Is altered central processing of afferent signals the cause of chest pain in syndromex?

S. D. Rosen, E. Paulesu, R. S J Frackowiak, P. G. Camici

Research output: Contribution to journalArticlepeer-review


The aetiology of syndrome X (SX, anginal pain and ischaemic-like changes in the stress ECG despite a normal coronary arteriogram) remains to be elucidated. There is increasing doubt over the myocardial ischemia hypothesis of chest pain in SX, whereas abnormalities of pain perception have been shown. To investigate the latter further, we have used positron emission tomography with H215O to measure regional cerebral blood flow (rCBF) changes as an index of neuronal activation: a) during chest pain in SX patients and b) during angina pectoris in coronary artery disease (CAD) patients. Nine SX patients [7 female, age 56 (11) mean (SD)] and 9 CAD patients [7 male, age 61(7) years] were studied. No patient had diabetes or other systemic disease. With stress, normal ventricular function was demonstrated in the SX patients despite an ischaemic-like ECG, but there were reversible wall motion abnormalities in the CAD patients. Intravenous dobutamine (D) was used to induce the chest pain. rCBF was measured during the following scan sequence: 1) rest; 2) placebo; 3) rest; 4) low dose D; 5) high dose D (provoking chest pain); and 6) rest. PET images were transformed into a standard stereotactic space and comparisons made across conditions by Statistical Parametric Mapping. Chest pain ocurred in response to low dose D in 4/9 SX but in no CAD patients (p=NS). During scan 5 (high dose D) chest pain was reported in all cases, being scored comparably by both groups (6.3 in CAD vs 7.6 in SX; p=NS). During scan 5, ischaemic-like ECG changes were noted in 9/9 CAD and 8/9 SX. The maximal D dose was equivalent for both groups. During chest pain, SX patients showed significantly greater increases in rCBF in the midbrain, right thalamus and right insular cortex and bilaterally in the frontal and prefrontal cortices. The central neural areas activated are similar in both SX and CAD, suggesting that in SX the afferent pain signals do originate from the heart. However the degree and extent of activation is disproportionately greater in SX and occurs in the absence of correlates of myocardial ischaemia such as ventricular wall motion abnormalites.

Original languageEnglish
Issue numberSUPPL. 1
Publication statusPublished - May 1997

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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