Coronary Care for Myocardial Infarction in Diabetics

Soler, Norman G.; Bennett, M.A.; Lamb, Patricia W.; Pentecost, B L; Fitzgerald, M. G.; Malins, J. M.

doi:10.1016/s0140-6736(74)92785-8

Cited by 129 publications

(59 citation statements)

References 10 publications

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“…Over the last 3 decades, epidemiologic data concerning the cardiac effects of SUs have been changing gradually. Previous studies indicated that "relatively old generation" SUs seemed to be detrimental to the heart, [12][13][14] however, recent studies suggest that "new generation" SUs may be neutral in this respect. [15][16][17][18] Overall, it remains to be established whether, and if so, which SUs increase the risk of cardiovascular complications in patients with type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Mitiglinide, a Novel Oral Hypoglycemic Agent, Preserves the Cardioprotective Effect of Ischemic Preconditioning in Isolated Perfused Rat Hearts

et al. 2007

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SUMMARYDiabetic patients often have manifestation of coronary heart disease. As a consequence, therapeutic strategies for diabetes should pay more attention to hypoglycemic agents which do not have adverse effects on myocardium. Mitiglinide is considered to have little or no impact on the cardioprotective effect of ischemic preconditioning (IP) because of its high selectivity for blocking sulfonylurea receptor1 (SUR1). However, glibenclamide, a nonselective SUR blocker, attenuates this beneficial effect.In the present study, we tested the hypothesis that mitiglinide preserves the protective action of IP evaluated by ischemia/reperfusion ventricular tachyarrhythmia (rVT) in isolated perfused rat hearts. After initial perfusion, the hearts were assigned to one of the following groups: 1) non-IP with control perfusion buffer (non-IP group); 2) IP with control perfusion buffer (IP-C group); 3) IP with perfusion buffer containing glibenclamide (IP-G group); and 4) IP with perfusion buffer containing mitiglinide (IP-M group). The protocol for the non-IP group consisted of 21 minutes of aerobic perfusion before 10 minutes of ischemia. In the other 3 groups (IP groups), there were 3 cycles of 2-minute ischemia followed by 5 minutes of reperfusion before 10 minutes of ischemia. The IP-C group had a significantly shorter rVT duration than the non-IP group (4.4 ± 1.8 minutes versus 14.3 ± 2.5 minutes; P < 0.05). rVT duration was the shortest in the IP-M group (3.9 ± 1.0 minutes), but among the longest in the IP-G group (14.0 ± 2.6 minutes).In conclusion, mitiglinide preserved the cardioprotective effect of IP, however, glibenclamide abolished this beneficial effect. Therefore, mitiglinide may offer a long-term benefit for myocardial ischemia in diabetic patients. (Int Heart J 2007; 48: 337-345)

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Section: Discussionmentioning

confidence: 99%

Mitiglinide, a Novel Oral Hypoglycemic Agent, Preserves the Cardioprotective Effect of Ischemic Preconditioning in Isolated Perfused Rat Hearts

et al. 2007

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“…These findings may explain the high incidence of congestive cardiac failure that occurs in diabetics 23 and also the fact that diabetics have a higher mortality rate from acute myocardial infarction than nondiabetics. 24 The Framingham study found that diabetic men aged 45-74 years have more than twice the expected frequency of congestive cardiac failure, and that diabetic women have a fivefold increase in risk. 23 The excess risks were still present when the history of CHD, rheumatic heart disease, blood pressure, weight, and cholesterol were taken into consideration.…”

Section: Nonatherosclerotic Heart Disease In Diabetesmentioning

confidence: 99%

Blood glucose and atherosclerosis.

Stout¹

1981

Arteriosclerosis

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“…In diabetes there is a chronic reduction in cardiac glycolytic capacity (3,4). Diabetics are prone to heart failure (5) and they suffer more damage following an infarction (6). It has been proposed that reduced cardiac glycolysis contributes to the heart failure and cardiac damage often suffered by diabetics (7,8).…”

mentioning

confidence: 99%

Cardiac Expression of Kinase-deficient 6-Phosphofructo-2-kinase/Fructose-2,6-bisphosphatase Inhibits Glycolysis, Promotes Hypertrophy, Impairs Myocyte Function, and Reduces Insulin Sensitivity

Donthi

et al. 2004

Journal of Biological Chemistry

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Glycolysis is important to cardiac metabolism and reduced glycolysis may contribute to diabetic cardiomyopathy. To understand its role independent of diabetes or hypoxic injury, we modulated glycolysis by cardiacspecific overexpression of kinase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (kd-PFK-2). PFK-2 controls the level of fructose 2,6-bisphosphate (Fru-2,6-P 2 ), an important regulator of glycolysis. Transgenic mice had over 2-fold reduced levels of Fru-2,6-P 2 . Heart weight/body weight ratio indicated mild hypertrophy. Sirius red staining for collagen was significantly increased. We observed a 2-fold elevation in glucose 6-phosphate and fructose 6-phosphate levels, whereas fructose 1,6-bisphosphate was reduced 2-fold. Pathways branching off of glycolysis above phosphofructokinase were activated as indicated by over 2-fold elevated UDP-N-acetylglucosamine and glycogen. The kd-PFK-2 transgene significantly inhibited glycolysis in perfused hearts. Insulin stimulation of metabolism and Akt phosphorylation were sharply reduced. In addition, contractility of isolated cardiomyocytes was impaired during basal and hypoxic incubations. The present study shows that cardiac overexpression of kinase-deficient PFK-2 reduces cardiac glycolysis that produced negative consequences to the heart including hypertrophy, fibrosis, and reduced cardiomyocyte function. In addition, metabolic and signaling responses to insulin were significantly decreased.

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Coronary Care for Myocardial Infarction in Diabetics

Cited by 129 publications

References 10 publications

Mitiglinide, a Novel Oral Hypoglycemic Agent, Preserves the Cardioprotective Effect of Ischemic Preconditioning in Isolated Perfused Rat Hearts

Mitiglinide, a Novel Oral Hypoglycemic Agent, Preserves the Cardioprotective Effect of Ischemic Preconditioning in Isolated Perfused Rat Hearts

Blood glucose and atherosclerosis.

Cardiac Expression of Kinase-deficient 6-Phosphofructo-2-kinase/Fructose-2,6-bisphosphatase Inhibits Glycolysis, Promotes Hypertrophy, Impairs Myocyte Function, and Reduces Insulin Sensitivity

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