Abstract

Ever since Cannon and Epstein (1) coined the term "microvascular angina" to describe syndrome X in 1988, the theory that a significant proportion of patients with syndrome X have microvascular dysfunction that leads to ischemia, ST depression, and chest pain have dominated the field of syndrome X research. This is surprising in view of the fact that the studies looking at the presence of ischemia and microvascular dysfunction are poorly conducted and have inconsistent results. Despite publication bias, there are numerous negative studies demonstrating the lack of ischemia in syndrome X patients when compared to controls. Indeed when Cannon himself did a well conducted study into microvascular dysfunction and found negative results, he concluded that invasive measurements of endothelium-dependent and endothelium-independent agonists is unlikely to be of value in determining the mechanisms of chest pain in patients with syndrome X (2). Microvascular dysfunction occurs in normal people with coronary risk factors but is not usually associated with objective ischemia, ST depression, or chest pain. Therefore, the question at the forefront of syndrome X research is no longer whether there is microvascular dysfunction but rather is the microvascular dysfunction responsible for ischemia, ST depression, and most importantly chest pain?