Abstract
Vascular calcification is a major contributor to mortality in end-stage renal disease (ESRD) patients. In this study, we investigated whether there was a correlation between the coronary artery calcium score (CACS) and the vascular calcification score (VCS), and whether higher VCS increased the incidence of interventions and major adverse cardiac and cerebrovascular events (MACCE). ECG-gated CT, including vascular access and the coronary vessel, was taken. CACS and VCS were calculated by the Agatston method. A comparison of CACS and survival analysis according to VCS groups was performed. Using a cutoff of VCS = 500, 77 patients were divided into two groups. The vintage was significantly older in the higher VCS group. The median CACS was higher in the higher VCS group (21 [0, 171] vs. 552 [93, 2430], p < 0.001). The hazard ratio (HR) for interventions and MACCEs in the higher VCS group increased by 3.2 and 2.3, respectively. Additionally, a longer duration of hemodialysis and higher magnesium levels (>2.5 mg/dL) showed lower HRs for interventions (<1). We quantified VCS and found that it was associated with the CACS. Additionally, higher VCS increased the risk of access interventions and MACCE. VCS of the access site may be suggested as a biomarker to predict ESRD patients.
Highlights
Cardiovascular events are known to be a major cause of mortality in patients with chronic kidney disease [1]
The motivation for this study was derived from a question regarding the clinical significance of vascular calcification (VC) at the vascular access site in end-stage renal disease (ESRD) patients
We speculated that cardiovascular mortality would be elevated in the higher vascular calcification score (VCS) group, as the calcification score (CACS) is linked to cardiovascular mortality
Summary
Cardiovascular events are known to be a major cause of mortality in patients with chronic kidney disease [1]. The coronary artery calcification score (CACS) is recognized as a strong predictor of cardiovascular mortality in ESRD patients, as well as in the general population [4,5]. VC is rare in the veins, but it does occur at vascular access sites in ESRD patients This phenomenon can be explained by arterialization of the remodeled vein of the vascular access due to the high levels of shear stress from strong blood flow [12]. 23% of patients presented with VC, and there was a significant difference in mortality between patients with and without calcification, a finding that demonstrated the clinical significance of vascular access calcification in ESRD patients [2]. Little research has investigated the correlation of VC at the vascular access site with the CACS, which is known to be a strong predictor of CV risk. We sought to analyze other risk factors for vascular access failure and MACCE within the framework of VC at the vascular access site
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