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Cardiovascular Research 2001 52(2):174-177; doi:10.1016/S0008-6363(01)00457-6
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

The pathophysiology of cardiac syndrome X — a tale of paradigm shifts

Stuart D Rosen*

Department of Heart Function, National Heart and Lung Institute, Imperial College School of Science, Technology and Medicine, London, UK

* Correspondence address: Department of Cardiology, Ealing Hospital, Uxbridge Road, Middlesex UB1 3HW, UK. Tel.: +44-20-8967-5359; fax: +44-20-8967-5007 stuart.rosen@ic.ac.uk

Received 24 August 2001; accepted 30 August 2001

The first 150 words of the full text of this article appear below.

See article by Gulli et al. [18] (pages 208–216) in this issue.


   1. Introduction
 
The aetiology of cardiac syndrome X — the problem of the patient with chest pain of anginal quality, ischaemic-like changes on the stress electrocardiogram (ECG) but a normal coronary arteriogram — continues to fascinate many engaged in cardiovascular research. It is a field of endeavour which has gone through a number of ‘paradigm shifts’ during the 28 years since the term was coined by Harvey Kemp [1], commenting on the ‘Group X’ subset of patients in Arbogast and Bourassa’s seminal paper on patients with angina and ‘normal or near normal’ coronary angiograms [2].

The first and most obvious mechanism of chest pain to be indicated was that of true myocardial ischaemia, but since the epicardial vessels were normal by definition, the microcirculation seemed the likely site of impairment of flow (or flow reserve) [3]. In . . . [Full Text of this Article]


   2. The sympathetic nervous system and the aetiology of cardiac syndrome X
 

   3. Studies of heart rate variability in cardiac syndrome X
 

   4. Pain perception and sympathetic activation in patients with syndrome X
 

   5. Conclusion
 

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