Does impaired glucose tolerance predict hypertension? A prospective analysis.

This study evaluates prospectively the relationship between impaired glucose tolerance (IGT) and blood pressure. From a population of 1376 men and women aged 40-59 years, all those with IGT (n = 54) plus 133 age- weight- and sex-matched normoglycaemic control subjects were selected after excluding treated hypertensive patients. Blood pressure, fasting and postload blood glucose and plasma insulin were measured. At 11.5 years after the first visit 76% of the IGT patients and 80% of the control subjects were re-examined. At baseline blood pressure was significantly higher in IGT patients than in control subjects (systolic 135.5 +/- 2.3 vs 127.9 +/- 1.4 mmHg, p < 0.001; and diastolic 88.0 +/- 1.5 vs 84.7 +/- 0.7 mm Hg, p < 0.05) independent of age, gender, weight, antihypertensive medication and insulinaemia. Accordingly, hypertension was more frequent in subjects with IGT (odds ratio 2.1, 95% confidence, interval (CI) 0.9-4.9). Postload insulin was significantly associated with hypertension--both at univariate and multivariate analysis--in normoglycaemic subjects, but not in those with IGT. At follow-up systolic blood pressure increased in both groups; the increase was smaller in patients with IGT (6.0 +/- 2.4 vs 12.3 +/- 1.6 mm Hg p < 0.05). Likewise, the 11.5 years' cumulative incidence of hypertension was not significantly different in subjects with baseline IGT or normoglycaemia; if anything it was lower in the IGT group (odds ratio 0.36, 95% CI 0.1-1.2). In multivariate analysis incidence of hypertension was associated positively with baseline blood pressure (p < 0.0003) and negatively with IGT status p < 0.03), while no significant association was found with insulin. In conclusion, the findings of this study question IGT as a risk factor for hypertension. Furthermore, these data do not indicate a major role for hyperglycaemia and hyperinsulinaemia per se in the aetiology of hypertension and suggest that IGT and hypertension share one or more pathogenetic factor(s) (i.e., insulin resistance, hyperactivity of the sympathetic nervous system, etc.), which induce deterioration of blood pressure control first, and hyperglycaemia later.