Superiority of high sensitivity cardiac troponin I over NT-proBNP and adiponectin for 7-year mortality in stable patients receiving haemodialysis.

Patients on haemodialysis (HD) have high mortality risk, and prognostic values of the major cardiovascular biomarkers cardiac troponin I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and adiponectin should be ascertained over longer follow-up periods using higher-sensitivity assays, which we undertook. In 221 HD patients, levels of high-sensitivity (hs)-cTnI, NT-proBNP, and adiponectin, were measured using high-sensitivity assays, and their associations with all-cause mortality (ACM) and cardiovascular mortality (CVM) were prospectively investigated for 7 years. Higher hs-cTnI and NT-proBNP levels were significant risk factors for ACM and CVM in the Kaplan-Meier analysis. Multivariate Cox proportional hazards analyses in a model including hs-cTnI and NT-proBNP identified log hs-cTnI, but not log NT-proBNP, as an independent risk factor for ACM (HR 2.12, P < 0.02) and CVM (HR 4.48, P < 0.0005). Stepwise analyses identified a high hs-cTnI tertile as a risk factor for ACM (HR 2.31, P < 0.01) and CVM (HR 6.70, P < 0.001). The addition of hs-cTnI to a model including age, CRP, DM, and NT-proBNP significantly improved the discrimination of ACM and CVM each over 7 years. Conclusively, hs-cTnI was superior to NT-proBNP and adiponectin in predicting ACM and CVM over 7 years in HD patients, suggesting the significance of baseline hs-cTnI measurements in long-term management.

A method for calculating left ventricular end-diastolic volume as an index of left ventricular preload from the pre-ejection period, ejection time, blood pressure, and stroke volume: a prospective, observational study.

BACKGROUND: Left ventricular end-diastolic volume (EDV) is a major determinant of cardiac preload. However, its use in fluid management is limited by the lack of a simple means to measure it noninvasively. This study presents a new noninvasive method that was validated against simultaneously measured EDV by transthoracic echocardiography (TTE). The goal of this study was to develop and validate a method to estimate EDV in humans non-invasively from left ventricular arterial coupling (Ees/Ea) and stroke volume (SV). METHODS: Ees/Ea can be calculated non-invasively from the four parameters of end-systolic arterial pressure (Pes), diastolic arterial pressure (DBP), pre-ejection period (PEP), and ejection time (ET), using the approximation formula. In addition, if SV can be assessed, EDV can be calculated. Therefore, using a vascular screening system (VaSera 1000/1500, Fukuda Denshi Co., Ltd., Tokyo, Japan), blood pressure, PEP, and ET were measured noninvasively, the SV value was obtained using an ultrasound diagnostic device, EDV was calculated (EDV calc), and it was compared with EDV obtained using the ultrasound diagnostic device (EDV echo). The results are shown as mean ± standard deviation values. RESULTS: There were 48 healthy subjects (40 men, 8 women), with a mean age of 24 ± 4 years, mean height of 169 ± 7 cm, and mean weight of 65 ± 12 kg. EDV echo was 91 ± 16 ml, and EDV calc was 102 ± 21 ml. There was a significant correlation between EDV echo and EDV calc (R2 = 0.81, p < 0.01). A Bland-Altman plot between EDV echo and EDV calc showed that the bias and limits of agreement were -11.2 ml (-36.6, + 14.2 ml). CONCLUSIONS: The results suggest that EDV can be measured non-invasively from Ees/Ea and SV. This suggests that continuous measurements may potentially work, using equipment available in the intraoperative setting.