Why the study?
Does oral glucose loading improve central hemodynamics in patients with known or suspected coronary artery disease, and is this response altered by diabetes status?
Does oral glucose loading improve central hemodynamics in patients with known or suspected coronary artery disease, and is this response altered by diabetes status?
Oral glucose loading acutely decreases central systolic blood pressure and arterial stiffness, but this beneficial hemodynamic response is blunted in patients with diabetes mellitus.
Glucose loading may differentially affect central BP by glycemic status; leaves open whether this alters postprandial risk assessment in DM.
BACKGROUND: Recent studies have shown that arterial stiffness is reduced after meal intake. We evaluated the acute response of central hemodynamics to glucose loading and the variation in their responses among normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and diabetes mellitus (DM). METHODS: The study enrolled 85 patients with known or suspected coronary artery disease who underwent a 75-g oral glucose tolerance test. Central hemodynamic measurements were assessed using radial applanation tonometry at fasting, 60, and 120 minutes after glucose loading. RESULTS: Glucose loading decreased the augmentation index normalized to a heart rate of 75 bpm (AIx@75) (81.6±13.9 to 74.5±14.1%, P < 0.01) and central systolic blood pressure (SBP) (115±22 to 109±21mm Hg, P < 0.01) at 120 minutes without a significant change in brachial SBP (126±25 to 125±25mm Hg, P = 0.93). Glucose loading decreased central SBP in NGT and IGT groups but did not affect the DM group. Change in AIx@75 at 120 minutes after glucose loading was blunted in IGT and DM groups compared with the NGT group (-5.7±4.4 vs. -3.6±4.1 vs. -9.3±6.2%, P < 0.01). Multivariate logistic regression analysis identified DM as an independent factor associated with the presence of blunted response of AIx to glucose loading. CONCLUSIONS: Oral glucose loading decreased central SBP and AIx@75 without a significant change in brachial SBP, and these central hemodynamic responses were blunted in patients with DM.
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Higaki et al. (2015) studied this question.
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