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Comparison Of Candesartan Versus Metoprolol For Treatment Of Systemic Hypertension After Repaired Aortic Coarctation.

E. Moltzer, F. M. Mattace Raso, Y. Karamermer, E. Boersma, G. Webb, M. Simoons, A. Danser, A. H. van den Meiracker, J. Roos‐Hesselink
Published 2010 · Medicine

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Even after successful repair, hypertension is one of the main determinants of cardiovascular morbidity and mortality in patients with aortic coarctation (CoA). We compared the effect of candesartan (angiotensin II receptor blockade) and metoprolol (beta-adrenergic receptor blockade) on blood pressure, large artery stiffness, and neurohormonal status in hypertensive patients after repair of CoA. In the present open-label, crossover study, hypertensive patients after CoA repair were first randomly assigned to treatment with candesartan 8 mg or metoprolol 100 mg once per day. After 8 weeks of treatment with one of the drugs, the other treatment was given for 8 weeks. The treatment effects were assessed with 24-hour ambulatory blood pressure monitoring, measurement of large artery stiffness, and neurohormonal plasma levels at baseline and after 8 weeks of either treatment. Sixteen patients (mean age 37 +/- 12 years, 26 +/- 15 years after repair, 63% men) completed the study. The 24-hour mean arterial pressure at baseline was 97.7 +/- 6.2 mm Hg. Metoprolol (mean dose 163 +/- 50 mg/day) decreased the mean arterial pressure (7.0 +/- 4.2 and 4.1 +/- 3.6 mm Hg, respectively) more than did candesartan (mean dose 13 +/- 4 mg/day; p = 0.018, 95% confidence interval 0.6 to 5.5). Large artery stiffness did not change with either treatment. With metoprolol, plasma B-type natriuretic peptide increased and plasma renin decreased. With candesartan, the plasma renin and noradrenaline levels increased and aldosterone levels decreased. In conclusion, in adult hypertensive patients after CoA repair, metoprolol had more of an antihypertensive effect than did candesartan. Moreover, the neurohormonal outcome did not support a significant role for the renin-angiotensin system in the causative mechanism of hypertension after CoA.
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