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There are new insights into the neural mechanisms responsible for enhanced cardiac pain perception in syndrome X
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 studies2,3 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 dysfunction11–14 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 cardiac stimuli could be the mechanism responsible for chest pain in cardiac syndrome X.16 Several studies consistently confirmed this finding,17–20 lending further support to the hypothesis that a reduced cardiac pain threshold might be the predominant cause of the syndrome. These observations generated some new questions:
Is enhanced perception of painful stimuli confined to the heart or is rather generalised?
Where does the abnormality responsible for enhanced …