How should we measure the “POT” of POTS, and how much does it matter?
A century and a half ago, a number of Civil War soldiers were noted to develop disabling fatigue with severe orthostatic intolerance after contracting dysentery. They were sometimes labeled as having “Soldier’s Heart” or “Da Costa Syndrome” [2]. Decades later, through careful clinical examination and using a then-new electrocardiograph, Sir Thomas Lewis determined that these soldiers had normal hearts. Lewis labeled the condition “effort syndrome,” and determined that “graduated exercise” was the key to recovery and rehabilitation [1].
In 1972, Streeten and colleagues reported a series of five patients with clinical symptoms and findings similar to those of Lewis’ effort syndrome. Streeten labeled this condition “hyperbradykininism” [3]. The term “postural tachycardia syndrome” was coined for one similar adult woman by Rosen and Cryer in 1982; she improved with increased salt intake [4]. Schondorf and Low labeled the condition “idiopathic postural orthostatic tachycardia syndrome” in a series of adults, suggesting the cause was “a mild form of an acute autonomic neuropathy” [5]. Postural orthostatic tachycardia syndrome (POTS) was later reported in an adolescent in 1999 [6].
Since then, POTS has been identified and characterized in adults and adolescents [7]. The diagnosis depends on a combination of chronic daily symptoms of orthostatic intolerance and excessive postural tachycardia (≥ 40 beats per minute (bpm) change in adolescents, ≥ 30 in adults) [8].
Perhaps prophetically, Lewis’ quotation cited above remains germane. Our current diagnostic labels of what he called “effort syndrome,” are, indeed, potentially nothing more than “temporary conceptions.” Two major issues remain in defining the diagnosis of what we now label as POTS: 1) how should “excessive postural tachycardia” be measured, and, 2) what difference does postural tachycardia make?
https://link.springer.com/article/10.1007/s10286-023-00977-3
A century and a half ago, a number of Civil War soldiers were noted to develop disabling fatigue with severe orthostatic intolerance after contracting dysentery. They were sometimes labeled as having “Soldier’s Heart” or “Da Costa Syndrome” [2]. Decades later, through careful clinical examination and using a then-new electrocardiograph, Sir Thomas Lewis determined that these soldiers had normal hearts. Lewis labeled the condition “effort syndrome,” and determined that “graduated exercise” was the key to recovery and rehabilitation [1].
In 1972, Streeten and colleagues reported a series of five patients with clinical symptoms and findings similar to those of Lewis’ effort syndrome. Streeten labeled this condition “hyperbradykininism” [3]. The term “postural tachycardia syndrome” was coined for one similar adult woman by Rosen and Cryer in 1982; she improved with increased salt intake [4]. Schondorf and Low labeled the condition “idiopathic postural orthostatic tachycardia syndrome” in a series of adults, suggesting the cause was “a mild form of an acute autonomic neuropathy” [5]. Postural orthostatic tachycardia syndrome (POTS) was later reported in an adolescent in 1999 [6].
Since then, POTS has been identified and characterized in adults and adolescents [7]. The diagnosis depends on a combination of chronic daily symptoms of orthostatic intolerance and excessive postural tachycardia (≥ 40 beats per minute (bpm) change in adolescents, ≥ 30 in adults) [8].
Perhaps prophetically, Lewis’ quotation cited above remains germane. Our current diagnostic labels of what he called “effort syndrome,” are, indeed, potentially nothing more than “temporary conceptions.” Two major issues remain in defining the diagnosis of what we now label as POTS: 1) how should “excessive postural tachycardia” be measured, and, 2) what difference does postural tachycardia make?
https://link.springer.com/article/10.1007/s10286-023-00977-3