¹Dept Clinical and Biological Sciences, University of Insubria, Varese, Italy

Abstract

Using digitized M-mode echocardiograms and 75-mg oral glucose tolerance test (OGTT), we evaluated the possible influence of post-prandial glycemia on left ventricular (LV) morphology and function in never-treated, non-obese, non-diabetic hypertensives. We enrolled 89 subjects (49 men, age 4511 years) with never-treated hypertension (24h BP > 135 and/or 85 mmHg), body mass index < 30 Kg/m2, glycemia at fast < 110 mg/dl and at 120 min during OGTT < 140 mg/dl. We measured glucose and insulin at fast, 30,60,90 and 120 min during OGTT, and metabolic clearance rate of glucose,an index of insulin sensitivity. With regard to the LV we evaluated: LV end-diastolic diameter, septal and posterior wall thickness, LV mass index, peak shortening and peak lengthening rate of LV diameter, peak thinning rate of LV posterior wall. Out of the 89 subjects, 31 had LV hypertrophy (LVMi > 134 g/m2 in men, > 110 g/m2 in women); LV systolic function was normal (peak shortening rate of LV diameter > 1.9 sec-1) in all the patients; 25 patients had preclinical LV diastolic dysfunction (peak lengthening rate of LV diameter < 3.6 sec-1 and/or peak thinning rate of LV posterior wall < 8.4 cm/sec). The metabolic parameters did not correlate with LV morphologic characteristics, nor with LV systolic function. With regard to diastolic function, peak thinning rate of LV posterior wall was inversely related to glycemia at 120 min (r = -0,20, p<0.05) and to glucose MCR (r=-0.25, p<0.01). From stepwise multiple regression analysis the main independent determinants of peak thinning rate of LV posterior wall (multiple R = 0.31, p=0.0092) were glucose MCR (beta = 0.23, p=0.02) and LVMi (beta = - 0.20, p=0.04), whereas post-prandial glycemia did not enter the equation.

In conclusion, in never-treated, non-obese, non-diabetic essential hypertensives, post-prandial glycemia is not related to LV remodeling. With regard to LV diastolic function, the influence of post-prandial glycemia is outweighted by insulin sensitivity, that appears to be an independent determinant of LV diastolic function.