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See detailA meta-analysis of glucose-insulin-potassium therapy for treatment of acute myocardial infarction.
Mamas, Mamas A.; Neyses, Ludwig UL; Fath-Ordoubadi, Farzin

in Experimental and Clinical Cardiology (2010), 15(2), 20-4

BACKGROUND: Glucose-insulin-potassium (GIK) therapy has been proposed to provide metabolic support to ischemic myocardium. A meta-analysis that included 1932 patients performed 10 years previously ... [more ▼]

BACKGROUND: Glucose-insulin-potassium (GIK) therapy has been proposed to provide metabolic support to ischemic myocardium. A meta-analysis that included 1932 patients performed 10 years previously demonstrated that GIK therapy may have an important role in reducing mortality after acute myocardial infarction (AMI). Since then, many larger randomized trials investigating the role of GIK in the setting of AMI have been published; hence, the present study repeats the previous meta-analysis performed by the current authors to include these trials. METHOD AND RESULTS: A systematic MEDLINE search for all randomized, placebo-controlled studies of GIK therapy in the setting of AMI was conducted and a meta-analysis of the mortality data was performed. A total of 16 randomized trials from 1966 to 2008 were identified, with 28,374 patients included in the current meta-analysis. There was a total of 1367 deaths (9.6%) in the GIK group, with 1351 deaths (9.6%) in the control group. Meta-analysis did not reveal any benefit from GIK treatment (OR 1.0; 95% CI 0.9 to 1.1; P=0.9). Subgroup analysis of patients given high-dose GIK and in patients in whom reperfusion was not obtained did not demonstrate a benefit from GIK therapy. CONCLUSION: A meta-analysis of 16 randomized trials that spanned 40 years and involved more than 28,000 patients did not reveal any mortality benefit for ST segment elevation AMI using GIK therapy when data from the modern thrombolysis/primary percutaneous coronary intervention era were included. [less ▲]

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See detailA molecular mechanism improving the contractile state in human myocardial hypertrophy.
Ritter, Oliver; Bottez, Nico; Burkard, Natalie et al

in Experimental and Clinical Cardiology (2002), 7(2-3), 151-7

BACKGROUND: Various molecular mechanisms are operative in altering the sarcomeric function of the heart under increased hemodynamic workload. Expression of the atrial isoform (ALC-1) of the essential ... [more ▼]

BACKGROUND: Various molecular mechanisms are operative in altering the sarcomeric function of the heart under increased hemodynamic workload. Expression of the atrial isoform (ALC-1) of the essential myosin light chain, a shift from alpha-myosin heavy chain (MHC) to beta-MHC, increased phosphorylation of the regulatory myosin light chains and increased troponin I (TnI) phosphorylation have been reported to modulate cardiac contractility in rodents. METHODS: TO ASSESS A POSSIBLE CONTRIBUTION OF THESE SARCOMERIC PROTEINS TO CARDIAC PERFORMANCE IN HUMAN MYOCARDIAL HYPERTROPHY, TWO DIFFERENT FORMS OF CARDIAC HYPERTROPHY WERE INVESTIGATED: 19 patients with hypertropic obstructive cardiomyopathy (HOCM) and 13 patients with aortic stenosis (AS) with marked left ventricular hypertrophy and normal systolic function. RESULTS: There was no change in MHC gene expression, regulatory myosin light chain or TnI phosphorylation status in normal heart (NH), HOCM and AS patients. However, patients with hypertrophied myocardium expressed ALC-1 that was not detectable in NH. ALC-1 protein expression correlated positively with the left ventricular ejection fraction. In patients with hypertrophied myocardium, there was a mean ALC-1 protein expression of 12.7+/-3% (range 3.6% to 32%). CONCLUSION: In humans, ALC-1 expression is in vivo a powerful molecular mechanism of the sarcomere to maintain or improve myocardial contractility under increased hemodynamic demands. [less ▲]

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