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Asian Cardiovasc Thorac Ann 2002;10:378
© 2002 Asia Publishing EXchange Pte Ltd


LETTER TO THE EDITOR

Unexplained Systemic Hypertension After Closure of Ductus Arteriosus

Ümrah Aydogan, MD

Department of Pediatric CardiologyIstanbul Medical Faculty Istanbul University Millet Caddesi, Çapa Istanbul 34390, Turkey
I read with interest the case of systemic hypertension after surgical closure of patent ductus arteriosus (PDA) reported by Davierwala and colleagues.1 We encountered the same complication after transcatheter occlusion of PDA with a Rashkind umbrella. With this experience, we conducted a prospective study to evaluate the possible role of the potent vasoconstrictor angiotensin II (AT-II) in this complication.

We monitored the blood pressure of 16 patients with PDA and took blood samples to measure the level of angiotensin I (AT-I), the precursor of AT-II, 10 days before, immediately before and after, and 10 days after the occlusion procedure.

We found no statistically significant difference in AT-I levels 10 days before and just before occlusion, which indicates that its levels were not affected by the stress induced by or the medication used in the catheterization procedure. There was also no significant difference in its levels immediately before and just after occlusion, which indicates that the patients were still under the effect of AT-II after occlusion, although its secretion was no longer necessary.

In all but 1 patient, preocclusion AT-I levels were higher than normal values (< 5 ng·dL-1), although nearly half of the patients had a pulmonary to systemic blood flow ratio (Qp/Qs) lower than 1.5. In addition, preocclusion AT-I levels significantly correlated (p < 0.05) with Qp/Qs ratios.

We also found that the systolic blood pressure increased significantly (p < 0.001) in 10 patients whose PDA was completely occluded after the procedure. It was above 160 mm Hg in 2 of them. AT-I levels were still high 10 days after the procedure in 6 of the 10 patients with complete occlusion.

Because the diastolic blood pressure is lower than normal in patients with PDA, we postulate from these results that the secretion of the vasoconstrictor AT-II is stimulated in order to maintain sufficient tissue perfusion in diastole, even in those with small shunts. There may be an adaptive response problem in the stimulation mechanism in some of these patients, which prolongs AT-II secretion for several days after PDA closure, resulting in hypertension. Patients with a wide PDA would have a higher risk of hypertension after closure since the AT-I level correlates with the Qp/Qs ratio.

REFERENCE

  1. Davierwala P, Thakur N, Babu P, Reddy S, Kumar P, Menon R, et al. Unexplained systemic hypertension after closure of ductus arteriosus. Asian Cardiovasc Thorac Ann 2002;10:78–9.[Abstract/Free Full Text]





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