1871
Jacob M. Da Costa’s published “On Irritable Heart: A Clinical Study of a Form of Functional Cardiac Disorder and its Consequences” in Am. J. Med. Sciences. Da Costa’s syndrome = irritable heart = neurocirculatory asthenia = soldier’s heart = effort syndrome = cardiac neurosis (Paul). It was investigated in WWI, especially in Britain by group under Thomas Lewis and James Mackenzie. Heart disease first attracted serious attention following British retreat from Mons in August 1914, when soldiers were sent back to England with chest pain. It eventually became third leading cause of discharge from British Army during WWI (Howell, 37). Lewis, in his MRC report on soldier’s heart, advocated the term “effort syndrome” for most cases, since the symptoms merely “exaggerated manifestations of healthy responses to effort” (Howell, 41; Lawrence, 31). Lewis summarized his experience in a monograph of 1919, The Soldier’s Heart and the Effort Syndrome. Among the symptoms, breathlessness and fatigue were universal; palpitation very frequent, and about half of patients had vague left chest distress with or after effort. Lewis believed the dominant etiological factor was “infection of one kind or another” (Paul, quoted at 310), which compromised the global functioning of the heart construed as a failure of cardiac reserve – this was in accord with the physiological perspective of the “new cardiology” of which Mackenzie was architect (Howell, 41-43; Lawrence, 31). Alfred Cohn of Rockefeller University first proposed that the symptom complex was neurotic, a viewpoint more fully elaborated in the work of Paul Wood beginning in 1941. Wood, after wartime experience with the condition, “came down squarely on the side of viewing Da Costa’s syndrome as a manifestation of emotion, more in keeping with the view of Cohn than that of Mackenzie or Lewis, and unlike that of White and Cohen, who considered that the issue was decidedly more complex” (Paul, 312). In 70s and 80s, there was some attempt to place Da Costa’s syndrome and mitral valve prolapse within a single rubric, but it “seems best to keep neurocirculatory asthenia and mitral valve prolapse as separate categories for the time being because they do not have sufficient similarities to justify a single label” (313). Treatment wise, “A program of reassurance, exercise, and physical fitness has been of value” (313).