DOES IMPAIRED GLUCOSE-TOLERANCE PREDICT HYPERTENSION - A PROSPECTIVE ANALYSIS

This study evaluates prospectively the relationship between impaired g lucose tolerance (IGT) and blood pressure. From a population of 1376 m en and women aged 40-59 years, all those with IGT (n = 54) plus 133 ag e- weight- and sex-matched normoglycaemic control subjects were select ed after excluding treated hypertensive patients. Blood pressure, fast ing 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 sign ificantly higher in IGT patients than in control subjects (systolic 13 5.5 +/- 2.3 vs 127.9 +/- 1.4 mm Hg, p < 0.001; and diastolic 88.0 +/- 1.5 vs 84.7 +/- 0.7 mm Hg, p < 0.05) independent of age, gender, weigh t, antihypertensive medication and insulinaemia. Accordingly, hyperten sion was more frequent in subjects with IGT (odds ratio 2.1, 95% confi dence, interval (CI) 0.9-4.9). Postload insulin was significantly asso ciated with hypertension - both at univariate and multivariate analysi s - in normoglycaemic subjects, but not in those with IGT. At follow-u p systolic blood pressure increased in both groups; the increase was s maller in patients with IGT (6.0 +/- 2.4 vs 12.3 +/- 1.6 mm Hg p < 0.0 5). Likewise, the 11.5 years' cumulative incidence of hypertension was not significantly different in subjects with baseline IGT or normogly caemia; 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 ne gatively with IGT status p < 0.03), while no significant association w as found with insulin. In conclusion, the findings of this study quest ion 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 hyperten sion share one or more pathogenetic factor(s) (i.e., insulin resistanc e, hyperactivity of the sympathetic nervous system, etc.), which induc e deterioration of blood pressure control first, and hyperglycaemia la ter.