sequencing (NGS) of 210 cardiovascular-related genes was conducted. Clinical data, including demographic details, family history, arrhythmic events, electrocardiographic parameters, and treatments, were collected. Results: Among 390 patients (152 probands) tested for LQTS, only 2 KCNH2 variants had over 5 carriers. The detailed clinical information of 22 carriers of this KCNH2 p.Ser261fs. has already been reported by our research group. Moreover, we identified 12 carriers of the KCNH2 c.77-2del variant, predicted to disrupt a splice site and not previously reported. Segregation analysis showed its high penetrance, supporting its classification as pathogenic. Conclusions: The newly identified KCNH2 c.77-2del variant is a pathogenic, as strongly supported by the segregation analysis. Our findings underscore the importance of further research into splice site variants to enhance clinical management and genetic counseling for affected families.

Paravalvular leakage (PVL) is yet a potential and serious complication after transcatheter aortic valve replacement. Percutaneous PVL closure may be the treatment of choice upon failure of balloon postdilation in patients with excessive surgical risk. If the retrograde approach fails, an antegrade strategy might provide the solution. Transcatheter heart valves with large frames pose specific challenges for transcatheter paravalvular leakage closure. When the retrograde approach fails despite the use of high‐support guidewires, an antegrade approach could help overcome this issue based on the diminished interaction with the transcatheter heart valve structures.

Growth differentiation factor-15 (GDF-15) is produced by cardiomyocytes and atherosclerotic lesions under stress conditions, but little is known about its relation with severity and complexity of coronary lesions. The aim of this study was to investigate the association between GDF-15 and the syntax score for risk prediction of major adverse cardiovascular events (MACE) at 2-year follow-up in patients with non–ST-segment elevation acute coronary syndrome (NSTEACS). This is a prospective cohort study of 502 patients with NSTEACS. The syntax score was calculated from baseline coronary angiography. Blood samples were obtained at study entry for the assessment of GDF-15 and high-sensitivity C reactive protein. One hundred and three patients (20.5%) showed MACE at 2-year follow-up. Patients who developed MACE had greater GDF-15 concentrations and syntax score (p <0.001) compared to patients who did not. There was a positive, but moderate, correlation between GDF-15 and syntax score (ρ = 0.45, p <0.0001). On Cox regression analysis, only GDF-15 levels (p <0.001), body mass index (p = 0.04), and syntax score (p <0.001) remained independent predictors of the MACE. The area under the curve of GDF-15 (0.912, 95% confidence interval 0.894 to 0.944) was significantly greater compared to high-sensitivity C reactive protein and syntax score. In conclusion, in patients with NSTEACS, levels of GDF-15 at admission were correlated with the syntax score and independently associated with an increased risk of MACE during 2-year follow-up.

Hypertrophic cardiomyopathy (HCM) is a monogenic disease with autosomal dominant inheritance. Genotype–phenotype relationships are complex, with variable penetrance even within the same family. The involvement of other modulating genetic and environmental factors is unknown. We aimed to analyze the HCM in monozygotic twins, carriers of the same founder pathogenic variant MYBPC3 p.G263*. The relationship was verified using the PowerPlex 16 HS System kit. Phenotypic differences and environmental differences (overloading conditions, coexistence and location, lifestyle, sport, and intensity) were analyzed. Three pairs of twins genetically identical for all markers and carriers of MYBPC3 G263* were identified. No environmental differences were identified. One of the 89-year-old twins had symptomatic severe obstructive HCM that required septal ablation, while her twin has remained asymptomatic with mild phenotype >80 years. A 49-year-old twin had a severe phenotype of obstructive HCM and pending myectomy, while his twin had a mild asymptomatic phenotype. In the last pair of twins, one presented a much larger left ventricular hypertrophy than his identical twin. In summary, we present three pairs of HCM twin patients sharing not only the genetic cause of the inherited disease but the entire genetic background. Despite identical genetic information and the absence of other known clinical, environmental, or lifestyle differences, the severity of the HCM phenotype is strikingly different. These unexplained differences should prompt the study of other unknown modulating factors, either epigenetic or environmental.