Vascular and cardiac function in young adults with classical congenital adrenal hyperplasia

Abstract

Introduction: Patients with classical congenital adrenal hyperplasia (CAH) have increased cardiovascular risk, but the vascular and cardiac function during longitudinal corticoids replacement therapy is not known thoroughly. Material and methods: Cross-sectional study of 19 Caucasian adults with CAH (age 23.7 ± 3.8 years; twelve males) compared to 20 healthy volunteers matched for origin, sex, age, and body mass index (BMI). All of the participants were assessed for flow mediated dilatation of the brachial artery (FMD), intima-media thickness of the common carotid artery (cIMT) and common femoral artery (fIMT), standard echocardiography, and global longitudinal left ventricular function using two-dimensional speckle-tracking echocardiography (LSTE). Results: The patients with CAH, compared with controls, had decreased FMD (9.4 ± 3.9 vs. 19.8 ± 5.2; p < 0.01), and the difference was still significant after correction for potential confounders. cIMT and fIMT were higher in the CAH group at baseline (for cIMT 0.47 ± 0.4 mm vs. 0.40 ± 0.03 mm; p < 0.01, for fIMT 0.47 ± 0.05 mm vs. 0.41 ± 0.04 mm; p < 0.01) but not after correction for potential confounders. The CAH subjects, compared with controls, had normal or similar left ventricular (LV) ejection fraction and LV mass index. The mean absolute value of LSTE differed in the CAH patients compared with controls (-20.5% ± 1.2 vs.-22.5% ± 1.7; p < 0.01), but it was still within the normal range. Conclusions: Young adults with CAH and glucocorticoid long-lasting treatment had impaired FMD, an insignificant increase of IMT, and subclinical changes in LV diastolic function in echocardiography.

Effect of long‐term glucocorticoid therapy on cardiac functions in children with congenital adrenal hyperplasia

“…Doppler tissue imaging of our patients revealed defective LV ventricular relaxation, rise of the diastolic pressures pointing to possible impairment of early filling of the ventricles 15 . Our results match those of Wierzbicka‐Chmiel et al, 31 and those by Nengom et al, 41 Marra et al 32 and Mooij et al 33 The reduced average mitral s´ velocity in our cohort compared to controls also supports the presence of possibly altered LV systolic function. A reduced s´ velocity was previously documented in subclinical LV systolic dysfunction in patients with hypertrophied myocardium where the average s´ velocity was found to be a good representative of LV contractile function besides being an independent predictor of LV diastolic dysfunction despite normal LV ejection fraction 42 .…”

“…Doppler tissue imaging of our patients revealed defective LV ventricular relaxation, rise of the diastolic pressures pointing to possible impairment of early filling of the ventricles. 15 Our results match those of Wierzbicka-Chmiel et al, 31 and those by Nengom et al, 41 Marra et al 32 and Mooij et al 33 The reduced average mitral Regarding RV, diastolic dysfunction was more pronounced in our patients with low tricuspid s´ velocity and e´/a´ ratio. It has been demonstrated that RV s´ velocity can additionally predict RV systolic function at ejection fractions below 45% with a sensitivity of 90% and specificity of 85%.…”

“…LV was significantly hypertrophied in the studied group as evidenced by larger LV mass, LVEDd and LVESd and thicker LVPW and IVST, in agreement with the results of others. 23,30 On the other hand, Wierzbicka-Chmiel et al 31 and Marra et al 32 reported no significant increase in LV dimensions. In their study,…”

Expression of selected angiogenesis-related small microRNAs in patients with abnormally increased secretion of glucocorticoids

“…About 1% of the general population are using long-term GC therapy at any given time, due to the increased preva-lence of diseases requiring such therapy [2][3]. There is growing concern that markedly increased use of GCs can lead to supraphysiological GC exposure and may induce specific adverse cardio-metabolic complications, such as dyslipidaemia, adiposity and central obesity, decreased insulin sensitivity, hyperglycaemia and diabetes, inflammation, immune dysregulation and platelet activation, and finally hypertension and atherosclerosis followed by cardio-vascular derangements, such as increased risk of coronary artery disease, heart insufficiency, or stroke [4][5]. These exogenous Miłosz P. Kawa, Pomeranian Medical University, Al.…”

“…Likewise, miRNA-223, the expression of which is dependent on intracellular cholesterol levels, has also been reported to play a role in endothelium, especially due to the fact that miRNA-223 negatively regulates the inflammatory response by blocking the NLRP3 inflammasome and IL-1b production [22]. Altogether, it seems that the involvement of miRNAs in angiogenesis and endothelial cell function in cardiovascular system is substantial, making miRNAs presumably major governing forces in the pathogenesis of endothelial dysfunction developing GC-related complications have been strictly linked to increased cardio-vascular morbidity or mortality [4][5]. Nevertheless, there is no medical consensus on the best strategies for the prevention and detection of GC-induced complications, and available data on these adverse events are rather poor, with many of the clinical studies being inconclusive, resulting in the lack of optimal treatment strategies for patients affected with glucocorticoid-induced adverse cardio-metabolic disorders.…”