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Diabetes Care 29:95-100, 2006
DOI: 10.2337/diacare.29.01.06.dc05-0955
© 2006 by the American Diabetes Association
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Pathophysiology/Complications
Original Article

Effects of Different Insulin Regimes on Postprandial Myocardial Perfusion Defects in Type 2 Diabetic Patients

Roldano Scognamiglio, MD, Christian Negut, MD, Saula Vigili de Kreutzenberg, MD, Antonio Tiengo, MD and Angelo Avogaro, MD

Metabolic Cardiology, Division of Metabolic Diseases, Department of Clinical and Experimental Medicine, University of Padova Medical School, Padua, Italy

Address correspondence and reprint requests to Roldano Scognamiglio, MD, Cardiologia Metabolica, Divisione di Malattie del Metabolismo, Policlinico Universitario, via Giustiniani 2, 35128 Padova, Italy. E-mail address: r.scognamiglio{at}unipd.it

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 (ß), myocardial blood volume (MBV), and myocardial blood flow (MBF) did not differ between control and type 2 diabetic subjects. Postprandial ß (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, ß 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: ß 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 ß (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.

Abbreviations: AUC, area under the curve • CVD, cardiovascular disesase • FFA, free fatty acid • MBF, myocardial blood flow • MBV, myocardial blood volume • MCE, myocardial contrast echocardiography


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