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Stroke. 2009;40:47-51
Published online before print October 16, 2008, doi: 10.1161/STROKEAHA.108.518670
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(Stroke. 2009;40:47.)
© 2009 American Heart Association, Inc.


Original Contributions

Temporary Reduction of Blood Pressure and Sympathetic Nerve Activity in Hypertensive Patients After Microvascular Decompression

Helga Frank, MD; Karsten Heusser, MD; Helmut Geiger, MD; Rudolf Fahlbusch, MD; Ramin Naraghi, MD Hans P. Schobel, MD

From Department of Nephrology (H.F.), Klinikum rechts der Isar, Technische Universitaet Muenchen, Germany; Department of Clinical Pharmacology (K.H.), Hannover Medical School, Hannover, Germany; Department of Nephrology (H.G.), University of Frankfurt, Germany; International Neuroscience Institute Hannover (R.F.), Germany; Department of Neurosurgery (R.N.), University of Erlangen-Nuremberg, Germany; Benedictus Krankenhaus Tutzing (H.P.S.), Germany.

Correspondence to Helga Frank, MD, Department of Nephrology, Klinikum rechts der Isar, Technische Universitaet Muenchen, Ismaninger Strasse 22, 81675 Munich, Germany. E-mail Helga.Frank{at}lrz.tum.de

Background and Purpose— Experimental studies suggested neurovascular compression of the brain stem as a cause of hypertension. The aim of our prospective study was to investigate the effect of microvascular decompression in patients with severe hypertension with neurovascular compression on blood pressure and central sympathetic nerve activity in the long-term.

Methods— Fourteen patients (4 males; mean age, 46±8 years) with essential hypertension underwent microvascular decompression of the brain stem. Vasoconstrictor muscle sympathetic nerve activity (recorded by microneurography: burst frequency, bursts/min) and blood pressure (24-hour profiles) were investigated before surgery and 7 days, 3 months, and every 6 months postoperatively.

Results— Muscle sympathetic nerve activity was preoperatively elevated and decreased significantly postoperatively (35±13 bursts/min vs 20±9 bursts/min; P<0.01). Sympathetic activity remained reduced 3 months (19±8bursts/min; P<0.01), 6 months (19±7 bursts/min; P<0.01), and 12 months (23±9 bursts/min; P<0.01) postoperatively. However, in the long-term, sympathetic nerve activity increased again (18 months after surgery: 28±10 bursts, not significant; 24 months postoperatively: 34±12 bursts/min, not significant). Systolic and diastolic blood pressure decreased from 162±6/98±5 mm Hg preoperatively to 133±6/85±4 mm Hg (7 days postoperatively; P<0.01); 136±5/86±4 mm Hg (3 months postoperatively; P<0.01); 132±4/85±4 mm Hg (6 months postoperatively; P<0.01); 132±3/85±5 mm Hg (12 months postoperatively; P<0.01); 132±5/84±5 mm Hg; P<0.01). Twenty-four months after microvascular decompression, blood pressure increased again up to 158±7/96±6 mm Hg, corresponding to the sympathetic nerve activity course.

Conclusion— Sympathetic nerve activity and blood pressure are temporary reduced by microvascular decompression in patients with severe hypertension with neurovascular compression. The data are a hint for sympathetic overactivity as a pathomechanism in this subgroup of patients.


Key Words: decompressive surgery • hypertension • sympathetic nervous system