Melissa G Y Lee1, Robyn A Hemmes2, Jonathan Mynard3, Elisabeth Lambert4, Geoffrey A Head5, Michael M H Cheung6, Igor E Konstantinov7, Christian P Brizard8, Gavin Lambert9, Yves d'Udekem10. 1. Department of Cardiac Surgery, The Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: mglee@student.unimelb.edu.au. 2. Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia. Electronic address: robyn.hemmes@allg.org.au. 3. Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: jonathan.mynard@mcri.edu.au. 4. Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Iverson Health Innovation Research Institute, Swinburne University of Technology, Melbourne, Australia. Electronic address: elisabethlambert@swin.edu.au. 5. Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia. Electronic address: geoff.head@bakeridi.edu.au. 6. Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia; Department of Cardiology, The Royal Children's Hospital, Melbourne, Australia. Electronic address: michael.cheung@rch.org.au. 7. Department of Cardiac Surgery, The Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: igor.konstantinov@rch.org.au. 8. Department of Cardiac Surgery, The Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: christian.brizard@rch.org.au. 9. Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Iverson Health Innovation Research Institute, Swinburne University of Technology, Melbourne, Australia. Electronic address: glambert@swin.edu.au. 10. Department of Cardiac Surgery, The Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research, Clinical Sciences, Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: yves.dudekem@rch.org.au.
Abstract
BACKGROUND: There is a high prevalence of late hypertension after coarctation repair. The relative contribution of elevated sympathetic tone and endothelial dysfunction to its development is unknown. This study aims to investigate the neural profile of coarctation patients including muscle sympathetic nerve activity testing to directly measure sympathetic nervous activity. METHODS: Twenty-three patients aged ≥18years with a coarctation repair underwent measurements of clinic and 24-h blood pressures, muscle sympathetic nerve activity, sympathetic and cardiac baroreflex functions, digital endothelial function, and ambulatory arterial stiffness index. Median age at repair was 1.2months (interquartile range: 0-9months). Patients were compared to 17 healthy matched controls. RESULTS: After 26±5years, 6% (1/18) and 44% (8/18) suffered clinic hypertension and prehypertension, respectively. On 24-h blood pressure monitoring, 15% (3/20) and 20% (4/20) had hypertension and prehypertension, respectively. Coarctation patients had elevated muscle sympathetic nerve activity compared with controls (49.6±24.9 vs. 29.9±14.0 bursts/100 heartbeats, p=0.02), dampened sympathetic baroreflex function (-2.2±2.1 vs. -7.0±5.6 bursts/100heartbeats·mm·Hg-1, p=0.007), normal cardiac baroreflex function (41.9±30.4 vs. 35.7±21.1ms·mm·Hg-1, p=0.6), endothelial dysfunction (pulse amplitude tonometry ratio: 0.39±0.32 vs. 0.81±0.50, p=0.004), and increased ambulatory arterial stiffness index (0.46±0.15 vs. 0.29±0.17, p=0.008). CONCLUSION: After coarctation repair patients have increased muscle sympathetic nerve activity, dampened sympathetic baroreflex response, endothelial dysfunction, and increased ambulatory arterial stiffness index, all of which may contribute to the development of late hypertension.
BACKGROUND: There is a high prevalence of late hypertension after coarctation repair. The relative contribution of elevated sympathetic tone and endothelial dysfunction to its development is unknown. This study aims to investigate the neural profile of coarctationpatients including muscle sympathetic nerve activity testing to directly measure sympathetic nervous activity. METHODS: Twenty-three patients aged ≥18years with a coarctation repair underwent measurements of clinic and 24-h blood pressures, muscle sympathetic nerve activity, sympathetic and cardiac baroreflex functions, digital endothelial function, and ambulatory arterial stiffness index. Median age at repair was 1.2months (interquartile range: 0-9months). Patients were compared to 17 healthy matched controls. RESULTS: After 26±5years, 6% (1/18) and 44% (8/18) suffered clinic hypertension and prehypertension, respectively. On 24-h blood pressure monitoring, 15% (3/20) and 20% (4/20) had hypertension and prehypertension, respectively. Coarctationpatients had elevated muscle sympathetic nerve activity compared with controls (49.6±24.9 vs. 29.9±14.0 bursts/100 heartbeats, p=0.02), dampened sympathetic baroreflex function (-2.2±2.1 vs. -7.0±5.6 bursts/100heartbeats·mm·Hg-1, p=0.007), normal cardiac baroreflex function (41.9±30.4 vs. 35.7±21.1ms·mm·Hg-1, p=0.6), endothelial dysfunction (pulse amplitude tonometry ratio: 0.39±0.32 vs. 0.81±0.50, p=0.004), and increased ambulatory arterial stiffness index (0.46±0.15 vs. 0.29±0.17, p=0.008). CONCLUSION: After coarctation repair patients have increased muscle sympathetic nerve activity, dampened sympathetic baroreflex response, endothelial dysfunction, and increased ambulatory arterial stiffness index, all of which may contribute to the development of late hypertension.
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