Children with congenital heart disease are at risk for developing increased arterial stiffness and this may be modulated by physical activity. OBJECTIVE: To compare arterial stiffness in high- and low-physically active children with congenital heart disease and healthy age- and sex-matched controls. PATIENTS: Seventeen children with congenital heart disease (12 ± 2 years; females = 9), grouped by low- and high-physical activity levels from accelerometry step count values, and 20 matched controls (11 ± 3 years; females = 9) were studied. OUTCOME MEASURES: Carotid-radial pulse wave velocity was assessed with applanation tonometry to determine arterial stiffness. Body composition and 6-min walk test measures were performed. Data were analyzed using analysis of variance and multiple regression. Significance was P < .05. RESULTS: Arterial stiffness was increased in low-physically active children with congenital heart disease (9.79 ± 0.97 m/s) compared to high-physically active children with congenital heart disease (7.88 ± 0.71 m/s; P = .002) and healthy-matched controls (8.67 ± 1.28 m/s; P = .015). There were no differences in body composition measures between groups (all P > .05), but 6-min walk test distance was less in both congenital heart disease groups (high-physically active: 514 ± 40 m; low-physically active: 539 ± 49 m) versus controls (605 ± 79 m; all P < .05). Average daily step count significantly predicted arterial stiffness in children with congenital heart disease (R2 = 0.358) with a negative correlation (R = -0.599, P = .011), while % fat mass (P = .519) and % lean mass (P = .290) did not predict arterial stiffness. CONCLUSIONS: Low-physically active children with congenital heart disease have increased arterial stiffness compared to high-physically active children with congenital heart disease and healthy-matched controls. Regular physical activity in children with congenital heart disease may modulate arterial stiffness.
Children with congenital heart disease are at risk for developing increased arterial stiffness and this may be modulated by physical activity. OBJECTIVE: To compare arterial stiffness in high- and low-physically active children with congenital heart disease and healthy age- and sex-matched controls. PATIENTS: Seventeen children with congenital heart disease (12 ± 2 years; females = 9), grouped by low- and high-physical activity levels from accelerometry step count values, and 20 matched controls (11 ± 3 years; females = 9) were studied. OUTCOME MEASURES: Carotid-radial pulse wave velocity was assessed with applanation tonometry to determine arterial stiffness. Body composition and 6-min walk test measures were performed. Data were analyzed using analysis of variance and multiple regression. Significance was P < .05. RESULTS: Arterial stiffness was increased in low-physically active children with congenital heart disease (9.79 ± 0.97 m/s) compared to high-physically active children with congenital heart disease (7.88 ± 0.71 m/s; P = .002) and healthy-matched controls (8.67 ± 1.28 m/s; P = .015). There were no differences in body composition measures between groups (all P > .05), but 6-min walk test distance was less in both congenital heart disease groups (high-physically active: 514 ± 40 m; low-physically active: 539 ± 49 m) versus controls (605 ± 79 m; all P < .05). Average daily step count significantly predicted arterial stiffness in children with congenital heart disease (R2 = 0.358) with a negative correlation (R = -0.599, P = .011), while % fat mass (P = .519) and % lean mass (P = .290) did not predict arterial stiffness. CONCLUSIONS: Low-physically active children with congenital heart disease have increased arterial stiffness compared to high-physically active children with congenital heart disease and healthy-matched controls. Regular physical activity in children with congenital heart disease may modulate arterial stiffness.
Authors: Erin Barbour-Tuck; Natasha G Boyes; Corey R Tomczak; Dana S Lahti; Chantelle L Baril; Charissa Pockett; Shonah Runalls; Ashok Kakadekar; Scott Pharis; Timothy J Bradley; Kristi D Wright; Marta C Erlandson Journal: BMC Cardiovasc Disord Date: 2020-05-19 Impact factor: 2.298