Background: Aortic stenosis is a degenerative condition with high mortality in its severe stages and no preventive treatment. While diabetes is a known risk factor, the role of elevated glucose levels below the diabetic threshold in the development of aortic stenosis remains unclear. This study investigated the association between dysglycaemia, including impaired fasting glucose, and the incidence of aortic stenosis.
Methods: This study included 324 449 participants from the Swedish Apolipoprotein Mortality Risk cohort (1985-1996) who were free of aortic valve disease at baseline and had fasting glucose and lipid levels recorded. Participants were followed for incident aortic stenosis through the National Patient and Cause of Death Registers until 31 December 2020. Fasting glucose was categorised into low (<3.9 mmol/L), normal (3.9-6.0 mmol/L), impaired fasting glucose (6.1-6.9 mmol/L), high glucose (≥7.0 mmol/L) and diabetes. HRs were calculated using Cox proportional hazards models, with adjustments for age, sex, lipids, socioeconomic status, hypertension and kidney disease.
Results: Over a mean follow-up of 25.9 years, 8523 participants developed aortic stenosis. Compared with normal glucose levels, adjusted HRs were 0.96 (95% CI 0.82 to 1.13) for low glucose, 1.36 (95% CI 1.24 to 1.50) for impaired fasting glucose, 1.79 (95% CI 1.60 to 1.99) for high glucose and 2.21 (95% CI 1.80 to 2.73) for diabetes. Spline analysis indicated a continuous increase in risk with rising glucose levels, even below the impaired fasting glucose threshold.
Conclusions: Dysglycaemia, including glucose levels below the diabetic range, is associated with a higher risk of aortic stenosis.
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http://dx.doi.org/10.1136/heartjnl-2024-325150 | DOI Listing |
J Am Coll Cardiol
March 2025
Cedars Sinai Medical Center, Los Angeles, California, USA. Electronic address:
This updated Heart Valve Collaboratory framework addresses the growing concern for transcatheter valve failure (TVF) following transcatheter aortic valve replacement (TAVR). With the increasing volume of redo-TAV and surgical TAV explantation, there is a critical need for standardized pathways and protocols for evaluating TVF using echocardiography and cardiac computed tomography (CT) angiography. This document clarifies prior definitions of bioprosthetic valve deterioration and bioprosthetic valve failure in a practical, imaging directed context for TAVR.
View Article and Find Full Text PDFCan J Cardiol
March 2025
Department of Cardiology, Rabin Medical Center, Petah Tikva, Israel; The Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Background: The use of transcatheter aortic valve implantation (TAVI) for severe aortic stenosis is expanding to patients across the entire spectrum of surgical risk. We aimed to perform a meta-analysis comparing TAVI and surgical aortic valve replacement (SAVR) in trials enrolling lower risk patients.
Methods: We conducted a meta-analysis of randomized controlled trials (RCTs) comparing safety and efficacy outcomes between TAVI and SAVR among lower risk patients (mean/median STS score <4).
Int J Cardiol
March 2025
Division of Cardiology, Yale University School of Medicine, Bridgeport Hospital, Bridgeport, CT, USA.
Background: Transcatheter Aortic Valve Implantation (TAVI) has become the routine standard of care in patients with severe aortic stenosis and prohibitive surgical risk worldwide. However, data on TAVI outcomes from Africa remain sparse. This study aimed to evaluate the outcomes of TAVI in Africa.
View Article and Find Full Text PDFSci Adv
March 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males.
View Article and Find Full Text PDFFabry disease (FD) is a lysosomal disorder due to alpha-galactosidase-A enzyme deficiency, accumulation of globotriaosylceramide (Gb3) and globotriaosylsphingosine (lyso-Gb3) which lead to proinflammatory effects. Males develop progressive hypertrophic cardiomyopathy (HCM) followed by fibrosis; females develop nonconcentric hypertrophy and/or early fibrosis. The inflammatory response to Gb3/lyso-Gb-3 accumulation is one of the suggested pathogenic mechanisms in FD cardiomyopathy when the secretion of inflammatory and transforming growth factors with infiltration of lymphocytes and macrophages into tissue promotes cardiofibrosis.
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