In 1973, Kemp [1], in an editorial, introduced the term ‘syndrome X’ to indicate the uncertain etiology of chest pain in patients who had a positive exercise ECG suggestive of myocardial ischemia but on coronary arteriograms had normal coronary arteries. In 1988, Reaven [2], in his Banting Lecture, used the same term ‘syndrome X’ to describe a metabolic syndrome characterized by glucose intolerance, insulin resistance, dyslipidemia, hypertension and coronary artery disease. Obviously Reaven [2] did not know about the existence of the term ‘syndrome X’ coined by Kemp [1] 15 years earlier. To avoid confusion, subsequent investigators added the qualifier ‘metabolic’ to Reaven's syndrome X [2] in order to distinguish it from the ‘cardiac’ syndrome X described by Kemp [1]. Until very recently, these two syndrome X's have always been considered as entirely separate entities which by accident share the same terminology. However, in recent years, more and more studies seem to indicate a potential link between the cardiac and metabolic syndrome X. In 1991 Dean and Jones [3] reported 11 patients with angina attributed to microvascular angina, another term for cardiac syndrome X, and hyperinsulinemia; they postulated that increased concentration of insulin may lead to coronary microvascular dysfunction, either endothelial or vascular. In 1998, Gaspardone et al. [4] further suggested a potential link between cardiac and metabolic syndrome X. They demonstrated that both enhanced activity of the sodium– lithium countertransport and stimulated hyperinsulinemia are present in the vast majority of patients with cardiac syndrome X. As enhanced activity of the sodium–lithium countertransport has the potential to cause both glucose intolerance and smooth muscle hyperactivity, they concluded that it might represent a common cause of the metabolic and vascular alterations frequently found in syndrome X [4].