Multilingual home environment and specific language impairment: a case-control study in Chinese children

published_or_final_versionMedical SciencesMasterMaster of Medical Science

Resting and exercise arterial dysfunction in anthracycline-treated adult survivors of childhood cancers

Abstract Background Emerging evidence suggests potential arterial damage with the use of anthracycline-based chemotherapeutic regimens. We determined arterial function at rest and during exercise in anthracycline-treated adult survivors of childhood cancers. Methods Ninety-six adult survivors (54 males) aged 25.0 ± 5.9 years and 60 (30 males) healthy controls were studied. Central systolic blood pressure (cSBP) and radial augmentation index (rAI) was determined by applanation tonometry. Carotid arterial stiffness and intima-media thickness (IMT) were assessed using high-resolution ultrasound. Results At rest, survivors had significantly greater carotid IMT (p  + 2SD of controls). The slopes of increase in carotid IMT (p < 0.001) and exercise-induced changes in carotid stiffness (p < 0.001) with age were significantly greater in survivors than controls. Multivariate analysis revealed carotid IMT (β = 0.32, p < 0.001) to be an significant correlate of dynamic percentage increase in stiffness index during exercise. Conclusions Arterial dysfunction is evident at rest and worsens during exercise in anthracycline-treated adult survivors of childhood cancers

Plasma high sensitivity troponin T levels in adult survivors of childhood leukaemias: determinants and associations with cardiac function.

We sought to quantify plasma high sensitivity cardiac troponin (hs-cTnT) levels, their determinants, and their associations with left ventricular (LV) myocardial deformation in adult survivors of childhood acute leukaemias.One hundred adult survivors (57 males) of childhood acute leukaemias, aged 24.1 ± 4.2 years, and 42 age-matched controls (26 males) were studied. Plasma cTnT was determined using a highly sensitive assay. Genotyping of NAD(P)H oxidase and multidrug resistance protein polymorphisms was performed. Left ventricular function was assessed by conventional, three-dimensional, and speckle tracking echocardiography. The medians (interquartile range) of hs-cTnT in male and female survivors were 4.9 (4.2 to 7.2) ng/L and 1.0 (1.0 to 3.5) ng/L, respectively. Nineteen survivors (13 males, 6 females) (19%) had elevated hs-cTnT (>95(th) centile of controls). Compared to those without elevated hs-TnT levels, these subjects had received larger cumulative anthracycline dose and were more likely to have leukaemic relapse, stem cell transplant, and cardiac irradiation. Their LV systolic and early diastolic myocardial velocities, isovolumic acceleration, and systolic longitudinal strain rate were significantly lower. Survivors having CT/TT at CYBA rs4673 had higher hs-cTnT levels than those with CC genotype. Functionally, increased hs-cTnT levels were associated with worse LV longitudinal systolic strain and systolic and diastolic strain rates.Increased hs-cTnT levels occur in a significant proportion of adult survivors of childhood acute leukaemias and are associated with larger cumulative anthracycline dose received, history of leukaemic relapse, stem cell transplant, and cardiac irradiation, genetic variants in free radical metabolism, and worse LV myocardial deformation

Comparisons of echocardiographic findings between survivors with (group I) and without (group II) elevated hs-cTnT levels.

<p>Abbreviations: A, peak mitral inflow velocity at late diastole; a, mitral annular late diastolic myocardial tissue velocity; E, peak mitral inflow velocity at early diastole; e, mitral annual early diastolic myocardial tissue velocity; EF, ejection fraction; FS, fractional shortening; IVA, isovolumic acceleration; LV, left ventricular; LVEDd, left ventricular end diastolic dimension; LVESd, left ventricular end systolic dimension; SR_d, early diastolic strain rate; SR_s, systolic strain rate.</p>*<p>statistically significant.</p

Comparisons of demographic and echocardiographic findings between survivors and control subjects.

<p>Abbreviations: A, peak mitral inflow velocity at late diastole; a, mitral annular late diastolic myocardial tissue velocity; E, peak mitral inflow velocity at early diastole; e, mitral annual early diastolic myocardial tissue velocity; EF, ejection fraction; FS, fractional shortening; IVA, isovolumic acceleration; LV, left ventricular; LVEDd, left ventricular end diastolic dimension; LVESd, left ventricular end systolic dimension; SR_d, early diastolic strain rate; SR_s, systolic strain rate.</p>*<p>statistically significant.</p

Relationships between high sensitivity cardiac troponin T (hs-cTnT) and indices of left ventricular (LV) deformation.

<p>Correlations between hs-cTnT and LV (a) global longitudinal systolic strain, (b) systolic strain rate, and (c) diastolic strain rate are shown. Solid lines represent the best-fit linear regression and dashed lines represent the 95% confidence interval for each parameter of the regression line.</p

Comparisons of demographic factors, clinical variables, and genotypic frequencies between survivors with (group I) and without (group II) elevated hs-cTnT levels.

<p>Abbreviations: AML, acute myeloid leukaemia; ALL, acute lymphoblastic leukaemia.</p>*<p>statistically significant.</p

Levels of high sensitivity cardiac troponin T (hs-cTnT) in survivors and controls by genders.

<p>Distributions of hs-cTnT in (a) male and (b) female survivors and controls are shown using scatter plots. Dashed lines represent 95^th percentile in controls.</p

Levels of high sensitivity cardiac troponin T (hs-cTnT) in survivors by NAD(P)H oxidase and multidrug resistance protein polymorphisms.

<p>Scatter plots showing distributions of hs-cTnT levels in relation to (a) <i>CYBA</i>, (b) <i>RAC2</i>, and (c) <i>NCF4</i> polymorphisms. Solid lines represent median hs-cTnT levels.</p