ABSTRACT
In 1988, during the Banting Award lecture of the American Diabetes Association, Gerald Reaven made a landmark contribution not only to the eld of endocrinology and metabolism but also to cardiovascular medicine when he introduced the notion of syndrome X.1 Reaven made the point that there is a signicant proportion of sedentary individuals who are characterized by insulin resistance and who are also at increased risk of cardiovascular disease (CVD) even if some of them never develop type 2 diabetes (T2DM). Thus, he proposed that beyond the well-recognized increased risk of T2DM associated with this condition, insulin resistance was also central to the development of abnormalities increasing the risk of CVD. As initial features of his metabolic syndrome X, Reaven made the link between insulin resistance and hypertriglyceridemia, low levels of high-density lipoprotein (HDL)-cholesterol, fasting hyperinsulinemia, and hypertension. Through a series of studies conducted over several decades he was able to document and expand the list of metabolic abnormalities associated with syndrome X, and they are presented in Table 50.1.2,3
After the introduction of Reaven’s syndrome X, the point was made that there was another syndrome X documented in cardiology (angina with normal coronary arteries),4-6 which led many groups to propose the term “insulin resistance syndrome” to avoid any confusion.7,8 However, to properly
acknowledge the seminal contribution of the father of this concept, we have suggested that this condition should be referred to as “Reaven’s syndrome.”9
