Abstract Background. The evaluation of long-term inflammatory response and function in postoperative patients with aortic valve replacement (AVR) deserves special analysis because it is important to try to prevent reoperation and improve durability and functionality of the prostheses. Methods In this study we included a cohort of patients with aortic valve damage treated by AVR with mechanical prosthesis, bioprosthesis and we included a control group. Results. We found that IL-4 and OPN levels were higher in patients with mechanical vs. biological prostheses (p = 0.01 and p = 0.04 respectively), OPG levels were decreased (p = 0.01), women had lower levels of ET-1 and IL-6, (p = 0.02) (p = 0.04) respectively. Patients older than 60 years had decreased levels of IL-1ß p <0.001) and a higher concentration of IL-4 p < 0.05). IL-1ß, OPG and TNFα were higher in patients with less than 5 years of evolution versus more than 10 years (p = 0.004, p = 0.02 and p = 0.03 respectively). Factors such as age, gender, prosthetic, and elevated IL-1B and ET-1 levels are associated with valve dysfunction prosthetic. These results indicate that the inflammatory involvement present prior to valve replacement may be perpetuated by various factors in the long term. Conclusions The findings provide us with the opportunity to effectively treat patients with AVR in the postoperative period, which could prolong the functionality of the bioprostheses.

Introduction The currently available evidence states that 12 months after kidney transplantation (KT), more than half of the patients have severe cardiac structural and functional abnormalities. Objective To assess the cardiac reverse remodeling using echocardiography in the long-term after KT and its association with fibroblast growth factor-23 (FGF-23), carboxy-terminal propeptide of procollagen type I (PIP), and parathyroid hormone (PTH). Methods Fifty-three patients with end-stage renal disease were assessed before and 28 months after KT by echocardiography and serum quantification of FGF-23, PIP, and PTH. Results Thirty men and 23 women, with a mean age of 34±11 years, were included in the study. At 28 months after KT, an increase in functional capacity, complete resolution of the left ventricle (LV) hypertrophy (LV mass:121 ± 48 vs. 65 ± 14 gr/m2), reduction in left atrial volume (46 vs. 30 ml/m2), improvement in LV ejection fraction (53 vs. 63 %), global longitudinal strain (-15.9 vs.-19.4 %), and diastolic function were observed. Multivariate analysis showed that pre-KT LV mass, graft function, hypertension, and post-KT PIP predicted post-KT LV mass (R2=0.65, F=12.1, p=0.001). Logistic regression showed that the pre-KT FGF-23 concentration was the only variable related to hypertension after KT (X2=12.1, R2=0.3, p=0.032). PTH levels were not associated with LV hypertrophy. Conclusions Long-term follow-up after KT demonstrated that type 4 cardiorenal syndrome is reversible. Myocardial interstitial expansion is a minor component of absolute LV mass and is dominated by cardiomyocyte hypertrophy. FGF-23 plays an important role in persistent hypertension after KT.

Objective: To determine the impact and usefulness of the combination of structural and functional biomarkers in the diagnosis of acute renal injury (AKI) and short-term prognosis of patients undergoing cardiac surgery (CS). Material and Methods. Prospective cohort study (March 2018 to December 2019). 63 adults older than 18 years old, on the Intensive Care Unit (ICU) were included. Interventions: Patients had undergone CS with extracorporeal circulation (ECC). Surgery was elective in 80% of cases; it was urgent in 18% and emergent in 3%. Exclusion criteria included chronic kidney disease, contrast medium application ≤24 hour before surgery, cancer, infectious and autoimmune diseases. On admission to the ICU, serum creatinine, urinary creatinine, urinary sediment, urinary NGAL, urinary cystatin, microalbuminuria and serum cystatin were measured. Results. AKI was found 31 cases (49%). ECC without renal damage was found when time of extracorporeal circulation was of 85 ± 25 minutes and with renal damage when it lasted 114 ± 32 (p = 0.0001). Serum creatinine has a likelihood ratio (LR) + of 5.5, the combination of serum cystatin c (cystatin C) and normalized NGAL, showed a better LR. In patients with severe irreversible AKI, the combination of cystatin C + NGAL adjusted to urinary creatinine (NGAL/uCr) + microalbuminuria had a LR+ of 18.75 and LR - of 0.26. Conclusions: The combination of biomarkers predicts and identifies severity of AKI and Biomarkers combination in Cardiac Surgery

Background: The left ventricle (LV) journey in their transition from hypertrophy to heart failure is marked by many subcellular events partially understood yet. The moment in which the structural abnormalities reach the umbral to induce myocardial dysfunction remains elusive. Aims: To evaluate the anatomic-functional relationship between LV wall thickness and longitudinal systolic dysfunction. Material and Methods: We prospectively performed clinical history and transthoracic echocardiogram on healthy individuals and patients with hypertension, left ventricle ejection fraction (LVEF) ≥50%, and absence of heart failure symptoms. Results: A total of 226 patients and 101 healthy individuals were recruited. The distribution for sex was similar between groups. The mean age was 67±13 years old in the patients, and 44% had concentric LV hypertrophy. LVEF was identical in both groups (63±6%); in contrast, global longitudinal strain (GLS) (-18.8±2.5% vs. -20.4±2%) and mitral annulus plane systolic excursion (MAPSE) (13.8±2.8 vs. 15.5±2mm) were lower. ROC curve classified optimally decreased GLS with LV septum thickness ≥13mm and decreased MAPSE with thickness ≥14mm. Multivariable logistic regression found that LV septum thickness is the only variable associated with longitudinal systolic dysfunction (OR= 1.1, CI95%= 1.05 – 1.15, p= 0.001, R squared= 0.38). Discussion: A progressive increase in LV wall thickness due to myocyte hypertrophy and interstitial expansion is associated with LV systolic longitudinal dysfunction. Conclusions: Patients with moderate or severe ventricular hypertrophy (septum ≥13mm) had longitudinal systolic dysfunction, GLS decreases with minor structural change than MAPSE, and LVEF is insensitive in detecting longitudinal myocardial dysfunction in patients with hypertension.