Clinical InvestigationArterioventricular interaction after coarctation repair
Section snippets
Study population
Patients treated with surgery or balloon angioplasty (BA) between 3 months and 16 years of age between 1969 and 2004 with a follow-up of at least 10 years were included in this study. Patients who had their primary CoA procedure before the age of 3 months were excluded from this study, as overall these patients had more severe CoA with varying degrees of LV dysfunction prior to repair. Patients with isthmus hypoplasia, aortic arch hypoplasia and/or severe associated heart defects (e.g.,
Study population
The study population consisted of 22 CoA-patients and 22 controls. Baseline characteristics of the study population are presented in Table I. Primary treatment of CoA-patients was performed with BA (10 patients) or surgery with end-to-end anastomosis (12 patients) at a mean age of 5.9 years (range 0.4–14.4 years). Mean follow-up at time of investigation was 23.9 years (range 10.8–42.2 years). Surgical patients were significantly older than BA patients (35 ± 9.5 versus 22 ± 6.7 years, P = .001),
Discussion
Increased aortic stiffness has been implicated in the development of hypertension in CoA-patients, even after anatomically successful repair.17., 18., 19., 20., 21., 22. Impaired aortic distensibility may also lead to increased LV afterload and adverse arterioventricular coupling.4., 6. The impact of increased aortic stiffness on LV function and the potential additive role of hypertension is however unclear in CoA-patients after anatomically satisfying repair. The purpose of this study was to
Conclusion
The data presented in this study highlight the growing understanding that although CoA may be repaired to anatomical satisfaction, patients are not ‘cured’ and demonstrate increased aortic stiffness proximal to the CoA repair-site, even if they are normotensive.4., 5. At long-term follow-up even well-repaired CoA-patients show increased PWV and decreased distensibility in the pre-coarctation aorta, associated with systemic hypertension. Despite these vascular pathologies, LV function was
Acknowledgements
This study was funded by a grant from the “Stichting Hartekind”; grand number: 2012.001.
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Cited by (0)
Funding: This study was funded by a grant from the “Stichting Hartekind”.
Conflicts of interest: None.