Insulin resistance linked to subtle myocardial dysfunction in normotensive Turner syndrome young patients without structural heart diseases

Abstract

Background Turner syndrome (TS) patients have increased cardiovascular risk. This cardiovascular risk is famously attributed to structural abnormalities of the left side of the heart such as aortic stenosis and aortic coarctation. However, due to insulin resistance and subsequent pathogenic mechanisms, normotensive TS patients without structural abnormalities may develop varying degrees of myocardial dysfunction. The aim of this research was to examine the role of speckle tracking echocardiography in early detection of Turner cardiomyopathy and to correlate this myocardial dysfunction with measures of insulin resistance. Methods This cross-sectional case control study included 30 children with TS and 30 age-matched healthy controls. TS patients were excluded if: hypertensive, with major structural abnormalities of the heart or other systemic diseases that may affect myocardial function. Conventional speckle tracking echocardiography and glucose-insulin ratio were performed for all study subjects. Results Routine echocardiographic parameters of left ventricular systolic function were similar in cases and controls while global longitudinal and circumferential strain (GLS and GCS) were lower in patients with TS than controls: (−13.2±1.1 vs. −18.3±2.4, p-value<0.000) and (−11.3±1.1 vs. −16.3±2.1, p-value<0.000), respectively. Fasting glucose:insulin ratio (FGIR) proved to be the best predictor of myocardial dysfunction in TS patients by multivariate analysis. Conclusions This study points towards the potential role of two-dimensional (2D) speckle tracking echocardiography in early detection of subtle systolic myocardial dysfunction in TS patients. It also points towards the implication of insulin resistance in precipitation of the observed dysfunction in TS patients.

Cardiac abnormalities in girls with Turner syndrome: ECG abnormalities, myocardial strain imaging, and karyotype–phenotype associations

“…The LVM z‐score in this study was relatively low, and not in line with previous studies reporting on normal left ventricular parameters or even left ventricular hypertrophy in girls and women with TS (AbdelMassih et al, 2018 ; Mortensen, Gravholt, et al, 2012 ; Oberhoffer et al, 2020 ; Sozen et al, 2009 ). This might be partly due to the differences in methods used to calculate the LVM (e.g., LVM/BSA, LV mass‐for‐height, LVM index).…”

“…Analysis was performed using echocardiographic quantification software (EchoPAC version 113; GE Medical Systems, Horten, Norway). Strain results were compared with age‐ and vendor‐specific normative values (Klitsie et al, 2013 ; Levy et al, 2016 ), and compared with results reported in other TS populations (AbdelMassih et al, 2018 ; Oberhoffer et al, 2020 ).…”

“…Myocardial strain analysis, mainly global longitudinal strain (GLS), can be used to detect subtle changes in left ventricular systolic function, that are not detectable with the left ventricular ejection fraction (EF) (Lang et al, 2015 ; Tops et al, 2017 ). However, this sensitive technique has only been investigated in very small cohorts of patients with TS, with contradicting results (AbdelMassih et al, 2018 ; Oberhoffer et al, 2020 ; Oz et al, 2014 ).…”

Clinical case report

“…[ 18 ] The reasons why the thyroid gland was an autoimmune target in TS patients have not yet been clearly identified, but the predilection could be elucidated based on the close connection between the thyroid autoimmunity and female gender. [ 19 ]…”

Left ventricular mass index and subendocardial myocardial function in children with chronic kidney disease, a transmural strain and three-dimensional echocardiographic study

“…Insulin resistance has been confirmed to aggravate CKD by altering renal hemodynamics, filtration pressure and aggravating sodium retention and therefore hypertension. The role hyperinsulinemia plays in myocardial remodeling is well known in the recent literature [16,17]. Insulin causes myocardial hypertrophy, impairs diastolic function and aggravates systemic hypertension by impairing endothelia function.…”