EDITORIAL

The complex link between brain and heart in cardiac syndrome X

G A Lanza, F Crea

Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma, Italy

Correspondence to:
Correspondence to:
Professor Filippo Crea, Istituto di Cardiologia, Università Cattolica del Sacro Cuore, L.go A. Gemelli, 8 00168 Roma, Italy;
f.crea@tiscalinet.it

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There are new insights into the neural mechanisms responsible for enhanced cardiac pain perception in syndrome X

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Keywords: cardiac syndrome X; chest pain; pain perception

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

In cardiac syndrome X, the presence of ischaemic-like ST segment changes during chest pain, in the absence of epicardial coronary stenoses, suggests that myocardial ischaemia caused by coronary microvascular dysfunction is responsible for angina.¹ This view is supported by the documentation of abnormalities in myocardial perfusion on radionuclide studies^2,3 and abnormal coronary blood flow response to vasoactive stimuli.^4–7 Furthermore, several abnormalities able to cause microvascular dysfunction have been reported, including increased adrenergic function,⁸ increased stress induced coronary sinus release of endothelin-1,⁹ and increased activity of sodium–hydrogen countertransport.¹⁰ Yet several studies failed to show myocardial lactate production and left ventricular dysfunction^11–14 during angina and ST segment depression, thus casting some doubts on the ischaemic origin of chest pain and ECG changes.¹⁵

In 1988, Shapiro and colleagues reported the observation that syndrome X patients refer chest pain during intra-atrial saline injection, suggesting that an abnormally increased perception of pain during usually painless . . . [Full text of this article]

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