Exercise-induced hypertension in the arms due to impaired arterial reactivity after successful coarctation resection

https://doi.org/10.1016/S0002-9149(99)80418-4Get rights and content

Abstract

Exercise-induced hypertension of the arms is a wellknown late complication after coarctation repair. Residual narrowing at the anastomosis site as well as abnormalities of the precoarctation arterial system may be the cause of this problem. Blood pressure response to exercise and flow-mediated arterial dilatation of the arms and legs were studied in 29 young adults after successful coarctectomy in childhood and compared with 13 control subjects. Peak exercise systolic blood pressure was significantly higher in patients than in control subjects: 238 versus 199 mm Hg (p = 0.007). Both groups had a positive systolic arm-leg gradient during exercise: 59 versus 37 mm Hg (p = 0.05). Flow-mediated dilatation of the brachial artery was significantly reduced in patients compared with that in control subjects: 4.2% (range 0% to 9.4%) versus 9.4% (range 3.7% to 16%) (p < 0.0001). Flow-mediated dilatation of the femoral artery was similar in both groups. Dilatation of the brachial artery was inversely correlated to peak exercise systolic pressure in the study patients (r = −0.427, p = 0.02). A positive arm-leg exercise gradient partly represents physiologic circulatory adaptation to ergometry and is therefore not appropriate for evaluation of residual narrowing. Exercise-induced hypertension of the arms late after coarctation repair is caused by impaired arterial reactivity, which results from structural or functional abnormality, or both.

References (21)

There are more references available in the full text version of this article.

Cited by (41)

  • Usefulness of exercise-induced hypertension as predictor of chronic hypertension in adults after operative therapy for aortic isthmic coarctation in childhood

    2011, American Journal of Cardiology
    Citation Excerpt :

    It is thought that exercise-induced hypertension in patients with CoA is caused by diminished arterial wall compliance and increased rigidity owing to the structural abnormal precoarctational wall, with more collagen and less smooth muscle tissue.16 Furthermore, it is hypothesized that the abnormal tissue in the precoarctational wall influences baroreceptor activity in the upper vascular bed, which might explain the pre- and postoperative hypertension.6,17–20 The prognostic significance of exercise-induced hypertension in patients with CoA is unknown.

  • Vascular Remodeling After "Successful" Repair of Coarctation. Impact of Aortic Arch Geometry

    2007, Journal of the American College of Cardiology
    Citation Excerpt :

    Hence, there is a rationale for understanding the mechanisms of increased IMT and stiffness after CoA repair. Abnormal findings in the vascular reactivity measures (FMD and GTN) are not consistently found in subjects who had CoA repair (4,9,10,24,25) and, indeed, there was a wide range of values in these parameters in the current study. Similarly, although long-term follow-up studies show a high prevalence of hypertension, a significant proportion of CoA survivors remain normotensive after 30 years (1,2,22).

View all citing articles on Scopus
View full text