Circulation: Heart Failure最新文献

Background: Studies have demonstrated that patients with myocarditis may have a higher burden of cardiomyopathy-associated genetic variants than the general population. However, data on children are limited. We compared the prevalence of rare predicted-damaging variants and clinically pathogenic variants in children with dilated cardiomyopathy (DCM) secondary to myocarditis with that in children with DCM alone and in heart-healthy controls.

Methods: Children with DCM secondary to myocarditis and children with DCM alone who underwent exome sequencing as part of a prior cross-sectional study were identified in the Pediatric Cardiomyopathy Registry, a large multicenter registry of children with cardiomyopathy. Controls from the Indiana University Biobank were matched 4:1 with myocarditis cases on genomic similarity. Rare predicted-damaging variants in cardiomyopathy-associated genes were identified using a bioinformatics approach. Clinical guidelines were used to determine clinical pathogenicity. The prevalence of variants was compared across the 3 groups.

Results: There were 32 patients with DCM secondary to myocarditis. The prevalence of rare predicted-damaging variants was 34.4% (11/32 [95% CI, 18.6%-53.2%]) in cases compared with 6.3% (8/128 [95% CI, 2.7%-11.9%]) in controls (P<0.001). Clinical review indicated all rare predicted-damaging variants in cases were pathogenic (1/12), likely pathogenic (3/12), or variants of uncertain significance (8/12), whereas most variants in controls were benign (2/8) or likely benign (4/8). The prevalence of pathogenic/likely pathogenic variants in cases was 12.5% (95% CI, 3.5%-29.0%) compared with 0% (95% CI, 0%-2.3%) in controls (P<0.01). Rare predicted-damaging and clinically pathogenic/likely pathogenic variant prevalence was not significantly different in children with DCM secondary to myocarditis and DCM without myocarditis (P=0.17 and P=1.00, respectively).

Conclusions: Children with DCM secondary to myocarditis had a higher burden of variants in cardiomyopathy-associated genes than that of heart-healthy controls. Larger studies will be needed to determine the utility of routine genetic testing in this population.

Air pollution is a major global environmental health threat and the leading environmental risk factor contributing to cardiovascular morbidity and mortality. Emerging evidence increasingly implicates air pollution as a critical, modifiable driver in the pathogenesis, progression, and prognosis of heart failure. Air pollution is increasingly recognized as part of the exposome-a complex interplay of environmental, social, and behavioral exposures accumulated across the life course. In this review, we synthesize experimental data demonstrating mechanistic links between air pollution and heart failure, along with growing experimental, clinical, and epidemiological evidence connecting both short- and long-term air pollution exposure with increased risk of heart failure progression across heart failure stages. We further examine how air pollution interacts with other exposomic risk domains-such as the social exposome, built environment, and access to greenery-compounding vulnerability in marginalized and underserved populations. The review will also summarize current approaches to communicate air pollution risk and propose practical strategies for both individuals and healthcare systems to mitigate its cardiovascular impact. Finally, we present a clinical framework for assessing and managing air pollution exposure in patients with heart failure, emphasizing the need for targeted risk stratification and the development of context-specific mitigation interventions.

Background: People with HIV (PWH) may have a higher risk of heart failure (HF) due to traditional and HIV-related factors. Incidence and risk prediction of HF in PWH are not well characterized. We aimed to quantify the risk of HF events in a global population of PWH with low-to-moderate estimated atherosclerotic cardiovascular disease risk.

Methods: HF incidence (events/1000 person years) was described overall and by demographic, HIV-specific, and HF factors, including estimated Predicting Risk of Cardiovascular Disease Events 10-year risk of HF. Confirmed HF events included adjudicated HF hospitalization and adverse events identified via a standardized Medical Dictionary for Regulatory Archives HF query.

Results: We analyzed 7769 REPRIEVE (Randomized Trial to Prevent Vascular Events in HIV) participants from 5 global regions (median, 50 years; 31% female). Over a median follow-up of 5.6 years (interquartile range, 4.3-5.9), HF incidence was higher in women, among Black participants in high-income regions, participants in sub-Saharan Africa, and among those with preexisting hypertension and obesity compared with the absence of these factors. Current and nadir CD4+T-cell count, and HIV-1 RNA level were not related to the incidence of HF events. Median (Q1-Q3) Predicting Risk of Cardiovascular Disease Events HF score was 1.66% (1.01-2.62). HF incidence was 1.65/1000 person-years (95% CI, 1.30-2.09). Expected number of HF events by Predicting Risk of Cardiovascular Disease Events HF (n=73) was consistent with observed (n=67).

Conclusions: Select demographics, clinical factors, and global regions contribute to a higher incidence of HF events among PWH. In PWH, the observed overall number of HF events aligned with the estimated Predicting Risk of Cardiovascular Disease Events HF risk rates.

Background: In patients with right ventricular (RV) outflow tract stenosis and pulmonary regurgitation (PR), percutaneous pulmonary valve implantation (PPVI) aims to preserve RV and left ventricular (LV) integrity and function. Our study aimed to assess acute changes in biventricular intrinsic myocardial function occurring with PPVI.

Methods: Twenty patients with RV outflow tract dysfunction (mean±1 SD; age, 23.0±10.9 years; mean peak echocardiographic RV outflow tract gradient, 64±25 mm Hg) underwent PPVI with biventricular assessment of pressure-volume loops using the conductance catheter technique during the same cardiac catheterization. Load-independent parameters of ventricular contractility (ventricular elastance) and ventricular compliance function, as well as pulmonary/systemic arterial elastance and ventriculoarterial coupling, were assessed before and directly after PPVI. Cardiac magnetic resonance for quantification of biventricular volumes, function, and PR was also performed.

Results: After PPVI, both RV ventricular elastance (median [interquartile range], 0.26 [0.16-0.83]-0.19 [0.13-0.42] mm Hg/mL per m²; P=0.029) and pulmonary systemic arterial elastance (0.32±0.20-0.25±0.19 mm Hg/mL per m²; P<0.001) decreased significantly, while right ventriculoarterial coupling (1.14±0.61-1.10±0.59; P=0.76) did not change statistically significant. LV ventricular elastance (1.31±0.93-1.23±0.72 mm Hg/mL per m²; P=0.68) and left ventriculoarterial coupling (0.75 [0.51-1.23]-0.82 [0.53-1.10]; P=0.98) were not affected by PPVI although systemic arterial elastance increased significantly (0.83±0.26-0.90±0.34 mm Hg/mL per m²; P=0.032). Both RV (P=0.37) and LV (P=0.20) compliance showed no significant change after PPVI. Patients with relevant PR (≥25%; n=10) had lower RV ventricular elastance (P=0.043) before and higher LV compliance (P=0.010) after PPVI compared with patients with minor PR (<25%; n=10), whereas ventriculoarterial coupling was similar between the 2 groups.

Conclusions: Acute reduction of RV overload by PPVI is accompanied by an instantaneous decline in RV contractility with persistent and inefficient ventriculoarterial coupling. The LV adequately adapts to an increase in pre- and post-load with nonsignificant changes in LV intrinsic function and ventriculoarterial coupling. The relevance of these response patterns on long-term biventricular remodeling requires further investigation.