Advances in understanding the mechanisms of angina pectoris in cardiac syndrome X

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This editorial refers to ‘Abnormal cortical pain processing in patients with cardiac syndrome X’† by M. Valeriani et al. , on page 975 Angina pectoris was initially described by Heberden in 1772 and is considered to be the hallmark of ischaemic heart disease. However, with the advent of selective coronary angiography, clinicians were confronted with a conundrum as some patients with ‘unmistakable’ angina had angiographically normal epicardial coronary arteries. This apparent disparity between the clinical symptoms and the angiographic findings appeared to be resolved when it was demonstrated that affected patients had electrocardiographic and metabolic evidence of ischaemia. Thus, it was hypothesized that the angina experienced by these patients was due to myocardial ischaemia secondary to coronary microvascular dysfunction. This new disorder was referred to as cardiac syndrome X and is typically characterized by exertional angina, electrocardiographic evidence of ischaemia on stress testing, angiographically smooth epicardial coronary arteries, and no other recognized cause for the chest pain. Multiple studies have subsequently demonstrated the presence of microvascular dysfunction in these patients. Controversy arose when several well-controlled studies failed to identify metabolic evidence of ischaemia in these patients despite reproducing the chest pain. This led to divided opinion among the researchers, with views ranging from an ‘ischaemic hypothesis’, where technical limitations account for the inability to detect the ischaemia, to a ‘non-ischaemic hypothesis’ where alternative mechanisms are proposed to be responsible for the chest pain. Recent technical advances have assisted in demonstrating surrogate markers of ischaemia in these patients, including subendocardial perfusion defects on magnetic resonance imaging,1 production of oxidative stress markers during pacing-induced angina,2 and a … *Corresponding author. Tel: +61 8 8222 7539; fax: +61 8 8222 7201. E-mail address : john.beltrame{at}adelaide.edu.au