European heart journal open最新文献

Aims: This study aimed to investigate the relationship between corticosteroid therapy and long-term outcomes in patients with cardiac sarcoidosis, stratified by left ventricular ejection fraction (LVEF) at diagnosis.

Methods and results: This study conducted a post hoc analysis of the ILLUstration of the Management and prognosIs of JapaNese PATiEnts with Cardiac Sarcoidosis, a retrospective multicentre registry. Cardiac sarcoidosis was diagnosed based on the 2016 Japanese Circulation Society and 2014 Heart Rhythm Society criteria. The primary endpoint was a composite of all-cause death, hospitalization for heart failure, and fatal ventricular arrhythmia events. Patients were divided into three groups based on LVEF: preserved LVEF (≥50%, n = 251), moderately impaired LVEF (LVEF, 35-49%; n = 149), and severely impaired LVEF (<35%, n = 99). Among 499 patients with cardiac sarcoidosis (mean age: 61.6 ± 11.4 years, male: 36.1%), 419 (84.0%) were treated with corticosteroids after diagnosis. During a median follow-up of 33.7 months (interquartile range, 16.8-62.7 months), 144 primary endpoints (28.9%) occurred. Corticosteroid therapy was associated with better prognosis when assessed in terms of primary endpoint in the entire cohort [hazard ratio (HR) 0.61, 95% confidence interval (CI) 0.41-0.89, P = 0.010]. When stratified by LVEF, corticosteroid therapy was significantly associated with a lower incidence of primary endpoints in the preserved LVEF group (HR, 0.30; 95% CI, 0.15-0.57, P < 0.001), but not in the moderately and severely impaired LVEF groups. This association remained robust, even after adjusting for confounders.

Conclusion: In this large cohort of cardiac sarcoidosis, corticosteroid therapy was associated with a lower incidence of long-term outcomes only in patients with preserved LVEF at diagnosis.

Clinical trial registration: UMIN000034974.

Aims: Mitral valve prolapse (MVP) is a common valvular disorder associated with significant morbidity and mortality, with a strong genetic basis. This study aimed to identify a mutation in a family with MVP and to characterize the valve phenotype in LTBP2 knockout (KO) mice.

Methods and results: Exome sequencing and segregation analysis were performed on a large family with MVP. Two mouse strains were generated: a complete KO of the LTBP2 gene and a knockin (KI) of the human mutation. At 6 months, phenotyping was conducted using echocardiography, histology, eye optical coherence tomography, and quantitative polymerase chain reaction analysis for TGF-β signalling targets (periostin/POSTN, RUNX2, and CTGF) in valve tissues. LTBP2 rs117800773 V1506M mutation exhibited segregation with MVP. LTBP2 KO mice had a higher incidence of myxomatous changes by histology (7 of 9 of KO vs. 0 of 7 control animals, P = 0.00186) and echocardiography (7 of 9 vs. 0 of 8, P = 0.0011). LTBP2 KI mice for the human mutation showed a significantly elevated myxomatous histological phenotype (8 of 8 vs. 0 of 9, P = 0.00004) as well as by echocardiography (6 of 8 vs. 0 of 9, P = 0.00123). Knockout mice demonstrated an increase in the depth of the anterior chamber as well as reduced visual acuity. LTBP2 KO mice demonstrated overexpression of both TGF-β signalling targets RUNX2 and periostin (P = 0.0144 and P = 0.001826, respectively).

Conclusion: We report a KO mouse strain with an LTBP2 mutation, demonstrating a valve phenotype, alongside a family with a novel mutation linked to MVP.

Aims: We aimed to perform a retrospective cohort study using the Centers for Disease Control and Prevention's (CDC's) Wide-Ranging Online Data for Epidemiologic Research (WONDER) database to analyse the trends in cardiovascular disease (CVD)-related mortality in patients with myeloproliferative neoplasms (MPNs) from 1999 to 2020.

Methods and results: We analysed the death certificate data from the CDC WONDER database from 1999 to 2020 for CVD with co-morbid myeloproliferative disorders in the US population. Age-adjusted mortality rates (AAMRs) and 95% confidence intervals (CIs) were computed per 1 million population by standardizing crude mortality rates to the 2000 US census population. To assess annual national mortality trends, we employed the Joinpoint regression model, calculating the annual per cent change in AAMR and corresponding 95% CIs. A total of 15 269 deaths related to CVD occurred in patients with co-morbid MPNs from 1999 to 2020. Overall, there was a decreasing trend in CVD-related AAMRs throughout these years. Males contributed to 51% of total deaths, and their AAMR was persistently higher than women throughout the study. Non-Hispanic (NH) Whites had the highest overall AAMR, followed by NH Blacks, NH American Indians or Alaska Natives, Hispanics or Latinos, and NH Asian or Pacific Islanders.

Conclusion: Our findings indicate a significant decline with notable gender, racial/ethnic, and regional differences in CVD-related mortality among patients with MPN over the past two decades. We emphasize the importance of a collaborative approach between oncologists and cardiologists in managing these patients, highlighting the potential benefits of integrating cardio-oncology services to enhance patient outcomes.

Aims: To better characterize functional consequences of the presence of COPD on cardiorespiratory fitness in patients with HF.

Methods and results: Patients with any clinical indication for cardiopulmonary exercise testing (CPET) were included in the international FRIEND registry. Diagnosis of COPD was confirmed by a ratio of forced expiratory volume in 1 s and forced vital capacity (FEV₁/FVC) < 0.70. HF was diagnosed in the presence of symptoms and signs of HF. A total of 10 957 patients were divided into four groups: patients without HF or COPD (n = 8963), patients with HF (n = 852) or COPD (n = 991) alone, and patients with both HF and COPD (n = 151). Maximal workload was the lowest in patients with both HF and COPD [78.09 (95% CI: 72.92, 83.64 watts)], and all pairwise comparisons with adjusted P < 0.05 between groups were statistically significant. Patients with both HF and COPD yielded the lowest PETCO₂ values [31.80 (95% CI: 31.00, 32.60)] mmHg and exhibited a higher VE/VCO₂ slope compared with HF (36.73 (95% CI: 35.78, 37.68) vs. 33.91 (95% CI: 33.50, 34.33 units, P  < 0.0001). Peak VO₂ was the lowest with concomitant HF and COPD 19.93 (95% CI: 18.60, 21.27) mL/kg/min and was significantly different compared with all other groups (P < 0.05).

Conclusion: Patients referred for CPET with COPD and concomitant HF exhibit a profound impairment in CRF compared with patients with COPD or HF alone. Early identification of pulmonary obstruction in patients with HF by more frequent usage of pulmonary function testing may contribute to providing better treatment for both COPD and HF in these high-risk individuals.

Aims: Causes of death remain largely unexplored in the atrial fibrillation (AF) population. We aimed to (i) thoroughly assess causes of death in patients with AF, especially those associated with sudden cardiac death (SCD) and (ii) evaluate the potential association between AF and SCD.

Methods and results: Linked primary and secondary care United Kingdom Clinical Practice Research Datalink dataset comprising 6 529 382 individuals aged ≥18. We identified 214 222 patients with newly diagnosed AF, and an equivalent number of non-AF patients matched for age, sex and primary care practice. The underlying primary cause of death for each patient was assessed in the form of International Classification of Diseases Tenth Revision (ICD-10) codes and also as part of broader disease categories (i.e. ICD-10 chapters).

Findings: Over a median follow-up of 2.7 (interquartile range: 0.7-6.0) years, 124 781 (58.25%) patients with AF died. Sudden cardiac death occurred in 13 923 patients with AF [6.50% patients with AF vs. 2.01% non-AF patients; odds ratio (OR) = 3.38, 95% confidence interval (CI): 3.27-3.50, P < 0.0001], contributing to 11.05% of all AF mortality. Diseases of the circulatory system, neoplasms and respiratory diseases explained 45% of AF mortality. Sudden cardiac death occurred more frequently in males (OR = 1.87, 95% CI: 1.80-1.93, P < 0.0001), and females with AF died more often of diseases of the circulatory, respiratory, digestive, and genitourinary system and less often of neoplastic disorders.

Interpretation: Conditions of the circulatory system are the main driver of mortality in the AF population. Females with AF experience higher cardiovascular and respiratory mortality but die less frequently of neoplasms. The risk of SCD is higher in the AF population, occurring more frequently in males.

Aims: Cavotricuspid isthmus (CTI) ablation is the current ablation treatment for typical atrial flutter (AFL). However, post-ablation atrial tachyarrhythmias, mostly in the form of atrial fibrillation (AF), are frequently observed after CTI ablation. We aimed to evaluate the effectiveness and safety of concomitant or isolated pulmonary vein isolation (PVI) in patients with typical AFL scheduled for ablation.

Methods and results: Electronic databases (PubMED, EMBASE, Clinicaltrials.gov) were searched through July, 2024. Randomized controlled trials (RCTs) were eligible if comparing PVI ± CTI ablation vs. CTI alone. The primary outcomes were any sustained atrial arrhythmia, typical AFL relapse, and AF. Secondary outcomes were need for redo-ablation or antiarrhythmic drugs. Random-effects and fixed-effects meta-analyses were undertaken for each individual outcome. Seven RCTs, with a total of 902 patients, were included. Comparing to CTI ablation alone, PVI ± CTI was more effective in preventing atrial tachyarrhythmias [risk ratio (RR) = 0.57, 95% CI: 0.41-0.79, P = 0.0007, I ² = 50%, number needed to treat (NNT) = 4.1]. The results were driven mainly by a reduction of new onset/recurrent AF (RR = 0.41, 95% CI: 0.27-0.61, P < 0.0001, I ² = 0%, NNT = 3.3), whereas there were no differences in typical AFL relapse (RR = 1.52, 95% CI: 0.63-3.66, P = 0.35, I ² = 9%). Major complication rate was low and comparable across groups, although uncomplicated pericardial effusion was higher in PVI ± CTI (1.8% vs. 0.0%, P = 0.04). Results were comparable for the sub-analysis of PVI alone vs. CTI ablation.

Conclusion: In patients with typical AFL, PVI ± CTI ablation is more effective than CTI alone in reducing the atrial tachyarrhythmias and subsequent AF during follow-up, without affecting major complications rate. These results set the rationale for a well-designed, larger-scale RCT comparing both strategies.

Electronic cigarette (EC) is widely advertised as a safe alternative to traditional cigarette (TC). We aimed to investigate the cardiovascular effect of EC with/without nicotine compared with TC. We systematically searched PubMed/MEDLINE, EMBASE, and Cochrane CENTRAL for randomized controlled trials that compared the effect of different smoking modalities on cardiovascular function up to 1 October 2024. Analysis used the weighted mean difference (WMD) with a 95% confidence interval (CI) via Comprehensive Meta-Analysis software, version 3.0. The study evaluated key cardiovascular parameters, including pulse wave velocity (PWV), augmentation index at 75 beats/min (AIx75), flow-mediated dilation (FMD), heart rate (HR), systolic blood pressure, and diastolic blood pressure. We analysed 9 trials involving 370 participants. Acute exposure to EC with nicotine (ECN) compared with nicotine-free EC (EC0) increased PWV (WMD = 0.26; 95% CI: 0.14-0.38, P < 0.001), AIx75 (WMD = 4.29; 95% CI: 2.07-6.51, P < 0.001), and HR (WMD = 5.06; 95% CI: 2.13-7.98, P = 0.001), significantly. In contrast, comparison between ECN and TC revealed no significant differences in FMD (WMD = 0.80; 95% CI: -0.09-1.70, P = 0.08). Our meta-analysis suggests that ECN acutely increases arterial stiffness more than EC0 does. Additionally, we found that the acute effect of ECN on endothelial dysfunction is not different from TC. Therefore, our study suggests that vaping cannot be considered as a safe substitute for TC. Further investigation is needed to explore the long-term cardiovascular effects of vaping and its modalities.

Aims: More than 220 Mio people live at altitudes above 2000 m, many of whom have pre-existing chronic diseases, including pulmonary vascular diseases (PVDs) such as pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH). We investigated the acute effects of high-dose supplemental oxygen on pulmonary haemodynamics assessed by echocardiography in patients with PVD permanently living at 2850 m.

Methods and results: In a randomized, single-blind, placebo-controlled crossover trial, patients with PVD diagnosed with PAH or CTEPH were allocated to receive 10 L/min supplemental oxygen (FiO₂ ≈ 95%) and placebo air administered via a facial mask with reservoir near their living altitude in Quito at 2850 m (FiO₂0.21, PiO₂ ≈ 60% of sea level) in random order with a washout period of >2 h. After >15 min of breathing the respective FiO₂, systolic pulmonary artery pressure (sPAP), cardiac output (CO), and other parameters were assessed by echocardiography. Furthermore, radial arterial blood gases were analysed. Twenty-eight patients with PVD (24 females, 26 PAH, age 45 ± 12 years) treated with phosphodiesterase-5 inhibitors (n = 28) and endothelin receptor antagonists (n = 9) were included. With oxygen vs. placebo air, sPAP was 57 ± 23 vs. 68 ± 24 mmHg, mean difference -11 mmHg (-15 to -6 mmHg, P < 0.001), CO was 3.2 ± 0.9 vs. 3.9 ± 1.1 L/min; -0.7 L/min (-0.9 to -0.4 L/min, P < 0.001), while sPAP/CO was unchanged, and the right ventriculo-arterial coupling was increased. PaO₂ was 22.5 ± 9.7 vs. 7.6 ± 1.5 kPa; 14.9 kPa (11.4-18.4 kPa, P < 0.001).

Conclusion: High-dose oxygen therapy in prevalent patients with PVD living near 2850 m significantly lowered sPAP but also CO by a reduced heart rate, resulting in an unchanged pulmonary resistance. Whether longer-term oxygen therapy would improve pulmonary vascular resistance requires further investigation.

Registration: NCT06084559 URL: https://clinicaltrials.gov/study/NCT06084559.