Objectives To investigate the impact of high level of postprandial plasma glucose on heart rate turbulence and cardiac structure and function in elderly essential hypertensive patients.
Methods Oral glucose tolerance test were performed in all 257 elderly essential hypertensives, aged from 60 to 79 years (mean: 66.8 ± 9.7 years). Then, according to the results of the test, participants were divided into three groups, namely, control group, high postprandial plasma glucose group and diabetes group. All participants were conducted physical examination, 24h ambulatory electrocardiogram, echocardiogram and blood test.
Results Compared to control group, turbulence onset (TO), total premature ventricular contraction of 24h, the end systolic diameters of left ventricle (LVESD), fractional shortening of the left ventricular minor semi axis (LVFS), interventricular septum thickness (IVST) and Tei index were markedly elevated, and turbulence slope (TS), the standard deviations of all normal RR intervals (SDNN), left ventricular ejection fraction (LVEF), and ratio of E/A were significantly decreased in high postprandial plasma glucose group and diabetes group (P < 0.01). TO, LVESD, left ventricular posterior wall thickness (LVPWT), and Tei index were significantly higher, and TS, LVEF, and ratio of E/A were significantly lower in diabetes group compared with high postprandial plasma glucose group (P < 0.01). Results of correlation analysis and multivariate linear regression analysis shown that level of postprandial plasma glucose markedly positively related to TO, total premature ventricular contraction of 24h, LVESD, IVST, LVPWT, A peak, and Tei index (r = 0.4217, 0.3052, 0.4175, 0.3862, 0.2847, 0.2415, and 0.4402, P < 0.01, respectively), and negatively related to TS, SDNN, LVFS, LVET, E peak and ratio of E/A (r = -0.4255, -0.3579, -0.4441, -0.3258, -0.2843 and -0.4033, P < 0.01, respectively).
Conclusions High level of postprandial plasma glucose may be an important risk factor for reducing heart rate turbulence, promote cardiac structure remolding, and inducing cardiac dysfunction.