ASSOCIATIONS BETWEEN PULSE WAVE VELOCITY, AORTIC CALCIFICATION AND CARDIAC STRUCTURE AND FUNCTION

NE M LIOUFAS1,2,3, S SM CHEN4,5, C M HAWLEY6,7, E PEDAGOGOS2,3, E M PASCOE6, A VALKS6, N D TOUSSAINT1,2

1Royal Melbourne Hospital, 2Department of Medicine (RMH), The University of Melbourne, 3Western Health, 4Epworth Healthcare, 5The Prince Charles Hospital, 6Australasian Kidney Trials Network, The University of Queensland, 7Department of Nephrology, Princess Alexandra Hospital

Aim: To evaluate associations between cardiovascular markers of ascending aortic distensibility (AAD), carotid-femoral pulse wave velocity (cfPWV) and abdominal aortic calcification (AAC), in participants with chronic kidney disease (CKD).
Background: CKD and abnormalities of mineral metabolism are associated with increased arterial stiffness and calcification, and cardiovascular disease (CVD). Advances in cardiovascular magnetic resonance (CMR) allow direct measurement of aortic stiffness and compliance, assessing aortic PWV and AAD. In healthy humans, reduction in AAD is an early marker of subclinical vascular alteration, but few studies in CKD have assessed local aortic stiffness and compliance by CMR.
Methods: IMPROVE-CKD was a multi-centre, placebo-controlled, randomised trial assessing effects of lanthanum carbonate on cardiovascular markers over 96 weeks in 278 participants with CKD3b/4. Primary outcome was cfPWV (SphygmoCor), and secondary outcomes included AAC (measured by CT). In a CMR sub-study (n=80), cardiac parameters of AAD, aortic PWV and left ventricular mass index (LVMI), were evaluated. We assessed relationships between baseline cardiac parameters of aortic stiffness and distensibility and arterial stiffness and calcification.
Results:  Participants recruited to the CMR sub-study (Australia 55; Malaysia 25) had mean age 60.3±12.7yrs, 68% male, 52% Caucasian, mean BMI 28.7±4.6kg/m2 and eGFR 26.6±8.3ml/min/1.73m². 44% had diabetes, 85% hypertension, and 21% CVD. Mean cfPWV was 10.8±4m/s and 80% had AAC, indicating high cardiovascular risk cohort. Mean LVMI was 67.3+/-16.0g/m², within normal reference range, but AAD was significantly reduced (2.1±1.7×10-3mmHg-1). Reduced AAD on CMR was associated with AAC (p=0.037) and higher cfPWV (p=0.008). On linear regression analysis however, AAD was not associated with cfPWV (0.03 [-0.15, 0.22], p=0.7).
Conclusions: AAD on CMR may be a useful early marker of vascular alteration in CKD patients despite normal LVMI.


Biography:
Dr Nicole Lioufas is a Research Fellow at the Royal Melbourne Hospital and works a Nephrologist and General Medical Consultant at Western Health. She is currently undertaking a PhD through the University of Melbourne in the role of phosphate binders on vascular calcification and cardiovascular outcomes in chronic kidney disease.

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