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Divorce of mitral prolapse and neurocirculatory asthenia
01.01.1988, Amer J Med 84: 183 (& M. Mäntysaari, T. Peltonen)
(ei kuvausta)

Divorce of mitral valve prolapse and neurocirculatory asthenia.

To the Editor:
The syndrome of symptoms referring to the cardiovascular system without findings of organic disease has been dealt with under many titles in the medical literature. Hartshorne and DaCosta started the series of studies in American literature during the Civil War, when the condition was called irritable heart and later DaCosta's syndrome. During World War 1, British and American lnvestigators introduced new names like neurocirculatory asthenia, soldier's heart, effort syndrome, and autonomic imbalance [1,2]. The new name in the 1940s was functional cardiovascular disease [2]. In the 1970s, mitral valve prolapse was considered as a possible organic cause of the syndrome, which we herein called neurocirculatory asthenia, and the term mitral valve prolapse syndrome was Introduced [3]. Finally, during this decade the importance of anxiety neurosis in the pathogenesis of the symptoms has received new Interest when the definition of panic anxiety has come close to the definition of neurocirculatory asthenia [4].

In their article, Weissman et al (Am J Med 1987; 82: 880-888) studied hemodynamic reactions to the Valsalva maneuver, deep breathing, and orthostatic testing as well as 24-hour urinary excretion of epinephrine and norepinephrine in control subjects, patients with mitral valve prolapse (MVP), patients with panic attacks, and patients with both MVP and panic attacks. The groups were age- and cardiac symptom-matched so that all groups had a similar frequency of atypical chest pain, palpitations, and dyspnea (symptoms during attacks in patients with panic attacks were not included in this comparison).

The clearest difference between the groups was seen in the orthostatic test, in which patients with panic attacks (with or without MVP) had higher heart rate and heart rate mean blood pressure product than patients without panic attacks (with or without MVP). The differences between control subjects and patients with MVP and between patients with panic attacks and patients with panic attacks plus MVP were very small. The authors concluded that circulatory regulation in patients with MVP is in some way different from that in patients with panic attacks. However, in the Comments section, the investigators did not pay any attention to the similarity between circulatory reactions in patients with MVP (without panic attacks) and controi subjects. Our impression of the control subjects, who thus had atypical chest pain, palpitations, and dyspnea without siqns of organic disease, is that they could have been patients with classic neurocirculatory asthenia. lf this suspicion of ours is correct, then one more conciusion could be made from this study: mitral valve prolapse has no importance in the etiology of neurocirculatory asthenia.

MATTI MÄNTYSAARI, M.D.
ESKO LÄNSIMIES, M.D.
Kuopio University Hospitai
SF-70210 Kuopio, Finland

TUOMAS PELTONEN, M.D.
University of Turku
Kiinamyllynkatu 10 SF-20520 Turku, Finland

1. Wooley CF: From irritable heart to mitral valve prolapse: World War 1 -the U.S. experience and the origin of neurocirculatory asthenia. Am J Cardiol 1987; 59: 1183-1186.
2. Friedman M: Functional cardiovascular disease. Baltimore: Williams and Wilkins, 1947.
3. Wooley CF: Where are the diseases of yesteryear? DaCosta's syndrome, soldier's heart, the effort syndrome, neurocirculatory asthenia and the mitral valve prolapse syndrome. Circulation 1976: 53: 749-751.
4. Brown JT, Mulrow CD, Stoudemire GA: The anxiety disorders. Ann Intern Med 1984; 100: 558-564. Submitted August 6, 1987, and accepted October 28, 1987 The


Reply:

Mäntysaari et al raise en interesting point concerning the relation between mitral valve prolapse (MVP) and neurocirculatory asthenia. Although we were aware of Wooley's [1] suggestion that these conditions were linked, our research protocol was designed at its inception in 1979 to assess study participants for panic and anxiety diagnoses. Using the family study method, we have shown that there was no difference between 81 adults with MVP and 232 contral subjects in the prevalence of panic disorder, high trait anxiety, atypical chest pain, or dyspnea [2]. In another study, we found diagnoses of MVP that had been based on such symptoms to be disproportionately likely to be faise positives [3]. This lack of association between MVP and several components of the neurocirculatory asthenia symptom complex leads us to believe, in accord with the suggestion of Mäntysaari et al, that mitral valve prolapse plays no role in the etiology of neurocirculatory asthenia.

RICHARD B. DEVEREUX, M.D.
NEIL J. WEISSMAN, B.S.
RANDI KRAMER-FOX, M.S. M.
KATHERINE SHEAR, M.D.
New York Hospital-Cornell Medical Center
New York, New York 10021

1. Wooley CF: VVhere are the diseases of yesteryear? DaCosta's syndrome, soldier's heart, the effort syndrome, neurocirculatory asthenia and the mitral valve prolapse syndrome. Circulation 1976; 53: 749-751.
2. Devereux RB. Kramer-Fox R, Brown WT, et al: Relation between clinical features of the "mitral prolapse syndrome" and echocardiographically documented mitral valve prolapse. J Am Coll Cardiol 1986; 8:763-772.
3. Devereux RB, Kramer-Fox R, Shear MK, Spitzer MC, KIIgfield P, Brown WT: Clinical over-diagnosis of mitral prolapse: relation to panic attacks and midsystollc murmurs (abstr). Clin Res 1987;35: 274A.
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