Potential determinants of the E/e′ ratio in non‐dialysis compared with dialysis patients

Abstract

Aim We hypothesized that arterial function and N‐terminal natriuretic peptide (NT‐proBNP) levels as a marker of volume overload, relate differently to E/e′ as an index of diastolic function in dialysis compared with non‐dialysis patients with chronic kidney disease. We further examined whether cardiovascular risk factors attenuated these relationships. Methods We assessed cardiovascular risk factors and determined arterial function indices by applanation tonometry using SphygmoCor software and E/e′ by echocardiography in 103 (62 non‐dialysis and 41 dialysis) patients. Results In established confounder adjusted analysis, dialysis status impacted the pulse wave velocity‐E/e′ relationship (interaction p = .01) but not the NT‐proBNP level‐E/e′ association (interaction p = .1). Upon entering arterial function measures and NT‐proBNP levels simultaneously in regression models, arterial function measures were associated with E/e′ (p = .008 to .04) in non‐dialysis patients whereas NT‐proBNP levels were related to E/e′ in dialysis patients (p = .009 to .04). Bivariate associations were found between diabetes (p < .0001) and E/e′ in non‐dialysis patients, and haemoglobin concentrations and E/e′ (p = .02) in those on dialysis. Upon adjustment for diabetes in non‐dialysis patients, only central pulse pressure remained associated with E/e′ (p = .02); when haemoglobin concentrations were adjusted for in dialysis patients, NT‐proBNP levels were no longer associated with E/e′ (p = .2). In separate models, haemoglobin levels were associated with E/e′ independent of left ventricular mass index and preload and afterload measures (p = .02 to .03). Conclusion The main determinants of E/e′ may differ in non‐dialysis compared with dialysis patients. These include arterial function and diabetes in non‐dialysis patients, and volume overload and anaemia in dialysis patients.

Aortic Stiffness and Pulsatile Pressures as Potential Mediators of Chronic Kidney Disease Induced Impaired Diastolic Function

“…Our study design was previously reported. [10][11][12][13] Briefly, 46 consecutive black CKD participants including 19 non-dialysis and 27 dialysis patients were enrolled at the Milpark Hospital in Johannesburg, South Africa. Patients with active infection or/and cancer were excluded.…”

“…We recorded demographic characteristics, traditional cardiovascular risk factors and cardiovascular events as previously reported [10][11][12][13] and detailed in the Supplementary Data Methods. Mean or distending arterial blood pressure for the peripheral waveform was determined electronically by the SphygmoCor device (see below) and using the formula…”

“…Central haemodynamic assessments were determined from central arterial pressure recordings obtained from pulse wave analysis by applanation tonometry and SphygmoCor software as previously described [10][11][12][13] and detailed in the Supplementary Data Methods. We recorded aortic pulse wave velocity (PWV) as an index of arterial stiffness, forward wave pressure (Pf), reflected wave pressure (Pb), central systolic blood pressure (CSBP) and central pulse pressure (CPP).…”

“…Measurement details were reported previously. [10][11][12][13] Intra-observer echocardiographic measurement variability is low in our setting with Pearson's correlation coefficients and variances (mean % difference (SD)) for left ventricular end-diastolic diameter, septal wall thickness, posterior wall thickness, E and e' of 0.92, 0.72, 0.76, 0.88 and 0.93 (p < 0.0001 for all), and −0.41 (4.16), 0.45 (7.74), 1.74 (6.08), 0.16 (9.95) and −1.46 (8.58), respectively. 16 Participants were examined in the partial left decubitus position.…”

“…In this study, we performed pulse wave analysis and echocardiography in black African CKD patients and matched healthy controls. [10][11][12] We determined early diastolic mitral annulus displacement velocity (e') and inflow velocity (E) by tissue and pulsed Doppler, respectively. E' was used as a measure of active relaxation, and we calculated E/e' as an index of left ventricular filling pressure or passive relaxation.…”