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Arm-leg pressure gradients on late follow-up after coarctation repair : Possible causes and implications

Guenthard, J. ; Zumsteg, U. ; Wyler, F.

In: European Heart Journal, 1996, vol. 17, no. 10, p. 1572-1575

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    Titre
    • Arm-leg pressure gradients on late follow-up after coarctation repair
      Possible causes and implications
    Auteur
    • Guenthard, J.. Departments of Cardiology and Endocrinology, University Children's Hospital of Basel, Basel, Switzerland
    • Zumsteg, U.. Departments of Cardiology and Endocrinology, University Children's Hospital of Basel, Basel, Switzerland
    • Wyler, F.. Departments of Cardiology and Endocrinology, University Children's Hospital of Basel, Basel, Switzerland
    Type de document
    • Postprint
    Identifiant OAI-PMH
    • oai:doc.rero.ch:302681
    Summary
    Seventeen years after coarctation repair, 36 patients were studied by magnetic resonance imaging and exercise testing to measure residual anatomical stenosis and hormonal response to exercise, and to evaluate their effect on arm-leg gradients and on exercise hypertension. The systolic arm pressure, leg pressure and arm-leg gradient were measured at rest and during exercise. Active renin and catecholamines were measured in the plasma at rest and after peak exercise. On magnetic resonance imaging 18 patients had residual stenosis of less than 30% (group I) and 18 had residual stenosis of equal to or more than 30% (group II). At peak exercise, the arm pressure was 235 (133-296) mmHg in group I and 241 (157-286) mmHg in group II (ns), the leg pressure was 138 (111-173) mmHg in group I and 114 (75-154)mmHg in group II (P=0·002). The adrenalin increase from rest to exercise was 32·7 ± 9·1 pg . ml −1 in the patients with exercise hypertension and 3·1 ± 4·7 pg. ml−1 in the patients who remained normotensive during exercise (P=0·02). In conclusion, residual anatomical stenosis leads to a pressure drop in the legs, which influences the arm-leg gradient. Arm hypertension is not related to anatomical narrowing but to interaction of enhanced sympathetic nerve activity and structural and functional abnormality of the precoarctation vessels. (Eur Heart J 1996; 17: 1572-1575)