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1.
J Med Life ; 2(3): 271-8, 2009.
Article in English | MEDLINE | ID: mdl-20112471

ABSTRACT

UNLABELLED: The diabetic patients represent a population with a high risk of morbidity and mortality because of vascular complications. Out of them, all the patients with acute ST-elevation myocardial infarction have a more reserved prognostic than those without diabetes mellitus. Moreover, the patients with impaired glucose tolerance have a more severe evolution in case of a myocardial infarction. AIM: We wondered about the progress of patients with myocardial infarction and high blood glucose levels in admittance who had not been previously diagnosed with diabetes mellitus. MATERIALS AND METHODS: We took 128 patients (who did not have diabetes) with acute ST-elevation myocardial infarction and divided them into three groups, according to the blood glucose level in admittance (<140 mg/dL, 140-200 mg/dL and > 200 mg/dL); we also analyzed a group of diabetics with acute myocardial infarction who were admitted in the same period in our clinic. We made a prospective analysis over a period of 30 days. We evaluated the mortality at 30 days (as primary objective), as well as the extent of the infarction and the change of the left ventricle systolic function (secondary objectives). RESULTS: Both mortality and the mass of myocardial necrosis grew relative to the blood glucose level in admittance; instead, the ejection fraction varied inversely to the initial blood glucose level. CONCLUSION: The admittance blood glucose level represents a useful and available marker for the initial stratification of risks in patients with acute myocardial infarction, even in those undiagnosed with diabetes mellitus.


Subject(s)
Blood Glucose/metabolism , Myocardial Infarction/blood , Diabetes Complications/blood , Female , Humans , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/physiopathology , Prognosis , Prospective Studies , Time Factors , Ventricular Function, Left
2.
Atherosclerosis ; 153(1): 191-201, 2000 Nov.
Article in English | MEDLINE | ID: mdl-11058715

ABSTRACT

Non-insulin-dependent diabetes mellitus (NIDDM) is frequently associated with macroangiopathies and coronary heart diseases. Lipoprotein lipase (LPL), an enzyme known to undergo significant functional alterations in diabetic state, is also a potential atherogenic protein. Since, to the best of our knowledge, there are no data concerning LPL secreted by macrophages of NIDDM patients we conducted a study to assess the expression and activity of LPL secreted by monocyte-derived macrophages from NIDDM patients with cardiovascular complications versus cardiovascular patients without diabetes (controls). Isolated cells from NIDDM patients, after 7 days in culture in the presence of 20% autologous serum, readily exhibit a foam cell phenotype, in contrast to the cells from controls. Macrophages were mainly loaded with triglycerides, whose cellular amount was well correlated to triglyceridemia of NIDDM subjects. Concomitantly, macrophages from NIDDM patients displayed a approximately six-fold decrease of mRNA expression and a approximately two-fold reduction of the activity of secreted LPL, as compared to control cells. These data suggest that in complicated diabetic state, macrophage loading leading to foam cell formation is accelerated, at least in part, due to a diminished expression and activity of LPL. These observations add and extend the data that may explain the occurrence of accelerated atherogenesis and of the atherosclerotic complications associated with diabetes.


Subject(s)
Diabetes Mellitus, Type 2/metabolism , Lipid Metabolism , Lipoprotein Lipase/metabolism , Macrophages/metabolism , Adult , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/pathology , Cell Line , Cells, Cultured , Diabetes Mellitus, Type 2/pathology , Diabetic Angiopathies/metabolism , Diabetic Angiopathies/pathology , Female , Foam Cells/pathology , Humans , Lipoprotein Lipase/genetics , Macrophages/pathology , Male , Microscopy, Electron , Monocytes/pathology , RNA, Messenger/metabolism
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