Type 2 Diabetes Mellitus Is Associated With Faster Degeneration of Bioprosthetic Valve

Abstract

resulted in 6184 patients (mean age 71.3Ϯ5.4 years, 60.1% male) being enrolled. Of these patients, 1731 (27.9%) had type 2 DM. The propensity score-matching algorithm successfully matched 1113 patients with type 2 DM with the same number of no-DM patients. The postmatching standard differences were less than 0.1 for each of the covariates, and 64.2% of DM patients were matched. The early (30 days) mortality rate was 7.8% (nϭ87) versus 2.9% (nϭ33) in patients with or without type 2 DM (PϽ0.001), respectively. Seven-year freedom from valve deterioration was significantly lower in patients with DM (73.2% [95% confidence interval, 61.6 -85.5] versus 95.4% [95% confidence interval, 83.9 -100], PϽ0.001). In Cox regression models with robust SEs that accounted for the clustering of matched pairs, DM was the strongest predictor of structural valve degeneration (hazard ratio 2.39 [95% confidence interval 2.28 -3.52]). When we allowed for interaction between type 2 DM and other key risk factors, DM remained a significant predictor beyond any potentially associated variable. Conclusions-Patients

Influence of osteoclasts and osteoprotegerin on the mode of calcific degeneration of aortic valves

“…Type 2 diabetes mellitus has recently emerged as a significant metabolic risk factor for calcific aortic valve disease and accelerated degeneration of bioprosthetic valves. 25,26 O'Sullivan et al 27 showed increased serum OPG levels in diabetic patients. Our results suggest the impact of diabetes on the mode of calcific valve remodeling irrespectively of the OPG level.…”

Molecular and Cellular Aspects of Calcific Aortic Valve Disease

“…Development of robust biomarkers for disease progression will not only provide the clinical tools necessary for patient risk stratification and assessment of response to therapeutic intervention, but may also illuminate novel pathways that can be targeted medically to prevent disease progression. The need to capture this risk of disease progression is particularly acute in patients with bioprosthetic valves 6 – but may be fundamentally different from patients with native valve sclerosis 11 . The seminal realization by Demer that oxylipids and cellular ROS signals are common to both bone loss and arterial calcium accrual 141, 142 suggests that cellular and/or molecular signatures indicative of vascular and skeletal oxidative stress will prove useful.…”

“…Genetics plays a direct role in that bicuspid aortic valve – a congenital risk factor for precocious CAS – has a significant genetic diathesis 3, 4 . Recently, type II diabetes (T2DM) has emerged as a particularly relevant and worrisome metabolic risk factor for native CAVD 5 as well as precocious degeneration of bioprosthetic valves 6 . It is becoming increasingly apparent that a diverse spectrum of cell-dependent mechanisms converge to regulate valvular calcium load; this is evidenced not only in histopathologic heterogeneity of CAVD 7, 8 but also from the multiplicity of cell types –interstitial cells, endothelial cells, cardiac chondrocytes and circulating osteoprogenitors – that participate in valve biomineralization 1, 9 .…”

Calcification and Oxidative Modifications Are Associated With Progressive Bioprosthetic Heart Valve Dysfunction

“…BHV calcification has been shown to be clinically associated with young age; children and younger adults have diminished implant durations over time, with a time‐dependent increased occurrence of BHV calcification . Renal failure is an important comorbidity of SVD via calcification, and earlier BHV failure due to SVD has been observed in diabetic patients . The mechanisms responsible for SVD in the absence of calcification have been studied to a limited extent …”