Patients with renovascular hypertension (RVH) have high cardiovascular mortality and morbidity. In these patients, overall sympathetic nerve activity is increased. It is unknown, however, whether this increase also involves the heart.
We tested the hypothesis that cardiac sympathetic activity is increased in patients with hypertension and renal artery stenosis.
A total of 14 patients with hypertension were studied before angioplasty of angiographically identified renal artery stenosis. Nine out of 14 patients had renovascular hypertension proven at the 1-year follow-up visit. A total of 19 healthy subjects served as a control group. A right heart catheterization, including the positioning of a coronary sinus thermodilution catheter was performed for hemodynamic recordings and blood sampling. Using a radiotracer dilution technique with infusion of tritiated noradrenaline ([3H]NA) and adrenaline ([3H]A), fractional extraction and clearance were calculated. Total body and cardiac NA spillovers were used as indices of systemic and cardiac sympathetic nervous activity. The study group had normal left ventricular ejection fraction and cardiac pressures. Cardiac NA spillover was increased by 127% in the hypertensive patients compared with healthy subjects (200 ± 53 versus 88 ± 10 pmol/min in controls, P < 0.05). Total body NA spillover was similar in both groups. Cardiac fractional extraction of [3H]NA and [3H]A was decreased by 26 and 47%, respectively, compared with normotensive subjects (P < 0.01 for both).
Patients with renovascular hypertension have altered cardiac sympathetic function with increased sympathetic drive and impaired catecholamine extraction. The increased cardiac sympathetic drive may have adverse long-term effects on prognosis in this patient group with high cardiovascular mortality.
Departments of aCardiology, bClinical Physiology and eNephrology, Sahlgrenska University Hospital, Göteborg, Sweden, cClinical Neurocardiology Section, National Institutes of Neurological Disorders and Stroke, Bethesda, Maryland, USA and dBaker Medical Research Institute, Prahran, Australia.
Sponsorship: This study was supported by grants from The Swedish Heart Lung Foundation, Sahlgrenska University Hospital and The Göteborg Medical Society.
Correspondence and requests for reprints to Magnus Petersson, Department of Cardiology, Sahlgrenska University Hospital, SE 413 45 Göteborg, Sweden. Tel: +46 31 3424222; fax: +46 31 827614; e-mail: firstname.lastname@example.org.
Received 22 October 2001
Revised 15 February 2002
Accepted 22 February 2002
See editorial commentary page 1071