Effects of diabetes on myocardial infarct size and cardioprotection by preconditioning and postconditioning.
In spite of the current optimal therapy, the mortality of patients with ischemic heart disease (IHD) remains high, particularly in cases with diabetes mellitus (DM) as a co-morbidity. Myocardial infarct size is a major determinant of prognosis in IHD patients, and development of a novel strategy to limit infarction is of great clinical importance. Ischemic preconditioning (PC), postconditioning (PostC) and their mimetic agents have been shown to reduce infarct size in experiments using healthy animals. However, a variety of pharmacological agents have failed to demonstrate infarct size limitation in clinical trials. One of the possible reasons for the discrepancy between the results of animal experiments and clinical trials is that co-morbidities, including DM, modified myocardial responses to ischemia/reperfusion and to cardioprotective agents. Here we summarize observations of the effects of DM on myocardial infarct size and ischemic PC and PostC and discuss perspectives for protection of DM hearts.
Second Department of Internal Medicine, Sapporo Medical University School of Medicine, South-1 West-16, Sapporo 060-8543, Japan. tmiki@sapmed.ac.jp
Takayuki
T
Miki
Takahito
T
Itoh
Daisuke
D
Sunaga
Tetsuji
T
Miura
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015897:Comorbidity; D003920:Diabetes Mellitus / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology* / Q000401:mortality; D004195:Disease Models, Animal; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D057775:Ischemic Postconditioning; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D012307:Risk Factors; D015398:Signal Transduction; D016896:Treatment Outcome
D001786:Blood Glucose; D007004:Hypoglycemic Agents