Childhood onset inflammatory bowel disease is more aggressive and has rapidly progressive clinical course than adult inflammatory bowel disease. Early-onset inflammatory bowel disease has more severe clinical progression as a subspecialised group of monogenic inflammatory bowel disease. We studied cardiac functions and aortic elasticity in children with early- and late-onset inflammatory bowel disease in remission period.

Thirty-three paediatric patients were divided into subgroups according to age of disease onset (<10 and >10 years of age). Twenty-five healthy children were admitted as control group. M-Mode echocardiography and pulsed wave Doppler echocardiography were performed. Strain, distensibility, stiffness index of ascending, and abdominal aorta were evaluated.

Interventricular septum (mm) and left ventricular end-systolic diameter were higher (6.9 ± 1.2, 26.2 ± 4.6) in early-onset inflammatory bowel disease patients than control patients (6.1 ± 1.27, 22.7 ± 4.12) (p = 0.050, p = 0.050). Mitral E/E′ ratio and myocardial performance index were increased in inflammatory bowel disease and early-onset inflammatory bowel disease groups than control group (p = 0.046, p = 0.04; p = 0.023, p = 0.033). Diastolic functions were found to be impaired in inflammatory bowel disease and early-onset inflammatory bowel disease groups according to control group, while there was no difference between late-onset inflammatory bowel disease and control groups in terms of diastolic functions. Mitral E/A ratio was lower in inflammatory bowel disease patients and early-onset inflammatory bowel disease patients (1.46 ± 0.32, 1.4 ± 0.21) than control patients (1.70 ± 0.27) (p = 0.013, p = 0.004). Aortic elasticity did not differ between groups.

Chronic low-grade inflammation has effects on left ventricular diameters and diastolic function in remission period. Aortic elasticity is not affected in our study groups.

We aimed to study the dimensions, systolic and diastolic functions of the left ventricle; dimensions and elasticity of the aorta; and carotid intima-media thickness and flow-mediated dilatation of the brachial artery in mitral valve prolapse.

The study group consisted of 43 patients (mean age=13.3±3.9) and 42 healthy children (mean age=12.9±3.4). Left ventricular end-diastolic, end-systolic, left atrial diameters, interventricular septum, and left ventricular posterior wall thickness were measured. Ejection and shortening fractions were calculated by M-mode. Measurements were adjusted to the body surface area. Mitral annulus, and systolic and diastolic diameters of the aortic annulus and aorta at each level were obtained; z-scores, aortic strain, distensibility, stiffness index were calculated. Carotid intima-media thickness and flow-mediated dilatation were studied. Patients were classified as classical/non-classical mitral valve prolapse and younger/older patients.

Left ventricular end-systolic, end-diastolic, and left atrial diameters (p=0.009, p=0.024, p=0.001) and aortic z-scores at annulus, sinus valsalva, and sinotubuler junction were larger (p=0.008, p=0.003, p=0.002, respectively) in the mitral valve prolapse group. Aortic strain and distensibility increased and stiffness decreased at the ascending aorta in the patient group (p=0.012, 0.020, p=0.019, respectively). Classical mitral valve prolapse had lower strain and distensibility and higher stiffness of the aorta at sinus valsalva level (p=0.010, 0.027, 0.004, respectively). Carotid intima-media thickness was thinner in the patient group, especially in the non-classical mitral valve prolapse group (p=0.037). Flow-mediated dilatation did not differ among the groups.

Mitral valve prolapse is a systemic disease of the connective tissue causing enlarged cardiac chambers and increased elasticity of the aorta. Decreased carotid intima-media thickness in this group may indicate low atherosclerosis risk.

Aortic dilation and dissection is reported in patients with Turner’s syndrome, both with and without cardiovascular risk factors. The bicuspid aortic valve is closely associated with dilated aortic root, although expression of aortic dilation is variable. The determinants for variable expression of aortic dilation in individuals with Turner’s syndrome, however, are unknown.

A primary mesenchymal defect is prevalent in individuals with Turner’s syndrome, suggested by having abnormalities in bone matrix, and lymphatic and peripheral blood vessels. We hypothesize that an abnormal intrinsic elastic property of aorta is a forerunner of aortic dilation in Turner’s syndrome.

Assess utility of aortic distensibility as a measure of aortic elasticity for the stratification of the risk for aortic dilation, and its relationship with age, karyotype, and hormonal therapy.

Prospective cross-sectional study.

We performed cross-sectional M-mode and Doppler echocardiography in 24 individuals with Turner’s syndrome. Dimensions of the aortic root, and its distensibility, were calculated using standard techniques. We also examined a control group of 24 age matched normotensive patients with structurally normal hearts, who had been referred for evaluation of cardiac murmurs or chest pain.

Aortic dilation was the most common cardiac anomaly, seen in 11 of 24 (46%) individuals with Turner’s syndrome, and none in control group. Of these individuals, 5 without cardiovascular risk factors had aortic dilation. In 2 young girls, aortic dimensions were normal, albeit with reduced distensibility. Aortic dilation correlated inversely with aortic distensibility, but not with age, karyotype or hormonal therapy.

Individuals with Turner’s syndrome, even without cardiovascular risk factors, do develop aortic dilation accompanied by decreased aortic distensibility, suggestive of an intrinsic abnormality in elastic property of the ascending aorta.