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(Circulation. 1997;96:1152-1156.)
© 1997 American Heart Association, Inc.
Articles |
Glucose-Insulin-Potassium Therapy for Treatment of Acute Myocardial Infarction
An Overview of Randomized Placebo-Controlled Trials
From the Medical Research Council Clinical Sciences Centre (F.F.-O.), Postgraduate Medical School, and Department of Cardiology (F.F.-O., K.J.B.), Hammersmith Hospital, London, UK.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background Glucose-insulin-potassium (GIK) therapy has been advocated for the treatment of acute myocardial infarction. However, the results from the clinical trials have been inconclusive, largely because of the small number of patients recruited and discrepancies between protocols used in these studies.
Method and Results A systematic MEDLINE search for all the randomized placebo-controlled studies of GIK therapy in acute myocardial infarction was made, and a meta-analysis of the mortality data was performed. Fifteen trials were identified, 5 were excluded because of poor randomization, and 1 was excluded because recruitment was limited to diabetic patients. The 9 remaining trials with a total of 1932 patients were included in the analysis. Hospital mortality was reduced from 21% (205 of 972 patients) in the placebo group to 16.1% (154 of 956) in the GIK group (P=.004; odds ratio, 0.72; 95% confidence interval [CI], 0.57 to 0.90). The proportional mortality reduction was 28% (CI, 10% to 43%). The number of lives saved per 1000 patients treated was 49 (95% CI, 14 to 83).
Conclusions The findings indicate that GIK therapy may have an important role in reducing the in-hospital mortality after acute myocardial infarction. The value of this therapy in the era of thrombolysis and acute revascularization by primary angioplasty can be fully resolved only by conducting a large randomized mortality study.
Key Words: glucose • myocardial infarction • insulin • metabolism • meta-analysis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Glucose-insulin-potassium (GIK) solution was initially advocated for the treatment of acute myocardial infarction as a polarizing agent to promote electrical stability1 and later as an agent to provide metabolic support. During the mid 1960s and 1970s, several clinical trials of GIK therapy in acute myocardial infarction were performed.2 3 4 5 6 7 8 9 10 11 12 13 14 15 However, results were inconclusive because of several factors, including a low number of recruits, poor design, and methodological discrepancies between different clinical trials, including varying times to the initiation of GIK therapy and the use of different GIK regimens (Table 1
). Many trials continued
recruitment as late as 48 hours after the onset of chest pain, and
several trials used oral glucose therapy with subcutaneous insulin
injections, whereas others used continuous intravenous
infusions (Table 1). Many of these studies may have used inadequate GIK
regimens. Dr Rackley and coworkers (Rogers et al12 )
demonstrated that to sufficiently suppress the plasma concentration of
harmful free fatty acids (FFA) and prevent myocardial uptake during
acute myocardial infarction, a mixture of 30% glucose, 50 U insulin,
and 80 mmol potassium at the rate of 
1.5 mL/kg per hour should
be infused. Largely due to discrepancies in reported results, lack of
commercial interest, and development of new and promising treatments,
such as ß-blockers and thrombolytic therapy, GIK
therapy for the treatment of acute myocardial infarction has been
abandoned.
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To further evaluate the effect of GIK therapy on mortality after acute myocardial infarction, we conducted a meta-analysis of all the properly conducted placebo-controlled, randomized trials of GIK therapy.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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A MEDLINE search (1966 through 1996) was performed using the search term "myocardial infarction" and a set of terms for GIK: glucose, insulin, glucose-insulin, GIK, GIP, PGI, glucose-insulin-potassium, metabolic support, and polarizing solution. In addition, references used by the selected studies and review articles on GIK therapy were scrutinized to ensure that all relevant studies were identified. All articles were reviewed, and studies that were placebo-controlled and properly randomized, with documented in-hospital mortality, were selected. Studies were excluded if they used inadequate means of randomization such as allocation on the basis of date of birth, admission to a particular unit, alternate numbers, or date of presentation. Trials that used a retrospective group or historic cases as the control group and those that limited the trial to a particular subgroup were also excluded (Table
2).
Statistical Analysis
For individual trials, the 
2
heterogeneity test16 was used to calculate
the significance, odds ratios, and 99% confidence interval (CI) values
for the differences in mortality between the GIK and placebo group,
except for trials in which the expected number of deaths was fewer than
five. For trials in which the number of deaths was fewer than five,
Fisher's exact test was used.17 In addition, for each
trial, the observed (O) minus expected (E) value for mortality (O-E)
and its variance were calculated.18 The expected value is
calculated as the average number of deaths of the combined groups. The
result is favorable when the observed value is less than the expected
value. The O-E value also corresponds to half the mortality reduction
achieved by the treated group. Results were pooled by adding O-E
values for each individual trial; this is called the grand total. Its
variance is the sum of each individual variance, and the SD is the
square root of this variance. A result is considered to be significant
when the grand total is 2 SD greater than zero. Although the
P value for the pooled data has been given, odds ratio and
CIs might be more relevant discriminators for this type of study (a
retrospective meta-analysis). Odds ratio is given by
exp(GT/VT) (where GT is grand total and VT is variance), and
for the pooled data, 95% CIs were used. These calculations correspond
to the Mantel-Haenszel method18 19 for combining
information from 2x2 tables. Proportional reduction in mortality is
given by the formula (1-odds ratio)x100. The number of extra lives
saved per 1000 patients was calculated by multiplying the event rate
difference by 10.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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A total of 15 trials were identified.2 3 4 5 6 7 8 9 10 11 13 14 15 20 21 Five trials4 5 6 7 10 were excluded because of poor randomization protocols, and 1 trial21 was excluded because only diabetic patients were included (Table 2
). The remaining 9
studies2 3 8 9 11 13 14 15 20 were included in the
meta-analysis. Studies were conducted between 1965 and 1987.
Two studies used a double-blind design,11 15 and the
remainder were open studies. Delays between the onset of chest pain and
initiation of treatment varied between 12 to 48 hours in different
studies. Duration of treatment varied from 6 hours to 14 days (Table 1). All trials reported the in-hospital mortality from an era in which
patients commonly remained in hospital for 3 to 4 weeks. Satler et
al20 reported the only trial in which
thrombolytic therapy was also given.
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In 6 trials, patients without myocardial infarction were withdrawn after randomization. In the study by Pentecost et al,9 most of 41 patients withdrawn had a diagnosis of severe angina, and none of these patients died. In the study by Hjermann,11 59 patients were withdrawn after excluding a myocardial infarction (26 in treated and 33 in control group): 4 because they were subsequently found to be diabetic (2 in each group) and 6 patients because they died within 3 hours of recruitment (2 in the treatment and 4 in the control group). The 6 patients who died were added to the mortality results in our analysis. In the MRC study,3 70 patients in the treatment group and 58 patients in the control group who did not have a myocardial infarction were withdrawn. Five of the patients from the treatment group and 6 from the control group died. These patients were included in the MRC mortality data in our analysis. In the study by Rogers et al,15 34 patients in the GIK group and 22 patients in the control group were withdrawn after excluding a myocardial infarction. In the study by Satler et al,20 of 27 patients, 10 who did not undergo a cardiac catheterization at 10 days after the infarction were excluded. None of these patients died, and exclusion of this study would not have affected the overall results. There were no patients reported as lost to follow-up and as dropouts because the data collection was limited to the in-hospital period.
The total number of patients included in the overall
meta-analysis was 1932 (Table 3): 956 patients
in the GIK group and 976 in the placebo group. The number of deaths in
the GIK group was lower than in the placebo group (154 [16.1%]
versus 205 [21%]; P=.004), with an odds ratio of 0.72 and
95% CI of 0.57 to 0.90 (Figure). Proportional mortality
reduction was 28% (95% CI, 10% to 43%) (Table 3). The absolute
reduction in mortality and number of lives saved per 1000 patients
treated with GIK was 4.9% and 49 lives (95% CI, 14 to 83),
respectively (Table 3). High-dose intravenous GIK therapy
has been advocated by Rogers et al12 to achieve adequate
suppression of plasma FFA levels. Only 4 trials13 14 15 20
used this regimen. Pooled data from these 4 trials included 288
patients and showed a mortality of 6.5% in the GIK group and 12% in
the placebo group. Although the proportional reduction in mortality
with GIK therapy was 48%, because of the small number of patients, the
95% CI barely exceeded unity (odds ratio, 0.52; 95% CI, 0.25 to
1.07). In the study by Mittra,2 a chart for random
allocation of the patients was used. However, a sequential
randomization protocol was used, in which the patients were paired
according to age and sex for comparison. This study was included in our
analysis, but the results would have remained positive after
its exclusion (P=.03; odds ratio, 0.77; 95% CI, 0.61 to
0.98).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The first controlled clinical mortality trial of GIK in myocardial infarction was published by Mittra2 in 1965; the result of this trial was promising. Since then, several studies have been conducted.3 4 5 6 7 8 9 10 11 12 13 14 15 However, many of the subsequent studies were poorly designed according to current standards. Of the optimally randomized placebo-controlled trials, only 1 study2 showed a significant benefit from GIK therapy. In the majority, a nonsignificant reduction in mortality with the use of this therapy could be demonstrated. Individually, however, none of these trials was sufficiently large to have power to be able to show a significant difference between the treated and control groups (Table 3
). With the
in-hospital mortality rates of 20% to 25% after an acute myocardial
infarction prevalent when these GIK trials were
conducted,3 it would have required 2000 to 3000 patients
to show a difference of 20% in mortality rate between the GIK and the
placebo groups. It is only after pooling the data from all the trials
that a number approaching this can be reached. The pooled data
consisted of >1900 patients and showed a reduction in absolute,
relative, and proportional hospital mortalities of 4.9%, 23.3%, and
28%, respectively, with the 95% CI of <1. This translates into a
saving of 49 lives per 1000 patients treated. Data available on the long-term effect of GIK therapy were very limited. We were not able to provide further information on any possible effect of GIK therapy in subgroups of patients, such as those with cardiac failure due to the lack of sufficient data. The side effects of GIK therapy were generally mild, with the most common being phlebitis at the site of intravenous infusion. Imbalances in plasma potassium or glucose were generally uncommon when plasma levels were monitored at regular intervals.
Mechanism of Action
In vitro and in vivo studies have identified several
mechanisms through which GIK therapy may exert its beneficial
effect.12 22 23 24 25 26 Exogenous glucose has been shown to be a
more efficient fuel than FFA or glycogen and is more likely to prevent
ischemic myocardial injury.27 Glycolysis-derived
ATP preferentially supports cell membrane function by protecting
membrane ion transport and hence helps to preserve cell
integrity.28 29 30 31 32 During myocardial ischemia, high
concentrations of FFA provoked by high sympathetic
activity33 34 35 have been shown to lead to increased
myocardial oxygen requirement and depression of myocardial mechanical
activity and contraction.33 36 37 38 They may also cause the
impairment of calcium homeostasis39 and the
production of free radicals, leading to electrical instability
and ventricular arrhythmias, including reperfusion
arrhythmias,40 41 42 and ultimately to cell membrane
damage (via a detergent effect).41 Insulin lowers the
plasma concentration of FFA by inhibiting lipolysis.43 44
Other possible mechanisms of action of GIK are (1) prevention of
ischemic contracture and improvement of myocardial
performance at a lower oxygen consumption45 ; (2)
protection of ischemic coronary vasculature, resulting
in preservation of low coronary resistance and myocardial
perfusion46 (this may be important, as recent studies have
shown that ischemic myocardial injury can be reduced by very
small increases in myocardial perfusion47 ); (3)
restoration of intracellular potassium; (4) promotion of wound healing
and reduction of tissue edema (via its hyperosmolar
effect)33 48 ; and (5) facilitating spontaneous
thrombolysis. Recent studies49 50 have
shown that insulin treatment reduces thromboxane A
production and decreases plasma plasminogen
activator inhibitor-I activity.
GIK and Reperfusion Strategies
Several recent trials support the complementary roles of GIK and
reperfusion therapy.25 26 45 46 51 It has been estimated
that GIK therapy has the potential to protect ischemic
myocardium before reperfusion for 10 hours or even
longer,46 thus lengthening the period during which
effective myocardial salvage is possible with reperfusion strategies
such as thrombolytic therapy or primary angioplasty.
Through reduction in the extent of ischemic myocardial
damage45 and suppression of FFA levels, GIK therapy helps
to prevent reperfusion injuries that may occur after successful
revascularization. Protection of the cell membrane
of ischemic myocytes and endothelial and
vascular smooth muscle cells may also improve reflow after reperfusion
and protect against no-reflow phenomenon by reducing cell swelling and
microvascular compression.46 Coronary reperfusion
may in turn add to the effectiveness of GIK therapy, as GIK treatment
only delays the onset of irreversible myocardial damage, and unless the
blood flow is reestablished, myocardial necrosis will eventually occur.
Reestablishment of blood flow by reperfusion strategies prevents
accumulation of lactic acid and hydrogen ions that may inhibit
glycolysis.25 36 52
The Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) trial21 has been the only substantial randomized placebo-controlled clinical trial of GIK therapy in acute myocardial infarction in the thrombolytic era. It showed a significant reduction in mortality in patients who were treated with glucose and insulin. However, only diabetic patients were studied, so it was not included in the meta-analysis.
Study Limitations
Limitations of meta-analysis studies have recently been
reviewed.53 54 The size of the pooled data is very
important; clearly, the margin for error decreases and the results
become more reliable as the size increases. Negative trials are less
likely to be published; this publication bias leads to overestimation
of the true difference between the groups.
Heterogeneity in patient populations and different
treatment protocols are additional concerns; however, discrepancies in
treatment protocol, particularly the use of oral therapy or extension
of the time of treatment to 48 hours after onset of chest pain,
undermines any potential benefit of GIK therapy. If anything, this will
lead to an underestimation rather than an overestimation of the
beneficial effect of GIK therapy. Many of the GIK studies were
performed in the mid 1960s and 1970s and were poorly designed compared
with current standards. We have therefore excluded all trials that were
not optimally randomized. Most of the trials were of open design
because of the need for regular blood monitoring; however, because
mortality was used as the end point, the results are unlikely to be
affected. Open design has been justifiably used in many modern and
successful studies with mortality end points, such as Gruppo Italiano
per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI)
study.55 Most of the studies included did not use the
principle of intention to treat. However, in at least 4
studies,3 9 11 20 information about excluded patients was
provided. In 1 study,3 we were able to include all the
excluded patients, and in another,11 excluded patients who
were known to have died were included in the overall analysis.
In addition, almost all the patients excluded after randomization were
those in whom diagnosis of myocardial infarction was ruled out. The
mortality rate in this group of patients is very small, and it could be
argued that their exclusion would not significantly affect the overall
results.
It should be recognized that the aim of meta-analyses such as the present study is not to provide definitive answers to complex clinical questions or to take the place of large properly conducted randomized clinical trials but rather to generate a hypothesis, stimulate interest in the subject, help determine whether there is a need to perform a proper clinical trial, and provide pointers toward the possible outcome.
Conclusions
The present study provides evidence that GIK therapy may have
an important role in reducing in-hospital mortality after acute
myocardial infarction. The sound theoretical rationale for this
beneficial effect, its complementary role with reperfusion strategies,
and very low incidence of serious side effects with proper monitoring
provide further arguments for the use of GIK. There is a need for a
large randomized mortality trial of this therapy as an adjunct to
thrombolysis or acute
revascularization by primary angioplasty for the
treatment of acute myocardial infarction.
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Footnotes |
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Reprint requests to Dr F. Fath-Ordoubadi, MRC Clinical Sciences Centre, RPMS, Hammersmith Hospital, London W12 0HS, UK.
Received October 9, 1996; revision received December 23, 1996; accepted February 21, 1997.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Sodi-Pallares D, Testelli MR, Fischleder BL. Effects of an intravenous infusion of a potassium-glucose-insulin solution on the electrocardiographic signs of myocardial infarction. Am J Cardiol. 1962;9:166-181.[Medline] [Order article via Infotrieve]
2. Mittra B. Potassium, glucose, and insulin in treatment of myocardial infarction. Lancet. 1965;2:607-609.[Medline] [Order article via Infotrieve]
3. Medical Research Council Working Party on the Treatment of Myocardial Infarction. Potassium, glucose, and insulin treatment for acute myocardial infarction. Lancet. 1968;2:1355-1360.[Medline] [Order article via Infotrieve]
4. Lundman T, Orinius E. Insulin-glucose-potassium infusion in acute myocardial infarction. Acta Med Scand. 1965;178:525-528.
5. Sievers J, Lindh J, Johansson BW, Karnell J. Acute myocardial infarction treated by glucose-insulin-potassium (GIK) infusion. Cardiology. 1966;49:239-247.[Medline] [Order article via Infotrieve]
6. Autio L, Hakkila J, Hartel G, Ikkala E. Anticoagulants and Sodi-Pallares infusion in acute myocardial infarction. Acta Med Scand. 1966;179:355-360.[Medline] [Order article via Infotrieve]
7. Malach M. Polarizing solution in acute myocardial infarction. Am J Cardiol. 1967;20:363-366.[Medline] [Order article via Infotrieve]
8. Pilcher J, Etishamudin M, Exon P, Moore J. Potassium, glucose and insulin in myocardial infarction. Lancet. 1967;1:1109.
9. Pentecost BL, Mayne NM, Lamb P. Controlled trial of intravenous glucose, potassium, and insulin in acute myocardial infarction. Lancet. 1968;1:946-948.[Medline] [Order article via Infotrieve]
10. Iisalo E, Kallio V. Potassium, glucose and insulin in the treatment of acute myocardial infarction. Curr Ther Res Clin Exp. 1969;11:209-215.[Medline] [Order article via Infotrieve]
11. Hjermann I. A controlled study of peroral glucose, insulin and potassium treatment in myocardial infarction. Acta Med Scand. 1971;190:213-218.[Medline] [Order article via Infotrieve]
12. Rogers WJ, Stanley AW, Breinig JB, Prather JW, McDaniel HG, Moraski RE, Mantle JA, Russell RO, Rackley CE. Reduction of hospital mortality rate of acute myocardial infarction with glucose-insulin-potassium infusion. Am Heart J. 1976;92:441-454.[Medline] [Order article via Infotrieve]
13.
Heng MK, Norris RM, Singh BN, Barratt Boyes C.
Effects of glucose and glucose-insulin-potassium on haemodynamics and
enzyme release after acute myocardial infarction. Br
Heart J. 1977;39:748-757.
14. Stanley AWH, Prather JW. Glucose-insulin-potassium, patient mortality and the acute myocardial infarction: results from a prospective randomized study. Circulation. 1978;57(suppl II):II-62. Abstract.
15. Rogers WJ, McDaniel HG, Mantle JA, Rackley CE. Prospective randomized trial of glucose-insulin-potassium in acute myocardial infarction: effects of hemodynamics, short and long-term survival. J Am Coll Cardiol. 1983;1:628. Abstract.
16. Armitage P, Berry G. Statistical Methods in Medical Research. Oxford, UK: Blackwell; 1987.
17. Bailey NTJ. Mathematics, Statistics and Systems for Health. New York, NY: Wiley; 1997.
18.
Antiplatelet Trialists' Collaboration.
Collaborative overview of randomized trials of antiplatelet
therapy: prevention of death, myocardial infarction and stroke by
prolonged antiplatelet therapy in various categories of
patients. BMJ. 1994;308:81-106.
19. Mantel N, Haenszel W. Statistical aspects of the analysis of data from retrospective studies of disease. J Natl Cancer Inst. 1959;22:719-748.
20. Satler LF, Green CE, Kent KM, Pallas RS, Pearle DL, Rackley CE. Metabolic support during coronary reperfusion. Am Heart J. 1987;114:54-58.[Medline] [Order article via Infotrieve]
21. Malmberg K, Ryden L, Efendic S, Herlitz J, Nicol P, Waldenstrom A, Wedel H, Welin L, on Behalf of the DIGAMI Study Group. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI): effect on mortality at 1 year. J Am Coll Cardiol. 1995;26:57-65.[Abstract]
22. Rackley CE, Russell RO, Rogers WJ, Mantle JA, McDaniel HG, Papapietro SE. Clinical experience with glucose-insulin-potassium therapy in acute myocardial infarction. Am Heart J. 1981;102:1038-1049.[Medline] [Order article via Infotrieve]
23. Opie LH. Metabolism of free fatty acids, glucose and catecholamines in acute myocardial infarction: relation to myocardial ischemia and infarct size. Am J Cardiol. 1975;36:938-953.[Medline] [Order article via Infotrieve]
24. Rogers WJ, McDaniel HG, Mantle JA, Russell RO, Rackley CE. Frontiers of therapy: use of glucose-insulin-potassium in treating myocardial infarction. J Cardiovasc Med. 1980;5:237-248.
25. Taegtmeyer H. Is there a rationale for glucose-insulin-potassium therapy in acute myocardial infarction? Cardiol Rev. 1995;26:307-313.
26. Opie LH. The glucose hypothesis: relation to acute myocardial ischemia. J Mol Cell Cardiol. 1970;1:107-115.
27. Runnman EM, Weiss JN. Exogenous glucose utilization is superior to glycogenolysis at preserving cardiac function during hypoxia. Circulation. 1988;78(suppl II):II-261. Abstract.
28. Opie LH. Hypothesis: glycolytic rates control cell viability in ischemia. J Appl Cardiol. 1988;3:407-414.
29.
Doorey AJ, Barry WH. The effects of inhibition
of oxidative phosphorylation and glycolysis on
contractility and high energy phosphate content in
cultured chick heart cells. Circ Res. 1983;53:192-201.
30. Hasin Y, Barry WH. Myocardial metabolic inhibition and membrane potential, contraction and potassium uptake. Am J Physiol. 1984;247:H322-H329.
31. Paul RJ, Hardin CH, Raeymackers L, Wuytack F, Casteels R. Preferential support of Ca++ uptake in smooth muscle plasma membrane vesicles by an endogenous glycolytic cascade. FASEB J. 1989;3:2298-2301.[Abstract]
32.
Weiss JN, Lamp ST. Glycolysis preferentially
inhibits ATP-sensitive K+ channels in isolated guinea
pig cardiac myocytes. Science. 1987;238:67-69.
33. Opie LH, Tansey M, Kennelly BM. Proposed metabolic vicious circle in patients with large myocardial infarction and high plasma free fatty acid concentrations. Lancet. 1977;2:890-892.[Medline] [Order article via Infotrieve]
34. Valori C, Thomas M, Shillingford J. Free noradrenaline and adrenaline excretion in relation to clinical syndromes following myocardial infarction. Am J Cardiol. 1967;20:605.[Medline] [Order article via Infotrieve]
35. Gupta DK, Jewitt DE, Young R. Increased plasma free fatty acid concentrations and their significance in patients with acute myocardial infarction. Lancet. 1969;2:1209.[Medline] [Order article via Infotrieve]
36. Oliver MF, Opie LH. Effects of glucose and fatty acids on myocardial ischaemia and arrhythmias. Lancet. 1994;343:155-158.[Medline] [Order article via Infotrieve]
37. Mjøs OD. Effect of free fatty acids on myocardial function and oxygen consumption in intact dog. J Clin Invest. 1971;50:1386.
38.
Henderson AH, Most AS, Parmley WW. Depression of
myocardial contractility in rats by free fatty acids
during hypoxia. Circ Res. 1970;26:439.
39. Saman S, Coetzee WA, Opie LH. Inhibition by stimulated ischaemia or hypoxia of delayed after depolarizations provoked by cyclic AMP: significance for ischaemic and reperfusion arrhythmias. J Mol Cell Cardiol. 1988;20:91-95.[Medline] [Order article via Infotrieve]
40. Oliver MF, Kurien VA, Greenwood TW. Relation between serum free fatty acids and arrhythmias and death after acute myocardial infarction. Lancet. 1968;1:710-714.[Medline] [Order article via Infotrieve]
41. Kurien VA, Oliver MF. A metabolic cause of arrhythmias during acute myocardial hypoxia. Lancet. 1970;1:813-1815.[Medline] [Order article via Infotrieve]
42. Kurien VA, Yates PA, Oliver MF. The role of free fatty acids in the production of ventricular arrhythmias after acute coronary occlusion. Eur J Clin Invest. 1971;1:225-241.[Medline] [Order article via Infotrieve]
43. McDaniel HG, Papapietro SE, Rogers WJ, Mantle JA, Smith RL, Russell RO, Rackley CE. Glucose-insulin-potassium induced alterations in individual plasma free fatty acids in patients with acute myocardial infarction. Am Heart J. 1981;102:10-15.[Medline] [Order article via Infotrieve]
44. Stanley AW, Moraski RE, Russell RO, Rogers WJ, Mantle JA, Kriesberg RA, McDaniel HG, Rackley CE. Effects of glucose-insulin-potassium on myocardial substrate availability and utilization in stable coronary artery disease: studies on myocardial carbohydrates, lipid and oxygen arterial-coronary sinus differences in patients with coronary artery disease. Am J Cardiol. 1975;36:929-937.[Medline] [Order article via Infotrieve]
45.
Vanoverschelde J-LJ, Janier MF, Bakke JE, Marshall DR,
Bergmann SR. Rate of glycolysis during ischemia
determines extent of ischemic injury and functional recovery
after reperfusion. Am J Physiol. 1994;267:H1785-H1794.
46.
Eberli FR, Weinberg EO, Grice WN, Horowitz GL, Apstein
CS. Protective effect of increased glycolytic substrate against
systolic and diastolic dysfunction and increased
coronary resistance from prolonged global underperfusion and
reperfusion in isolated rabbit hearts perfused with erythrocyte
suspensions. Circ Res. 1991;68:466-481.
47.
Apstein CS, Deckelbaum L, Mueller M, Hagapian L, Hood
WB. Graded global ischemia and reperfusion: cardiac
function and lactate metabolism.
Circulation. 1977;55:864-872.
48. Wildenthal K, Mierzwiak DS, Mitchell JH. Acute effects of increased serum osmolarity on left ventricular performance. Am J Physiol. 1969;216:898-904.
49. Davi G, Catalan I, Averna M. Thromboxane biosynthesis and platelet function in type II diabetes mellitus. N Engl J Med. 1990;322:1769-1774.[Abstract]
50. Jain SK, Nagi DK, Slavin BM, Lumb PJ, Yudkin JS. Insulin therapy in type 2 diabetic subjects suppresses plasminogen activator inhibitor (PAI-1) activity and proinsulin-like molecules independently of glycemic control. Diabetic Med. 1993;10:27-32.[Medline] [Order article via Infotrieve]
51. Stanley A, Arciniegas J, Cooper T, Corley N, Hess R, MacLean W, Papapietro S. Glucose-insulin-potassium following successful coronary reperfusion improves survival during myocardial infarction). Circulation. 1984;70(suppl II):II-153. Abstract.
52.
Rovetto MJ, Lamberton WF, Neely JR. Mechanism of
glycolytic inhibition in ischemic rat heart. Circ
Res. 1975;37:742-751.
53.
Yusuf S, Flather M. Magnesium in acute
myocardial infarction: ISIS 4 provides no grounds for its use.
BMJ. 1995;310:751-752.
54.
Egger M, Smith GD. Misleading
meta-analysis: lessons from `an effective, safe, simple'
intervention that wasn't. BMJ. 1995;310:752-754.
55. GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Micocardico). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986;1:397-401.[Medline] [Order article via Infotrieve]
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 |
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 L. Zhou, H. Huang, T. A. McElfresh, D. A. Prosdocimo, and W. C. Stanley Impact of anaerobic glycolysis and oxidative substrate selection on contractile function and mechanical efficiency during moderate severity ischemia Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H939 - H945. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Ussher and G. D. Lopaschuk The malonyl CoA axis as a potential target for treating ischaemic heart disease Cardiovasc Res, July 15, 2008; 79(2): 259 - 268. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Gandhi, B. A. Finegan, and A. S. Clanachan Role of glucose metabolism in the recovery of postischemic LV mechanical function: effects of insulin and other metabolic modulators Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2576 - H2586. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Kloner and R. W. Nesto Glucose-Insulin-Potassium for Acute Myocardial Infarction: Continuing Controversy Over Cardioprotection Circulation, May 13, 2008; 117(19): 2523 - 2533. [Full Text] [PDF]
|
|
|
|
 |
|
 C. J. Zuurbier, F. J. Hoek, J. van Dijk, N. G. Abeling, J. C. M. Meijers, J. H. M. Levels, E. de Jonge, B. A. de Mol, and H. B. Van Wezel Perioperative hyperinsulinaemic normoglycaemic clamp causes hypolipidaemia after coronary artery surgery Br. J. Anaesth., April 1, 2008; 100(4): 442 - 450. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Chai, Y. Wu, G. Li, W. Cao, Z. Yang, and Z. Liu Activation of p38 mitogen-activated protein kinase abolishes insulin-mediated myocardial protection against ischemia-reperfusion injury Am J Physiol Endocrinol Metab, January 1, 2008; 294(1): E183 - E189. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Diaz, A. Goyal, S. R. Mehta, R. Afzal, D. Xavier, P. Pais, S. Chrolavicius, J. Zhu, K. Kazmi, L. Liu, et al. Glucose-Insulin-Potassium Therapy in Patients With ST-Segment Elevation Myocardial Infarction JAMA, November 28, 2007; 298(20): 2399 - 2405. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Asadollahi, N. Beeching, and G. Gill Hyperglycaemia and mortality J R Soc Med, November 1, 2007; 100(11): 503 - 507. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. P. Patel, M. E. Pugh, S. Goldberg, and G. Eiger Hyperinsulinemic Euglycemia Therapy for Verapamil Poisoning: A Review Am. J. Crit. Care., September 1, 2007; 16(5): 498 - 503. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. V Parikh, S. M Abdullah, E. C Keeley, J. E Cigarroa, T. A Addo, J. J Warner, A. Khera, J. A De Lemos, and D. K McGuire Effect of glucose-insulin-potassium (GIK) infusion on biomarkers of cardiovascular risk in ST elevation myocardial infarction (STEMI): insight into the failure of GIK Diabetes and Vascular Disease Research, September 1, 2007; 4(3): 222 - 225. [Abstract] [PDF]
|
|
|
|
|
|
H. Su, X. Sun, H. Ma, H.-F. Zhang, Q.-J. Yu, C. Huang, X.-M. Wang, R.-H. Luan, G.-L. Jia, H.-C. Wang, et al. Acute hyperglycemia exacerbates myocardial ischemia/reperfusion injury and blunts cardioprotective effect of GIK Am J Physiol Endocrinol Metab, September 1, 2007; 293(3): E629 - E635. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Authors/Task Force Members, L. Ryden, E. Standl, M. Bartnik, G. V. d. Berghe, J. Betteridge, M.-J. de Boer, F. Cosentino, B. Jonsson, M. Laakso, et al. Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: full text: The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD) Eur. Heart J. Suppl., June 1, 2007; 9(suppl_C): C3 - C74. [Full Text] [PDF]
|
|
|
|
|
|
M. T. Dirksen, G. J. Laarman, M. L. Simoons, and D. J.G.M. Duncker Reperfusion injury in humans: A review of clinical trials on reperfusion injury inhibitory strategies Cardiovasc Res, June 1, 2007; 74(3): 343 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Inzucchi Management of Hyperglycemia in the Hospital Setting N. Engl. J. Med., November 2, 2006; 355(18): 1903 - 1911. [Full Text] [PDF]
|
|
|
|
|
|
G. Li, I. S. Ali, and R. W. Currie Insulin induces myocardial protection and Hsp70 localization to plasma membranes in rat hearts Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1709 - H1721. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sulfi and A. D Timmis Review: Heart failure complicating acute myocardial infarction in patients with diabetes: pathophysiology and management strategies The British Journal of Diabetes & Vascular Disease, September 1, 2006; 6(5): 191 - 196. [Abstract] [PDF]
|
|
|
|
 |
|
 H. B. Van Wezel Glucose-insulin-potassium techniques in cardiac surgery: historical overview and future perspectives. Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2006; 10(3): 224 - 227. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Barsheshet, M. Garty, E. Grossman, A. Sandach, B. S. Lewis, S. Gottlieb, A. Shotan, S. Behar, A. Caspi, R. Schwartz, et al. Admission Blood Glucose Level and Mortality Among Hospitalized Nondiabetic Patients With Heart Failure. Arch Intern Med, August 14, 2006; 166(15): 1613 - 1619. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D.L. Folmes, A. S. Clanachan, and G. D. Lopaschuk Fatty Acids Attenuate Insulin Regulation of 5'-AMP-Activated Protein Kinase and Insulin Cardioprotection After Ischemia Circ. Res., July 7, 2006; 99(1): 61 - 68. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Jhund and J. J.V. McMurray Does Aspirin Reduce the Benefit of an Angiotensin-Converting Enzyme Inhibitor?: Choosing Between the Scylla of Observational Studies and the Charybdis of Subgroup Analysis Circulation, June 6, 2006; 113(22): 2566 - 2568. [Full Text] [PDF]
|
|
|
|
 |
|
 Z. T. Bloomgarden Cardiovascular Disease Diabetes Care, May 1, 2006; 29(5): 1160 - 1166. [Full Text] [PDF]
|
|
|
|
|
|
J. R. Timmer, T. Svilaas, J. P. Ottervanger, J. P.S. Henriques, J.-H. E. Dambrink, S. A.J. van den Broek, I. C.C. van der Horst, and F. Zijlstra Glucose-Insulin-Potassium Infusion in Patients With Acute Myocardial Infarction Without Signs of Heart Failure: The Glucose-Insulin-Potassium Study (GIPS)-II J. Am. Coll. Cardiol., April 18, 2006; 47(8): 1730 - 1731. [Full Text] [PDF]
|
|
|
|
 |
|
 J. D. Schipke, R. Friebe, and E. Gams Forty years of glucose-insulin-potassium (GIK) in cardiac surgery: a review of randomized, controlled trials. Eur. J. Cardiothorac. Surg., April 1, 2006; 29(4): 479 - 485. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. W. Cheung, V. W. Wong, and M. McLean The Hyperglycemia: Intensive Insulin Infusion In Infarction (HI-5) Study: A randomized controlled trial of insulin infusion therapy for myocardial infarction Diabetes Care, April 1, 2006; 29(4): 765 - 770. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. Pittas, R. D. Siegel, and J. Lau Insulin Therapy and In-Hospital Mortality in Critically Ill Patients: Systematic Review and Meta-analysis of Randomized Controlled Trials JPEN J Parenter Enteral Nutr, March 1, 2006; 30(2): 164 - 172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. Hamdulay, A. A. Khafaji, and H. Montgomery Glucose-Insulin and Potassium Infusions in Septic Shock Chest, March 1, 2006; 129(3): 800 - 804. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Lautamaki, K.E. J. Airaksinen, M. Seppanen, J. Toikka, R. Harkonen, M. Luotolahti, R. Borra, J. Sundell, J. Knuuti, and P. Nuutila Insulin Improves Myocardial Blood Flow in Patients With Type 2 Diabetes and Coronary Artery Disease Diabetes, February 1, 2006; 55(2): 511 - 516. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. W. Quinn, D. Pagano, R. S. Bonser, S. J. Rooney, T. R. Graham, I. C. Wilson, B. E. Keogh, J. N. Townend, M. E. Lewis, P. Nightingale, et al. Improved myocardial protection during coronary artery surgery with glucose-insulin-potassium: A randomized controlled trial J. Thorac. Cardiovasc. Surg., January 1, 2006; 131(1): 34 - 42. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kosiborod, S. S. Rathore, S. E. Inzucchi, F. A. Masoudi, Y. Wang, E. P. Havranek, and H. M. Krumholz Admission Glucose and Mortality in Elderly Patients Hospitalized With Acute Myocardial Infarction: Implications for Patients With and Without Recognized Diabetes Circulation, June 14, 2005; 111(23): 3078 - 3086. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. W. Quinn, D. Pagano, and R. S. Bonser Glucose and Insulin Influences on Heart and Brain in Cardiac Surgery Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2005; 9(2): 173 - 178. [Abstract] [PDF]
|
|
|
|
|
|
S. R. Mehta, S. Yusuf, R. Diaz, and E. Paolasso Glucose-Insulin-Potassium Infusion and Mortality in the CREATE-ECLA Trial--Reply JAMA, June 1, 2005; 293(21): 2598 - 2598. [Full Text] [PDF]
|
|
|
|
|
|
P. Wang, S. G. Lloyd, and J. C. Chatham Impact of High Glucose/High Insulin and Dichloroacetate Treatment on Carbohydrate Oxidation and Functional Recovery After Low-Flow Ischemia and Reperfusion in the Isolated Perfused Rat Heart Circulation, April 26, 2005; 111(16): 2066 - 2072. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Malmberg, L. Ryden, H. Wedel, K. Birkeland, A. Bootsma, K. Dickstein, S. Efendic, M. Fisher, A. Hamsten, J. Herlitz, et al. Intense metabolic control by means of insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI 2): effects on mortality and morbidity Eur. Heart J., April 1, 2005; 26(7): 650 - 661. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M Conner, K. R Flesner-Gurley, and J. C Barner Hyperglycemia in the Hospital Setting: The Case for Improved Control Among Non-Diabetics Ann. Pharmacother., March 1, 2005; 39(3): 492 - 501. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
The CREATE-ECLA Trial Group Investigators* Effect of Glucose-Insulin-Potassium Infusion on Mortality in Patients With Acute ST-Segment Elevation Myocardial Infarction: The CREATE-ECLA Randomized Controlled Trial JAMA, January 26, 2005; 293(4): 437 - 446. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. M. Califf Simple Principles of Clinical Trials Remain Powerful JAMA, January 26, 2005; 293(4): 489 - 491. [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. Nikolaidis, A. Doverspike, T. Hentosz, L. Zourelias, Y.-T. Shen, D. Elahi, and R. P. Shannon Glucagon-Like Peptide-1 Limits Myocardial Stunning following Brief Coronary Occlusion and Reperfusion in Conscious Canines J. Pharmacol. Exp. Ther., January 1, 2005; 312(1): 303 - 308. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Woods, J. M. Smith, S. Sohail, A. Sarah, and A. Engle The Influence of Type 2 Diabetes Mellitus in Patients Undergoing Coronary Artery Bypass Graft Surgery: An 8-Year Prospective Cohort Study Chest, December 1, 2004; 126(6): 1789 - 1795. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. W. Wong, M. McLean, S. C. Boyages, and N. W. Cheung C-Reactive Protein Levels Following Acute Myocardial Infarction: Effect of insulin infusion and tight glycemic control Diabetes Care, December 1, 2004; 27(12): 2971 - 2973. [Full Text] [PDF]
|
|
|
|
|
|
G. Carvalho, T. Schricker, H. L. Lazar, S. R. Chipkin, C. A. Fitzgerald, Y. Bao, H. Cabral, and C. Apstein Letter Regarding Article by Lazar et al, "Tight Glycemic Control in Diabetic Coronary Artery Bypass Graft Patients Improves Perioperative Outcomes and Decreases Recurrent Ischemic Events" Circulation, November 16, 2004; 110(20): e505 - e505. [Full Text] [PDF]
|
|
|
|
 |
|
 W. Bothe, M. Olschewski, F. Beyersdorf, and T. Doenst Glucose-Insulin-Potassium in Cardiac Surgery: A Meta-Analysis Ann. Thorac. Surg., November 1, 2004; 78(5): 1650 - 1657. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. G. Pittas, R. D. Siegel, and J. Lau Insulin Therapy for Critically Ill Hospitalized Patients: A Meta-analysis of Randomized Controlled Trials Arch Intern Med, October 11, 2004; 164(18): 2005 - 2011. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. B. Hirsch Were We Wrong About Insulin and Acute Myocardial Infarction? DOC News, October 1, 2004; 1(2): 4 - 5. [Full Text]
|
|
|
|
 |
|
 J.-T. Kim, C.-W. Jung, and K.-H. Lee The Effect of Insulin on the Resuscitation of Bupivacaine-Induced Severe Cardiovascular Toxicity in Dogs Anesth. Analg., September 1, 2004; 99(3): 728 - 733. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. T. Bloomgarden Inpatient Diabetes Control: Rationale Diabetes Care, August 1, 2004; 27(8): 2074 - 2080. [Full Text] [PDF]
|
|
|
|
|
|
J. F. LaDisa Jr., J. G. Krolikowski, P. S. Pagel, D. C. Warltier, and J. R. Kersten Cardioprotection by glucose-insulin-potassium: dependence on KATP channel opening and blood glucose concentration before ischemia Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H601 - H607. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Bolli, L. Becker, G. Gross, R. Mentzer Jr, D. Balshaw, and D. A. Lathrop Myocardial Protection at a Crossroads: The Need for Translation Into Clinical Therapy Circ. Res., July 23, 2004; 95(2): 125 - 134. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Kloner and S. H. Rezkalla Cardiac protection during acute myocardial infarction: Where do we stand in 2004? J. Am. Coll. Cardiol., July 21, 2004; 44(2): 276 - 286. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. S Lewis, S. L Kane-Gill, M. B. Bobek, and J. F Dasta Intensive Insulin Therapy for Critically Ill Patients Ann. Pharmacother., July 1, 2004; 38(7): 1243 - 1251. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. G. Lloyd, P. Wang, H. Zeng, and J. C. Chatham Impact of low-flow ischemia on substrate oxidation and glycolysis in the isolated perfused rat heart Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H351 - H362. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R Timmer, J. P. Ottervanger, K. Thomas, J. C.A Hoorntje, M.-J. de Boer, H. Suryapranata, F. Zijlstra, and on behalf of the Zwolle myocardial infarction stud Long-term, cause-specific mortality after myocardial infarction in diabetes Eur. Heart J., June 1, 2004; 25(11): 926 - 931. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. R. Chaitman, S. L. Skettino, J. O. Parker, P. Hanley, J. Meluzin, J. Kuch, C. J. Pepine, W. Wang, J. J. Nelson, D. A. Hebert, et al. Anti-ischemic effects and long-term survival during ranolazine monotherapy in patients with chronic severe angina J. Am. Coll. Cardiol., April 21, 2004; 43(8): 1375 - 1382. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Lee, J. Horowitz, and M. Frenneaux Metabolic manipulation in ischaemic heart disease, a novel approach to treatment Eur. Heart J., April 2, 2004; 25(8): 634 - 641. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Ramanathan, S. Morita, Y. Huang, K. Shirota, T. Nishimura, X. Zheng, and S. N. Hunyor Glucose-insulin-potassium solution improves left ventricular energetics in chronic ovine diabetes Ann. Thorac. Surg., April 1, 2004; 77(4): 1408 - 1414. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. L. Lazar, S. R. Chipkin, C. A. Fitzgerald, Y. Bao, H. Cabral, and C. S. Apstein Tight Glycemic Control in Diabetic Coronary Artery Bypass Graft Patients Improves Perioperative Outcomes and Decreases Recurrent Ischemic Events Circulation, March 30, 2004; 109(12): 1497 - 1502. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. T Dirksen, G. Laarman, A. W.J van 't Hof, G. Guagliumi, W. A.L Tonino, L. Tavazzi, D. J.G.M Duncker, M. L Simoons, and on behalf of the PARI-MI Investigators The effect of ITF-1697 on reperfusion in patients undergoing primary angioplasty: Safety and efficacy of a novel tetrapeptide, ITF-1697 Eur. Heart J., March 1, 2004; 25(5): 392 - 400. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. K. Andersen, J. Gjedsted, C. Christiansen, and E. Tonnesen The roles of insulin and hyperglycemia in sepsis pathogenesis J. Leukoc. Biol., March 1, 2004; 75(3): 413 - 421. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Clement, S. S. Braithwaite, M. F. Magee, A. Ahmann, E. P. Smith, R. G. Schafer, and I. B. Hirsch Management of Diabetes and Hyperglycemia in Hospitals Diabetes Care, February 1, 2004; 27(2): 553 - 591. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Westerbacka, R. Bergholm, M. Tiikkainen, and H. Yki-Jarvinen Glargine and Regular Human Insulin Similarly Acutely Enhance Endothelium-Dependent Vasodilatation in Normal Subjects Arterioscler Thromb Vasc Biol, February 1, 2004; 24(2): 320 - 324. [Abstract] [Full Text]
|
|
|
|
|
|
B. J. Riedel, J. Gal, G. Ellis, P. J. Marangos, A. W. Fox, and D. Royston Myocardial Protection Using Fructose-1,6-Diphosphate During Coronary Artery Bypass Graft Surgery: A Randomized, Placebo-Controlled Clinical Trial Anesth. Analg., January 1, 2004; 98(1): 20 - 29. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Schneider, N. Ad, U. Izhar, I. Khaliulin, J. B. Borman, and H. Schwalb Protection of myocardium by cyclosporin A and insulin: in vitro simulated ischemia study in human myocardium Ann. Thorac. Surg., October 1, 2003; 76(4): 1240 - 1245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Brady and A. Jovanovic The sulfonylurea controversy: Much ado about nothing or cause for concern? J. Am. Coll. Cardiol., September 17, 2003; 42(6): 1022 - 1025. [Full Text] [PDF]
|
|
|
|
|
|
I. C. C. van der Horst, F. Zijlstra, A. W. J. van't Hof, C. J. M. Doggen, M.-J. de Boer, H. Suryapranata, J. C. A. Hoorntje, J.-H. E. Dambrink, R. O. B. Gans, H. J. G. Bilo, et al. Glucose-insulin-potassium infusion inpatients treated with primary angioplasty for acute myocardial infarction: The glucose-insulin-potassium study: a randomized trial J. Am. Coll. Cardiol., September 3, 2003; 42(5): 784 - 791. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Apstein The benefits of glucose-insulin-potassium for acute myocardial infarction (and some concerns) J. Am. Coll. Cardiol., September 3, 2003; 42(5): 792 - 795. [Full Text] [PDF]
|
|
|
|
|
|
I. L Williams, B. Noronha, and A. G Zaman Review: The management of acute myocardial infarction in patients with diabetes mellitus The British Journal of Diabetes & Vascular Disease, September 1, 2003; 3(5): 319 - 324. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Aldemir, A. Gurel, H. Buyukbayram, and I. TaAyildiz The Effects of Glucose-Insulin-Potassium Solution and BN 52021 in Intestinal Ischemia-Reperfusion Injury Vascular and Endovascular Surgery, September 1, 2003; 37(5): 345 - 351. [Abstract] [PDF]
|
|
|
|
|
|
S. Lloyd, C. Brocks, and J. C. Chatham Differential modulation of glucose, lactate, and pyruvate oxidation by insulin and dichloroacetate in the rat heart Am J Physiol Heart Circ Physiol, June 5, 2003; 285(1): H163 - H172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Dandona, A. Aljada, A. Chaudhuri, and A. Bandyopadhyay The Potential Influence of Inflammation and Insulin Resistance on the Pathogenesis and Treatment of Atherosclerosis-Related Complications in Type 2 Diabetes J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2422 - 2429. [Full Text] [PDF]
|
|
|
|
|
|
T. Doenst, C. Schlensak, and F. Beyersdorf Cardioplegia in pediatric cardiac surgery: do we believe in magic? Ann. Thorac. Surg., May 1, 2003; 75(5): 1668 - 1677. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. N. Sack and D. M. Yellon Insulin therapy as an adjunct toreperfusion after acute coronary ischemia: A proposed direct myocardial cell survival effect independent of metabolic modulation J. Am. Coll. Cardiol., April 16, 2003; 41(8): 1404 - 1407. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Bovill Anesthesia for Patients with Impaired Ventricular Function Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2003; 7(1): 49 - 54. [PDF]
|
|
|
|
|
|
H. B. van Wezel and S. W. M. d. Jong Clinical Use of Glucose-Insulin-Potassium in Cardiac Surgery andAcute Myocardial Infarction: An Overview Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2003; 7(1): 77 - 83. [PDF]
|
|
|
|
|
|
C. J. Tack Insulin Resistance and Acute Cardiovascular Complications Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2003; 7(1): 85 - 90. [PDF]
|
|
|
|
|
|
T. Doenst, W. Bothe, and F. Beyersdorf Therapy with insulin in cardiac surgery: controversies and possible solutions Ann. Thorac. Surg., February 1, 2003; 75(2): S721 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Sundell and J. Knuuti Insulin and myocardial blood flow Cardiovasc Res, February 1, 2003; 57(2): 312 - 319. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
The Task Force on the Management of Acute Myocardi, F. Van de Werf, D. Ardissino, A. Betriu, D. V. Cokkinos, E. Falk, K. A.A. Fox, D. Julian, M. Lengyel, F.-J. Neumann, et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation Eur. Heart J., January 1, 2003; 24(1): 28 - 66. [Full Text] [PDF]
|
|
|
|
|
|
R. Ferrara, G. Guardigli, and R. Ferrari Myocardial metabolism: the diabetic heart Eur. Heart J. Suppl., January 1, 2003; 5(suppl_B): B15 - B18. [Abstract] [PDF]
|
|
|
|
|
|
N. N. Wahab, E. A. Cowden, N. J. Pearce, M. J. Gardner, H. Merry, J. L. Cox, and ICONS Investigators Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era? J. Am. Coll. Cardiol., November 20, 2002; 40(10): 1748 - 1754. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Ryden and K. Malmberg Who are the enemies? Diabetes mellitus -- a major risk factor for ischaemic myocardial injury: new directions in the management of acute coronary syndromes in the diabetic patient Eur. Heart J. Suppl., November 1, 2002; 4(suppl_G): G21 - G25. [Abstract] [PDF]
|
|
|
|
 |
|
 J Sala, R Masia, F-J Gonzalez de Molina, J M Fernandez-Real, M Gil, D Bosch, W Ricart, M Senti, and J Marrugat Short-term mortality of myocardial infarction patients with diabetes or hyperglycaemia during admission J Epidemiol Community Health, September 1, 2002; 56(9): 707 - 712. [Abstract] [Full Text] [PDF]
|
|
|
|
|
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J. L. Carson, P. M. Scholz, A. Y. Chen, E. D. Peterson, J. Gold, and S. H. Schneider Diabetes mellitus increases short-term mortality and morbidity in patients undergoing coronary artery bypass graft surgery J. Am. Coll. Cardiol., August 7, 2002; 40(3): 418 - 423. [Abstract] [Full Text] [PDF]
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I. B. Hirsch, A. Coviello, J. E. Mazuski, J. A. Bailey, M. J. Shapiro, K. C. McCowen, J. A. Maykel, B. R. Bistrian, N. J. Nusbaum, G. van den Berghe, et al. Intensive Insulin Therapy in Critically Ill Patients N. Engl. J. Med., May 16, 2002; 346(20): 1586 - 1588. [Full Text] [PDF]
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W. A. Lell, V. G. Nielsen, D. C. McGiffin, F. E. Schmidt Jr, J. K. Kirklin, and A. W. Stanley Jr Glucose-insulin-potassium infusion for myocardial protection during off-pump coronary artery surgery Ann. Thorac. Surg., April 1, 2002; 73(4): 1246 - 1251. [Abstract] [Full Text] [PDF]
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J. Sundell, P. Nuutila, H. Laine, M. Luotolahti, K. Kalliokoski, O. Raitakari, and J. Knuuti Dose-Dependent Vasodilating Effects of Insulin on Adenosine-Stimulated Myocardial Blood Flow Diabetes, April 1, 2002; 51(4): 1125 - 1130. [Abstract] [Full Text] [PDF]
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I. B. Hirsch In-Patient Hyperglycemia--Are We Ready to Treat It Yet? J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 975 - 977. [Full Text] [PDF]
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 Y. Cottin, I. Lhuillier, L. Gilson, M. Zeller, C. Bonnet, C. Toulouse, P. Louis, L. Rochette, C. Girard, and J.-E. Wolf Glucose insulin potassium infusion improves systolic function in patients with chronic ischemic cardiomyopathy Eur J Heart Fail, March 1, 2002; 4(2): 181 - 184. [Abstract] [Full Text] [PDF]
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Q. Liu, J. C. Docherty, J. C. T. Rendell, A. S. Clanachan, and G. D. Lopaschuk High levels of fatty acids delay the recoveryof intracellular pH and cardiac efficiency inpost-ischemic hearts by inhibiting glucose oxidation J. Am. Coll. Cardiol., February 20, 2002; 39(4): 718 - 725. [Abstract] [Full Text] [PDF]
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T. Ramanathan, K. Shirota, S. Morita, T. Nishimura, Y. Huang, and S. N. Hunyor Glucose-insulin-potassium solution improves left ventricular mechanics in diabetes Ann. Thorac. Surg., February 1, 2002; 73(2): 582 - 587. [Abstract] [Full Text] [PDF]
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H.-P. Hermann, O. Zeitz, S. E Lehnart, B. Keweloh, N. Datz, G. Hasenfuss, and P. M.L Janssen Potentiation of beta-adrenergic inotropic response by pyruvate in failing human myocardium Cardiovasc Res, January 1, 2002; 53(1): 116 - 123. [Abstract] [Full Text] [PDF]
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I. B. A. Menown and A. A. J. Adgey Cardioprotective therapy and sodium-hydrogen exchange inhibition: current concepts and future goals J. Am. Coll. Cardiol., November 15, 2001; 38(6): 1651 - 1653. [Full Text] [PDF]
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R. Ramasamy, Y. Hwang, S. Bakr, and S. R. Bergmann Protection of ischemic hearts perfused with an anion exchange inhibitor, DIDS, is associated with beneficial changes in substrate metabolism Cardiovasc Res, August 1, 2001; 51(2): 275 - 282. [Abstract] [Full Text] [PDF]
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I. Gustafsson and P. Hildebrandt Blood glucose in the CCU: time to measure Eur. Heart J., July 1, 2001; 22(13): 1061 - 1062. [PDF]
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