Albuminuria is independently associated with preclinical left ventricular systolic dysfunction: The TESEO study

BACKGROUND Global longitudinal strain (GLS) of the left ventricular is a highly sensitive and reliable marker of systolic function and GLS outperforms ejection fraction (EF) in detecting preclinical left ventricular systolic dysfunction (LVSD). In patients with type 2 diabetes (DM2) albuminuria is a predictor of symptomatic heart failure, but data on the relationship between GLS and albuminuria are conflicting. AIM To explore the relationship between GLS and albuminuria in a contemporary cohort of DM2 patients. METHODS The study was performed on DM2 patients consecutively enrolled in the TESEO study. Patients with symptoms/signs of heart failure, EF < 50%, coronary artery, other cardiac diseases, or non-adequate acoustic window for GLS assessment were excluded. We collected clinical data, screened for complications, and measured GLS by speckle-tracking echocardiography. Univariate and multiple linear regression analyses were performed to identify independent explanatory variables associated with GLS. Logistic regression analysis was used to assess whether albuminuria was independently associated with GLS-diagnosed (GLS > -18%) LVSD. RESULTS Patients (n = 193, age: 60.6 +/- 8.1, male: 57%) had a short DM2 duration (3.8 +/- 4.9 years) and good metabolic control (glycated haemoglobin A1c: 6.5% +/- 1.0). Preclinical GLS-LVSD was present in 21.8% of the patients. GLS values were significantly higher in patients with albuminuria (-19.88 +/- 2.16 vs -18.29 +/- 2.99, P < 0.001) and in multivariate analysis natural logarithm of albumin-creatinine ratio and uric acid were independent predictors of GLS. In logistic regression analysis, albuminuria was associated with a 6.01 (95% confidence interval: 1.874-19.286) increased odds ratio of GLS-LVSD, independent of age, sex, diastolic blood pressure, chronic kidney disease, EF, mitral annulus velocity lateral, uric acid, and treatments. CONCLUSION Albuminuria was independently associated with subclinical LVSD in our contemporary cohort of DM2 patients.