Attention was drawn to postural orthostatic tachycardia syndrome (POTS) in 1993 by Philip Low's team at Mayo Clinic.1 Postural orthostatic tachycardia syndrome has remained difficult to treat despite almost 2 decades of expanding research and recognition.
The typical patient is a young female, 15–40 years of age, whose symptoms are usually multiple. In combination, the symptoms are very debilitating and those most common are fatigue, orthostatic intolerance, palpitation manifest as sinus tachycardia, oedema and discolouration of the lower limbs, and occasionally syncope.
Two sub-types of POTS have been described. In the first of these, a primary neurological defect is present, possibly triggered by a viral infection. This defect takes the form of a partial autonomic denervation leading to excessive venous pooling in the legs and, sometimes, additional affection of the renal innervation resulting in a reduced plasma renin activity. The second sub-type is considered to have central sympathetic activation, termed the hyperadrenergic type.2,3
Publication information
Sutton R, Salukhe T. Ivabradine in the treatment of orthostatic intolerance. Europace. 2011 Mar;13(3):306-7.