Abstract P040: Muscle Metaboreflex Regulation of Arterial Blood Pressure in Children with Congenital Heart Defects

• Published in: Circulation (New York, N.Y.) N.Y.), 2016-03, Vol.133 (suppl_1)
• Main Authors: Tomczak, Corey R, Fusnik, Stephanie, Hogeweide, Elizabeth, Haykowsky, Mark J, Stickland, Michael K, Runalls, Shonah, Kakadekar, Ashok, Pharis, Scott, Pockett, Charissa, Erlandson, Marta
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.133.suppl_1.p040

Abstract only Introduction: Metabolically sensitive afferent fibers in skeletal muscle can signal an increase the sympathetic control of arterial blood pressure during exercise. This process, called the muscle metaboreflex, is augmented in adults with cardiovascular disease and contributes to exercise intolerance. The role of the muscle metaboreflex on blood pressure control in children with congenital heart defects (CHD) is not known. Hypothesis: We tested the hypothesis that the mean arterial pressure (MAP) response to the muscle metaboreflex would be augmented in children with CHD compared to healthy controls. Methods: Twenty-six children with CHD (11±2 years; males=14; females=12) and 21 age- and sex-matched controls (11±3 years; males=10; females=11) were studied. CHD diagnoses included Tetralogy of Fallot (n=7), pulmonary or aortic stenosis (n=3), hypoplastic left or right heart syndrome (n=5), Ebstien’s anomaly (n=1), atrial or ventricular septal defect (n=5), transposition of the great arteries (n=2), double inlet left ventricle (n=1), heart transplantation (n=2), tricuspid or pulmonary atresia (n=2), coarctation of the aorta (n=2), and dilated cardiomyopathy (n=1). Testing included a 3 min rest period followed by isometric handgrip exercise at 30% of maximal voluntary contraction for 2 min. Exercise was followed by 3 min of either a free flow control condition or circulatory occlusion to isolate the muscle metaboreflex. Beat-by-beat MAP was recorded using finger plethysmography. Analyses were completed using mixed designs factorial ANOVA with P < 0.05 as the level of significance. Data are mean ± SD. Results: During the free flow control condition, there was no significant difference in resting MAP (75±9 mmHg vs. 78±9 mmHg), exercise MAP (86±14 mmHg vs. 87±12 mmHg), or free flow MAP (72±10 mmHg vs. 78±9 mmHg) between children with CHD vs. controls, respectively ( P > 0.05). MAP significantly increased from rest to exercise and returned to resting levels during the free flow control condition for both groups. For the circulatory occlusion condition, there was no significant difference in resting MAP (73±11 mmHg vs. 74±8 mmHg), exercise MAP (84±15 mmHg vs. 81±11 mmHg), or circulatory occlusion MAP (79±13 mmHg vs. 79±13 mmHg) between children with CHD vs. controls, respectively ( P > 0.05). MAP significantly increased from rest to exercise and MAP remained elevated above resting levels during circulatory occlusion for both children with CHD and contr