& u through the third year. That is, there is no latent period as in the type 1 diabetic patients. Coronary heart disease mortality increased progressively with duration of diabetes. These types of curves suggested that accelerated atherosclerosis was already present at the time of diagnosis of type 2 diabetes and that it progresses with duration of the diabetes.
That concept had been suggested earlier by the prospective data from the Whitehall study of approximately 18,000 civil servant men that showed almost a twofold increase in CHD mortality in nondiabetic men in the upper 5% of the 2-h blood glucose value (>5.3 mmol/L or 95 mg/dL) after a 50-g oral glucose load (33). The Paris Prospective Study followed 7164 working men for a mean of 11.2 years and observed annual CHD mortality rates of 1.4, 2.7, and 3.2 per 1000 persons in normoglycemic persons, impaired glucose tolerance individuals, and new and known type 2 diabetic patients, respectively (34). Many subsequent studies have confirmed that individuals with IGT have approximately a 1.5- to 2.0-fold increased risk of death from CVD when compared to normoglycemic individuals. Coutinho et al. have examined in detail the relationship between nondiabetic plasma glucose values and incident cardiovascular events by doing a metaregression analysis of published data from 20 studies of 95,783 individuals followed for a mean of 12.4 years (5). Their analysis indicated that a fasting plasma glucose of 6.1 mmol/L (110 mg/dL) and a 2-h plasma glucose of 7.8 mmol/L (140 mg/dL) were associated with a relative cardiovascular event risk of 1.33 and 1.58, respectively. Thus, there are overwhelming data to support the concept that accelerated atherosclerosis occurs many years prior to the onset of type 2 diabetes. The data can be interpreted to mean that subdiabetic levels of plasma glucose are responsible for the vascular disease or that type 2 diabetes is preceded by some metabolic state that causes both type 2 diabetes and accelerated atherosclerosis.
Many population-based epidemiological studies published in the 1980s had suggested that high fasting or postprandial plasma insulin levels predicted the development of type 2 diabetes. In 1990, Haffner and associates presented data from the ongoing San Antonio Heart Study that indicated that individuals who were going to develop type 2 diabetes had an increase in many of the components of the insulin resistance syndrome years before the onset of their diabetes (35). The prediabetic individuals were older, more generally and centrally obese, had a dyslipidemia that manifested itself as higher plasma triglyceride and a lower -o plasma HDL cholesterol, higher (though still normal) systolic and diastolic blood pressure, and a greater prevalence of hypertension. The mean fasting and 2-h post-glucose-challenge plasma glucoses were approximately 5.6 mmol/L (101 g mg/dL) and 8.3 mmol/L (149 mg/dL) as compared to 5.0 mmol/L (91 mg/dL) <j and 5.3 mmol/L (95 mg/dL) in the normal population. The prediabetic individuals had fasting plasma insulin levels that were 66% higher in the men and 102%
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