Use of the aldosterone-to-renin ratio (ARR) has suggested that at least one in 10 hypertensive subjects have primary aldosteronism (PA). There is thus a timely need to review the literature for effective drug therapies and to speculate on other therapeutic options by taking into account recent advances in understanding of the PA disease pathophysiological process.
A MEDLINE and EMBASE search of all articles published from the start of the databases until July 1999 and reviews of the bibliographies of textbooks.
Primary research articles on the medical treatment of PA with emphasis on diagnosis, treatment option, drug dosage, therapeutic response and adverse drug effect.
Study design and quality were assessed. Relevant data on diagnostic methodology, drug usage and response were analysed and compared.
A select number of subjects with aldosterone-producing adenoma (APA) can be expected to respond well to surgical treatment. For the majority of PA cases especially subjects with idiopathic hyperaldosteronism (IHA), long-term medical treatment is now safe and feasible although no randomized controlled trials have been carried out to date. The best therapeutic response is obtained by directly antagonizing aldosterone at the receptor level using medium to low dose spironolactone and this response can be predicted by a raised ARR. The response to other potassium-sparing diuretics and calcium channel blockers are modest. IHA responds better than angiotensin II-unresponsive APA to angiotensin converting enzyme inhibitors and this may also be true with angiotensin II receptor blockers. The discovery of the aldosterone synthase gene opens up the possibility for gene therapy.
The diagnosis of PA allows appropriate management with resultant blood pressure control in many hypertensive subjects who otherwise have resistant hypertension despite multiple drug therapy.
aDepartment of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff, CF14 4XN, cHypertension Research Centre, Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, United Kingdom. bDivision of Hypertension and Endocrinology/Metabolism, Mayo Clinic, Rochester, Minnesota, USA.
Received 7 August 2000
Revised 6 November 2000
Accepted 7 November 2000
Correspondence and requests for reprints to Dr Pitt O. Lim, Department of Cardiology, Wales Heart Research Institute University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, United Kingdom. Tel: +44 29 2074 7747 ext. 6060; Fax: +44 29 2074 3500; E-mail: email@example.com