New potential biomarkers for early chronic kidney disease diagnosis in patients with different glucose tolerance status

Background: The purpose of the present study was to investigate the role of oxidative stress, platelet activation, and endocan levels in renal dysfunction in normal glucose tolerance (NGT) patients with 1-h plasma glucose values ≥155 mg/dl (NGT ≥ 155), compared to NGT < 155, impaired glucose tolerance (IGT), and type 2 diabetes mellitus (T2DM) newly diagnosed subjects. We enlisted 233 patients subjected to an oral glucose tolerance test (OGTT). Materials and methods: The serum levels of platelet activation (glycoprotein VI and sP-selectin), oxidative stress biomarkers (8-isoprostane and Nox-2), and endocan were evaluated using an ELISA test. Results: Among NGT < 155 patients and the T2DM group, there was a statistically significant increase in 8-isoprostane (p < 0.0001), Nox-2 (p < 0.0001), glycoprotein VI (p < 0.0001), and sP-selectin (p < 0.0001) serum levels. Higher serum endocan levels were found with the worsening of metabolic profile (p < 0.0001); specifically, NGT ≥ 155 patients presented higher serum endocan values when compared to NGT < 155 patients (p < 0.0001). From the multivariate linear regression analysis, 1-h glucose resulted in the major predictor of estimated glomerular filtration rate (e-GFR) justifying 23.6% of its variation (p < 0.0001); 8-isoprostane and Nox-2 added respectively another 6.0% (p < 0.0001) and 3.2% (p = 0.001). Conclusion: Our study confirmed the link between 1-h post-load glucose ≥155 mg/dl during OGTT and the possible increased risk for chronic kidney disease (CKD) in newly diagnosed patients. The novelty is that we demonstrated a progressive increase in oxidative stress, platelet activation, and serum endocan levels with the worsening of metabolic profile, which becomes evident early during the progression of CKD

Right ventricular outflow tract reconstruction using a valved biological conduit (Hancock conduit) late after Tetralogy of Fallot surgical correction

OBJECTIVES: The most appropriate strategy in the management of right ventricular outflow tract (RVOT) reconstruction in patients with tetralogy of Fallot early repair and late failure of right ventricle to pulmonary artery continuity is still debated. This study addresses this issue by evaluating retrospectively 12 years experience in this kind of reconstruction, focusing exclusively on the performance of Hancock conduits. METHODS: Data from 32 patients with an early repaired Tetralogy of Fallot, 23 males and 9 females, who underwent 34 RVOT reconstruction (2 were reinterventions) with Hancock conduit at Fondazione Toscana "G. Monasterio" Pediatric Cardiac Surgery department, Massa, Italy between February 2003 and May 2015 were retrospectively reviwed. Median age was 17,6 +/- 11,32 years (range 13 months to 41 years and 8 months), mean BSA 1,4 +/- 0,54m2 (0,34 m2 minimum and 2,12 m2 most), mean height 148,1 +/- 33,6 cm (range 61 cm to 195 cm) and mean weight 49,5 +/- 26,35 Kg (range 6,9 Kg to 96 Kg). The RV-PA peak gradient, RV mean pressure and pulmonary regurgitation were measured before and after the surgical conduit implantation and on follow-up, in addition RV end-diastolic volume index was measured, when feasible, before and after Hancock implantation. RESULTS: The early 30 days mortality was 6,25% and not related to conduit failure. Complete follow-up was feasible in 27 patients and the mean duration was 31,6 +/- 34,42 months. The observed RV-PA peak gradient means were 60,4 +/- 30,06 mmHg preoperatively, 29,1 +/- 11,48 mmHg postoperatively and 45,3 +/- 26,02 mmHg on the last follow-up; RV mean pressures were 53,3 +/- 27,73 mmHg preoperatively 41,6 +/- 12,71 mmHg postoperatively and 53,6 +/- 18,8 mmHg on the last follow-up; RV end-diastolic volume index means were 218,3 +/- 57,94 ml/m2 before surgery and 126,1 +/- 14,49 ml/m2 after surgery. Conduit failure was observed in 5 patients in which the the mean freedom from conduit failure was 70,56 +/- 15,02 months (mean age at failure 6,86 +/- 1,78 years), in 4 of them percutaneous intervention were attempted (2 ballooning and 2 melody), 2 successful. DISCUSSION: From our series the Hancock conduit can be actually considered as a valuable solution for RVOT reconstruction in already operated patients with ToF, considering good RV pressures and gradients values even after up to 9 years of follow up

One-hour post-load glucose and subclinical left atrial myocardial dysfunction in hypertensive patients

Background: Recently, studies demonstrated that normal glucose-tolerant subjects (NGT) with 1-h post-load plasma glucose value = 155 mg/dL during oral glucose tolerance test (OGTT) (NGT = 155) present an impaired cardio-metabolic profile, with subclinical myocardial damage. Atrial morphological and functional alterations, closely related to diastolic dysfunction, are important predictors of atrial fibrillation (AF), cardiovascular (CV) events and mortality in the entire population as well as in diabetic patients. The aim of our study was to evaluate subclinical atrial myocardial damage, assessed with speckle tracking echocardiography, in NGT= 155 mg/dL patients, comparing to NGT < 155 mg/dL subjects, impaired glucose tolerant (IGT) individuals and patients with newly diagnosed type 2 diabetes (T2DM).Methods: We enrolled 229 Caucasian patients. All subjects underwent anthropometrical and haemodynamic parameters evaluation, OGTT, advanced Colour-Doppler echocardiography with evaluation of main atrial and ventricular parameters.Results: As expected, from first to the fourth group there was a worsening of the metabolic profile as attested by fasting, 1- and 2-h post-load plasma glucose levels, during OGTT. Moreover, from NGT < 155 to T2DM group there was an impairment in reservoir and pump atrial function (PALS and PACS, respectively) (p < .0001).Conclusion: Present data demonstrated for the first time that NGT= 155 subjects present subclinical atrial dysfunction. These results may be clinically relevant because they highlight how atrial myopathy occurs early in pre-diabetes stage regardless of fibrotic and morphological alterations of the ventricular myocardium