SO083VASCULAR STIFFNESS ESTIMATED NON-INVASIVELY USING PULSE WAVE PROPAGATION CORRESPONDS TO VASCULAR BIOPSY FINDINGS

Background and Aims Patients with chronic kidney disease (CKD) are at high risk of cardiovascular disease (CVD) due to complex processes in the uremic milieu linked to CKD - mineral and bone disorders (CKD-MBD). These processes alter structure and function of heart and vasculature e.g. by causing ectopic calcification that makes vessels stiffer thus affecting pulse (pressure) wave profiles. Our study aimed to derive patient-specific parameters using pulse wave propagation model including arterial stiffness and compare those parameters with cardiovascular status including biopsy proven severity of vascular calcification. Method In a group of 81 CKD (stage 5) patients undergoing living donor kidney transplantation, the degree of medial calcification in epigastric artery was histologically graded as 0 (n=22), 1 (n=31), 2 (n=21) and 3 (n=7) representing no, minimal, moderate and extensive signs of vascular calcification, respectively. Concomitantly 82 features were determined including demographic and anthropometric features, blood biomarkers related to CKD - MBD and other measurements. Pressure profiles (circles in Fig. 1) in radial artery were recorded using applanation tonometer (SphygmoCor, AtCor Medical, Australia) and used to derive patient-specific parameters from a mathematical model describing blood flow and pressure in 55 major arteries. Results The model was able to reproduce all recorded pressure profiles with high accuracy with average relative error less than 8% (compare solid line and circles in Fig. 1). Vascular stiffness, derived from the model, in arterial branches located in the area of artery for which calcification was histologically quantified, was significantly higher for higher calcification score (p-value < 0.001). The estimated stiffness correlated with the level of troponin T (rho=0.65**), advanced glycation end-products (by skin autofluorescence, rho=0.55*), osteoprotegerin (rho=0.44**), hepcidin 25 (rho=0.32*, interleukin 6 (rho=0.29*) and choline (rho=0.28**), (‘**’ and ‘*’ denote p-value < 0.01 and 0.05, respectively). Stiffer arteries were found in patients with diagnosed CVD (p-value < 0.01). Conclusion We demonstrate that a mathematical model based on a single peripheral recording of pulse pressure profile has the potential to provide information about cardiovascular status in the individual patient. Also, the estimated stiffness correlates well with several well-established CVD risk factors. Our mathematical model of the arterial tree, if validated in larger cohorts of patients, may be used as computational tool to predict vascular stiffness without need of arterial biopsy.