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Background: Evaluate the impact of valvular calcifications measured on cardiac computed tomography (CCT) in patients with infective endocarditis (IE).
Methods: Seventy patients with native IE (36 aortic IE, 31 mitral IE, 3 bivalvular IE) were included and explored with CCT between January 2016 and April 2018. Mitral and aortic valvular calcium score (VCS) were measured on unenhanced calcium scoring images, and correlated with clinical, surgical data, and 1-year death rate.
Results: VCS of patients with mitral IE and no peripheral embolism was higher than those with peripheral embolism (868 (25-1725) vs. 6 (0-95), < 0.05). Patients with high calcified mitral IE (mitral VCS > 100; = 15) had a lower rate of surgery (40.0% vs.78.9%; = 0.03) and a higher 1-year-death risk (53.3% vs. 10.5%, = 0.04; OR = 8.5 (2.75-16.40) than patients with low mitral VCS ( = 19). Patients with aortic IE and high aortic calcifications (aortic VCS > 100; = 18) present more frequently atypical bacteria on blood cultures (33.3% vs. 4.8%; = 0.03) than patients with low aortic VCS ( = 21).
Conclusion: The amount of valvular calcifications on CT was associated with embolism risk, rate of surgery and 1-year risk of death in patients with mitral IE, and germ's type in aortic IE raising the question of their systematic quantification in native IE.
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http://dx.doi.org/10.3390/jcm10194458 | DOI Listing |
Arq Bras Cardiol
September 2025
Escola Bahiana de Medicina e Saúde Pública, Salvador, BA - Brasil.
Background: Chronic kidney disease (CKD) is associated with a higher prevalence of valvular diseases and increased mortality from cardiovascular causes. Factors that influence the genesis of cardiac valve calcification (CVC) in these patients are not well-defined.
Objective: To determine the risk factors for valvular calcification in patients with CKD.
Eur Heart J Open
July 2025
Amsterdam UMC Location University of Amsterdam, Department of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences, Meibergdreef 9, 1105AZ Amsterdam, Netherlands.
Aims: Calcific aortic valve disease is the most common valvular heart disease characterized by an inflammatory response in the leaflets followed by fibro-calcific remodelling of valvular interstitial cells (VICs). Lipoprotein(a) [Lp(a)] is a well-recognized risk factor for CAVD, however the role of metabolism in driving Lp(a)-induced inflammation remains largely elusive. Therefore, we aim to investigate the role of Lp(a) in driving inflammatory and metabolic changes in VICs and examine how alterations in cellular metabolism can alter their inflammatory phenotype.
View Article and Find Full Text PDFJ Cell Mol Med
September 2025
Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania.
Calcific aortic valve disease (CAVD) is a growing global health burden, with no approved pharmacological treatments to date, indicating a substantial therapeutic gap and the need for deeper insight into its underlying mechanisms. Transcriptomic approaches, particularly RNA sequencing (RNAseq) and single-cell sequencing (scRNAseq), are emerging as powerful tools for unravelling the complex biology of the aortic valve (AV) in both normal and diseased states. This review summarises recent advances in our understanding of AV structure and function, with emphasis on valvular cell plasticity, heterogeneity and intercellular interactions-especially between valvular endothelial cells (VECs) and monocytes under physiological and pathological conditions.
View Article and Find Full Text PDFCJC Open
August 2025
Institut Universitaire de Cardiologie et Pneumologie de Québec (Quebec Heart & Lung Institute), Université Laval, Québec City, Québec, Canada.
Background: Valvular lesions in calcific aortic valve stenosis are sex-specific: female patients reach a similar level of severity as male patients but with less valvular calcification and more valvular fibrosis. We thus aim to assess the transcriptome of stenotic aortic valves according to patients' sex.
Methods: A total of 300 valves were collected, and genomewide gene expression was quantified using a microarray on 240.
Sex differences in aortic valve stenosis (AVS) progression have been documented clinically, but the underlying cellular mechanisms that drive sex-dependent calcification in aortic valve tissue remain poorly understood. Here, we harnessed single cell and spatial transcriptomics to investigate mechanisms that drive sex dependent spatial organization of valvular interstitial cell (VIC) and macrophage gene expression near calcification sites in human male and female aortic valve tissue. Histological analyses of aortic valve tissues stratified into healthy and diseased cohorts based on degree of calcification reveal increased valve calcification area in diseased male aortic valves relative to female, and increased valve thickening in diseased female aortic valves.
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