Cardiovascular Comorbidities Are the Main Predictors of Cardiac Reverse Remodeling following Kidney Transplantation.

BACKGROUND: End-stage renal disease is associated with cardiac remodeling, which is partly reversible after kidney transplantation (KT). We aimed to determine the association of cardiovascular comorbidities or kidney-related factors with cardiac reverse remodeling after KT. METHODS: We performed echocardiography in 56 patients (aged 48 ± 15 years, mean ± SD) before and 24 months after undergoing their first KT. Echocardiograms were reviewed using a standardized process with blinding for the patient characteristics and evaluation timing. Multivariable linear regression analysis was used to evaluate the association between comorbidities and changes in cardiac structure and systolic/diastolic function. RESULTS: Left ventricular mass index (LVMI) and diastolic parameters did not change significantly, while left ventricular ejection fraction (LVEF) increased from 63.9 to 69.6% (p = 0.046). Multivariable analysis revealed associations of histories of valvular heart disease with a smaller reduction in LVMI (ß = -27.3, p = 0.04), of coronary artery disease or heart failure with a smaller increase in LVEF (ß = 7.17, p = 0.02), and of diabetes mellitus with less improvement in E wave (ß = -0.19, p = 0.05), e' (ß = 4.15, p = 0.046), and E/e' (ß = -5.00, p < 0.01). CONCLUSION: Cardiovascular comorbidities were -associated with less improvement in cardiac structure and function following KT. Our findings suggest that patients with CV comorbidities may experience limited "favorable" reverse cardiac remodeling following KT.

Memory Alterations and White Matter Hyperintensities in Elderly Patients With Hypertension: The ADELAHYDE-2 Study.

OBJECTIVES: The longitudinal ADELAHYDE-2 study aims to identify the factors associated with cognitive impairment/decline and white matter hyperintensities burden. METHODS: Longitudinal single-center study comprising two visits separated by approximately 7 years. A total of 131 patients completed the two visits. The primary outcome was global memory composite scale, while the secondary outcome was white matter hyperintensities (WMH/Fazekas scale) load. RESULTS: Global memory at visit 2 (V2) was largely influenced by age, smoking status, glycated hemoglobin, and history of stroke already present at visit 1 (V1). These variables accounted for ∼51% of the memory alterations at V2. WMH at V2 was likely influenced by age, left ventricular hypertrophy, diabetes mellitus, carotid intima-media thickness, and body mass index at V1. These findings accounted for ∼37% of the WMH changes at V2. Increase in pulse wave velocity from V1 to V2 showed a trend for association with memory deterioration (adjusted estimates = 0.06; P = .067), whereas smoking and increase in systolic blood pressure (trend) were associated with an increment in WMH (adjusted estimates = 0.49; P = .047 and adjusted estimates = 0.01; P = .08, respectively). On the other hand, angiotensin-converting enzyme inhibitor/angiotensin receptor blockers and statins (trend) were likely to be protective (adjusted estimates for angiotensin-converting enzyme inhibitor/angiotensin receptor blockers = -0.49; P = .049, and adjusted estimates for statins = -0.46; P = .055). CONCLUSIONS: Several readily identifiable factors are associated with memory deterioration and WMH, many of which are potentially modifiable. Interventions aimed to control these risk factors need to be tested prospectively in order to assess their cognitive protective value.