Why the study?
Does an insulin analog improve postprandial myocardial perfusion abnormalities compared to regular insulin or placebo in type 2 diabetic patients?
Does an insulin analog improve postprandial myocardial perfusion abnormalities compared to regular insulin or placebo in type 2 diabetic patients?
In patients with type 2 diabetes, an insulin analog partially reversed postprandial myocardial perfusion abnormalities compared to regular insulin, likely by improving glucose control.
Answers are grounded in this paper and cite their sources.
Insulin analogs may improve postprandial myocardial perfusion in T2D; extends RCT evidence on insulin formulation effects on coronary flow.
OBJECTIVE: Postprandial glycemia is an independent risk factor for cardiovascular disease that is more powerful than fasting glycemia and determines myocardial perfusion defects in type 2 diabetes. We examined the efficacy of two different insulin regimes (regular insulin and insulin analog) in controlling postprandial hyperglycemia and in preventing myocardial perfusion abnormalities. RESEARCH DESIGN AND METHODS: A total of 20 consecutive type 2 diabetic patients and 20 control subjects were enrolled in this randomized, three-way, cross-over, placebo-controlled study. Myocardial perfusion was assessed by myocardial contrast echocardiography (MCE) in fasting and postprandial (120 min) state. RESULTS: Insulin analog was associated with lower, but not statistically significant, postprandial glycemia than regular insulin (glucose increase: 116 +/- 8 vs. 136 +/- 5%, P = NS). However, the area under the curve following insulin analog was significantly lower than regular insulin (18,354 +/- 702 vs. 20,757 +/- 738 mg per 120 min, P = 0.032). Fasting myocardial flow velocity (beta), myocardial blood volume (MBV), and myocardial blood flow (MBF) did not differ between control and type 2 diabetic subjects. Postprandial beta (0.67 +/- 0.24 vs. 0.92 +/- 0.25, P < 0.01), MBV (8.4 +/- 2 vs. 10.9 +/- 1.2, P < 0.01), and MBF (5.6 +/- 2 vs. 9.9 +/- 2.8, P < 0.01) increased significantly in control subjects. In type 2 diabetes, during placebo in the postprandial state, beta increased (0.65 +/- 0.27 vs. 0.89 +/- 0.24, P < 0.01), while MBV (8.34 +/- 1.2 vs. 4.3 +/- 1.3, P < 0.01) and MBF (5.4 +/- 1.5 vs. 3.4 +/- 0.9, P < 0.01) decreased. Similar changes in MCE variables were observed after regular insulin: beta increased (0.65 +/- 0.22 vs. 0.92 +/- 0.12, P < 0.01) and MBV (8.2 +/- 2 vs. 5.2 +/- 1.16, P < 0.01) and MBF (5.4 +/- 1.9 vs. 4.2 +/- 0.86, P < 0.01) were reduced. After insulin analog, postprandial beta (0.66 +/- 0.18 vs. 0.9 +/- 0.18, P < 0.01), MBV (8.2 +/- 1.6 vs. 9.6 +/- 1.2, P < 0.01), and MBF (5.4 +/- 2 vs. 7.2 +/- 1.9, P < 0.01) increased. Values of postprandial MBV and MBF were higher after insulin analog than regular insulin treatment. CONCLUSIONS: Insulin analog partially reversed myocardial perfusion abnormalities observed in postprandial state by improving glucose control.
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Scognamiglio et al. (2006) studied this question.
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