Tight Glycemic Control Reduces Heart Inflammation And Remodeling

1,146 views

Published on

Tight Glycemic Control Reduces Complications in AMI setting

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
1,146
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
32
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Tight Glycemic Control Reduces Heart Inflammation And Remodeling

  1. 1. TIGHT GLYCEMIC CONTROL REDUCES HEART INFLAMMATION AND REMODELING DURING ACUTE MYOCARDIAL INFARCTION IN HYPERGLYCEMIC PATIENTS http://www.cardiosource.com/pops/jaccjump.asp ?vol=53&issue=16&page=1425&journal=JACC
  2. 2. Methods Eighty-eight patients with first acute  myocardial infarction (AMI) undergoing bypass surgery were studied: 38 normoglycemic patients served as the control group; hyperglycemic patients (glucose = 140 mg/dl) were randomized to intensive glycemic control (IGC) (n = 25; glucose 80-140 mg/dl) or conventional glycemic control (CGC) (n = 25; glucose 180-200 mg/dl) for almost 3 days before surgery, with insulin infusion followed by subcutaneous insulin treatment
  3. 3. Echocardiographic parameters were  investigated at admission and after treatment period. During surgery, oxidative stress  (nitrotyrosine, superoxide anion [O2–] production, inducible nitric oxide synthase [iNOS]), inflammation (nuclear factor kappa B [NFκB], tumor necrosis factor [TNF]-α, and apoptosis (caspase-3) were analyzed in biopsy specimens taken from the peri-infarcted area.
  4. 4. Results Compared with normoglycemic  patients, hyperglycemic patients had higher myocardial performance index (MPI) (p < 0.05), reduced ejection fraction (p < 0.05), more nitrotyrosine, iNOS, and O2– production, more macrophages, T- lymphocytes, and HLA-DR cells, and more NFκB-activity, TNF-α, and caspase-3 levels (p < 0.01) in peri-infarcted specimens.
  5. 5. After the treatment period, plasma glucose  reduction was greater in the IGC than in the CGC group (p < 0.001). Compared with IGC patients, CGC patients had higher MPI (p < 0.02), lower ejection fraction (p < 0.05), and more markers of oxidative stress, inflammation, and apoptosis (p < 0.01) in peri-infarcted specimens.
  6. 6. Conclusions Tight glycemic control, by reducing oxidative  stress and inflammation, might reduce apoptosis in peri-infarcted areas and remodeling in AMI patients.
  7. 7. Perspective This mechanistic study suggests that tight  glycemic control during the ischemic insult may be associated with reduction of early post-infarction remodeling. The study, while promising, needs to be validated in larger cohorts, and the clinical implications of the reduction in remodeling needs to be defined..
  8. 8. The NICE-SUGAR study recently suggested  that intensively lowering blood glucose to a target of 81-108 mg/dl does not benefit critically ill patients and increase their risk of dying.
  9. 9. For now, it seems prudent to follow the  American Heart Association Scientific Statement recommendations on hyperglycemia and acute coronary syndrome (ACS) (Circulation 2008;117:1610-9), which states that in patients admitted to an intensive care unit (ICU) with ACS, approximation of normoglycemia appears to be a reasonable goal (suggested range for plasma glucose 90- 140 mg/dl), as long as hypoglycemia is avoided.
  10. 10. In patients hospitalized in the non-ICU  setting, efforts should be directed at maintaining plasma glucose levels <180 mg/dl with subcutaneous insulin regimens
  11. 11. Relationship Between Spontaneous and Iatrogenic Hypoglycemia and Mortality in Patients Hospitalized With Acute Myocardial Infarction JAMA Vol. 301 No. 15, April 15, 2009 Retrospective cohort study using data from  Health Facts, a contemporary database of patients hospitalized across the United States in 40 hospitals between January 1, 2000, and December 31, 2005.
  12. 12. Of all the patients in the database, 7820  patients were hospitalized with AMI andwere hyperglycemic on admission (glucose level 140 mg/dL). Patients were stratified based on whether they  developed a hypoglycemic event (random glucose level <60 mg/dL) during subsequent hospitalization. Logistic regression models were used to  evaluate the association between hypoglycemia and in-hospital mortality within subgroups of patients who were and were not
  13. 13. Among patients treated or not treated with  insulin, those with hypoglycemia were older and had more comorbidity. Hypoglycemia was associated with increased mortality in patients not treated with insulin (18.4% [25/136] mortality in patients with hypoglycemia vs. 9.2% [425/4,639] in those without hypoglycemia; p < 0.001),
  14. 14. Insulin Induced Hypoglycemia does not increase mortality in AMI setting but not in those treated with insulin (10.4%  [36/346] mortality in patients with hypoglycemia vs. 10.2% [276/2,699] in those without hypoglycemia; p = 0.92).
  15. 15. After multivariable adjustment, there was a  significant interaction between hypoglycemia and insulin therapy (p value for interaction = 0.01). Hypoglycemia was a predictor of higher mortality in patients who were not treated with insulin (odds ratio, 2.32 [95% confidence interval, 1.31-4.12] vs. patients without hypoglycemia), but not in patients treated with insulin (odds ratio, 0.92 [95% confidence interval, 0.58-1.45] vs. patients without hypoglycemia).
  16. 16. Conclusions While hypoglycemia was associated with  increased mortality in patients with AMI, this risk was confined to patients who developed hypoglycemia spontaneously. In contrast, iatrogenic hypoglycemia after  insulin therapy was not associated with higher mortality risk.

×