Impaired systolic and diastolic left ventricular function in children and adolescents with congenital adrenal hyperplasia receiving corticosteroid therapy

2019 ◽  
Vol 29 (3) ◽  
pp. 319-324
Author(s):  
Hale Tuhan ◽  
Tülay Demircan ◽  
Ayca Altıncık ◽  
Gönül Çatlı ◽  
Özgür Kızılca ◽  
...  
Keyword(s):  
Relaxation Time ◽  
Congenital Adrenal Hyperplasia ◽  
Bone Age ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Control Group ◽  
Adrenal Hyperplasia ◽  
Isovolumic Relaxation Time ◽  
17 Hydroxyprogesterone ◽  
Isovolumic Relaxation

AbstractAimThe present study aimed to evaluate systolic and diastolic myocardial function in children and adolescents with congenital adrenal hyperplasia.MethodsThe study included 44 children with the diagnosis of classic congenital adrenal hyperplasia and 39 healthy children whose age, pubertal status, and gender were similar to those of the patient group. Anthropometric parameters and 17-hydroxyprogesterone levels were measured, and bone age was calculated. The average daily hydrocortisone dose was calculated over the last 1-year file records. Hyperandrogenic state was defined according to bone age SD score (⩾2) and 17-hydroxyprogesterone levels (>10 ng/ml). Echocardiographic examinations were assessed by conventional two-dimensional Doppler echocardiography and tissue Doppler imaging.ResultsPatients had higher morphological parameters, such as left ventricular end-systolic diameter, interventricular septal thickness at end diastole, left ventricular posterior wall thickness at end diastole, left ventricular mass and index, than the control group (p<0.05). On pulsed-wave and tissue Doppler echocardiography, significant subclinical alterations were observed in systolic (isovolumic contraction time), diastolic (isovolumic relaxation time), and global left ventricular functional (myocardial performance index) parameters in the congenital adrenal hyperplasia group compared to the control group (p<0.05). In partial correlation analyses, after controlling the effect of hyperandrogenism, the mean hydrocortisone dosage was positively correlated with isovolumic relaxation time in congenital adrenal hyperplasia group (p<0.05).ConclusionThis study demonstrated that the patients with congenital adrenal hyperplasia are at risk for left ventricular hypertrophy, systolic and diastolic myocardial subclinical alterations. Overtreatment may be responsible for the increased risk of myocardial dysfunction in patients with congenital adrenal hyperplasia.

Influence of heart rate on left ventricular isovolumic relaxation time: a Doppler study in healthy newborns

2004 ◽  
Vol 17 (4) ◽  
pp. 330-331 ◽  
Author(s):  
Antonio De Merulis ◽  
Giulio Calcagni ◽  
Paolo Versacci ◽  
Renato Lucchini ◽  
Flavia Ventriglia ◽  
...  
Keyword(s):  
Heart Rate ◽  
Relaxation Time ◽  
Left Ventricular ◽  
Isovolumic Relaxation Time ◽  
Doppler Study ◽  
Isovolumic Relaxation

Pulsed Doppler assessment of left ventricular diastolic function in normal and cardiomyopathic cats

1999 ◽  
Vol 35 (4) ◽  
pp. 285-291 ◽  
Author(s):  
JM Bright ◽  
ME Herrtage ◽  
JF Schneider
Keyword(s):  
Relaxation Time ◽  
Diastolic Function ◽  
Peak Velocity ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
P Value ◽  
Pulsed Doppler ◽  
Time Data ◽  
Isovolumic Relaxation Time ◽  
Isovolumic Relaxation

Left ventricular (LV) diastolic function was evaluated in 16 cats with primary hypertrophic cardiomyopathy (HCM) using pulsed Doppler (PD) assessment of transmitral flow and isovolumic relaxation time. Data obtained was compared to data from 12 healthy, adult, research cats. Compared to normal cats, the HCM group showed significantly (p value less than 0.05) reduced early LV inflow velocities (mean +/- standard error [SE], peak velocity of 0.70+/-0.04 m/s versus 0.54+/-0.04 m/s and integrated velocity of 0.48+/-0.08 m/s versus 0.37+/-0.03 m/s); a reduced rate of deceleration of early inflow (mean+/-SE, -12.0+/-1.0 m/s2 versus -5.1+/-1.1 m/s2); prolonged isovolumic relaxation time (mean +/- SE, 45.7+/-3.3 ms versus 76.0+/-3.1 ms); and increased atrial systolic flow velocities (mean +/- SE, peak velocity of 0.29+/-0.04 m/s versus 0.48+/-0.04 m/s and integrated velocity of 0.21+/-0.03 m/s versus 0.34+/-0.03 m/s). The results suggest that PD provides a noninvasive method of identifying and quantifying functional diastolic impairment in cats with HCM.

Brain Natriuretic Peptide: Effect on Left Ventricular Filling Patterns in Healthy Subjects

1995 ◽  
Vol 88 (2) ◽  
pp. 159-164 ◽  
Author(s):  
Peter B. M. Clarkson ◽  
Nigel M. Wheeldon ◽  
Catherine MacLeod ◽  
Wendy Coutie ◽  
Thomas M. MacDonald
Keyword(s):  
Relaxation Time ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Double Blind ◽  
Isovolumic Relaxation Time ◽  
Isovolumic Relaxation

1. Elevated plasma concentrations of brain natriuretic peptide are found in conditions associated with impaired left ventricular diastolic function. The purpose of this study was to determine whether this peptide actually plays a physiological role in improving myocardial performance in diastole. 2. Nine normal subjects received infusions of brain natriuretic peptide or placebo in a randomized, double-blind, crossover study. Brain natriuretic peptide infusion produced a significant reduction in isovolumic relaxation time (means and 95% confidence interval for difference−10.8 ms, −14.5 to −7.0 ms) (P < 0.01) and significantly increased both the peak E/A velocity (0.54, 0.14–0.94) (P < 0.05) and the E/A time velocity integral (1.09, 0.20–1.98) (P < 0.05). 3. These responses were evident at concentrations of brain natriuretic peptide that produced no associated effects on blood pressure, heart rate or stroke distance. 4. Brain natriuretic peptide infusion in normal subjects significantly reduces isovolumic relaxation time and improves transmitral Doppler flow profiles, suggesting that this peptide may be important in the control of left ventricular diastolic relaxation in man.

Adverse Effects of Hypoxaemia on Diastolic Filling in Humans

1995 ◽  
Vol 89 (2) ◽  
pp. 165-169 ◽  
Author(s):  
Robert I. Cargill ◽  
David G. Kiely ◽  
Brian J. Lipworth
Keyword(s):  
Heart Rate ◽  
Relaxation Time ◽  
Confidence Interval ◽  
Left Ventricular ◽  
Mean Difference ◽  
Oxygen Mixture ◽  
Diastolic Filling ◽  
Isovolumic Relaxation Time ◽  
Isovolumic Relaxation ◽  
Deceleration Time

1. Abnormalities of myocardial relaxation may occur as a consequence of myocyte hypoxia. We have therefore examined the effects of hypoxaemia on right and left ventricular diastolic function in 10 healthy male subjects. 2. After resting to reach baseline haemodynamics, subjects were rendered hypoxaemic by breathing a variable nitrogen/oxygen mixture. Oxygen saturation (SaO2) was maintained at 85–90% for 20 min and then at 75–80% for a further 20 min. Haemodynamic and diastolic filling parameters were measured non-invasively at baseline and at the end of each period of hypoxaemia. 3. Diastolic filling of both ventricles was significantly impaired by hypoxaemia. In comparison with baseline, left ventricular isovolumic relaxation time and transmitral E-wave deceleration time corrected for heart rate were significantly prolonged at SaO2 75–80%: mean difference in corrected relaxation time, 9.8 ms (95% confidence interval 1–19); mean difference in corrected deceleration time, 34 ms (95% confidence interval 11–56). Similarly, right ventricular isovolumic relaxation time and transtricuspid E-wave deceleration time were significantly prolonged at SaO2 values of 75–80% compared with baseline: mean difference in relaxation time, 20.3 ms (95% confidence interval 3–38); mean difference in deceleration time, 33 ms (95% confidence interval 11–55). 4. During hypoxaemia there were dose-related increases in heart rate, cardiac output and mean pulmonary artery pressure, but no effects on mean arterial pressure. 5. Hypoxaemia significantly impairs relaxation of left and right ventricles in normal humans. These changes may reflect impairment of intracellular calcium transport secondary to the effects of myocyte hypoxia.

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