Background:
Glucagon-like peptide 1 (GLP1) analogues are promising new treatment options for patients with type 2 diabetes, but may have both potentially beneficial and harmful cardiovascular effects. This may also be the case for the analogues of GLP1 for clinical use. The present study examined the effect of treatment with Liraglutide, a long-acting GLP1 analogue, on myocardial ischemia and reperfusion in a porcine model.
Methods:
Danish Landrace Pigs (70-80 kg) were randomly assigned to Liraglutide (10 g/kg) or control treatment given daily for three days before ischemia-reperfusion. Ischemia was induced by balloon occlusion of the left anterior descending artery for 40 minutes followed by 2.5 hours of reperfusion. The primary outcome parameter was infarct size in relation to the ischemic region at risk. Secondary endpoints were the hemodynamic parameters mean pulmonary pressure, cardiac output, pulmonary capillary wedge pressure as measured by a Swan-Ganz catheter as well as arterial pressure and heart rate
Results:
The infarct size in relation to ischemic risk region in the control versus the Liraglutide group did not differ significantly: 0.46 (0.14) and 0.54 (0.12) (mean and standard deviation (SD), p=0.21]. Heart rate was significantly higher in the Liraglutide group during the experiment, while the other hemodynamic parameters did not differ significantly.
Conclusion:
Liraglutide has a neutral effect on myocardial infarct size in a porcine ischemia-reperfusion model.

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Background:
The impact of reducing door-to-balloon time on hospital revenues, costs, and net income is unknown.
Methods:
We prospectively determined the impact on hospital finances of (1) emergency department physician activation of the catheterization lab and (2) immediate transfer of the patient to an immediately available catheterization lab by an in-house transfer team consisting of an emergency department nurse, a critical care unit nurse, and a chest pain unit nurse. We collected financial data for 52 consecutive ST-elevation myocardial infarction (STEMI) patients undergoing emergency percutaneous intervention from October 1, 2004-August 31, 2005 and compared this group to 80 consecutive STEMI patients from September 1, 2005-June 26, 2006 after protocol implementation.
Results:
Per hospital admission, insurance payments (hospital revenue) decreased ($35,043+/-$36,670 vs. $25,329+/-$16,185, P=0.039) along with total hospital costs ($28,082+/-$31,453 vs. $18,195+/-$9,242, P=0.009). Hospital net income per admission was unchanged ($6962 vs. $7134, P=0.95) as the drop in hospital revenue equaled the drop in costs. For every $1000 reduction in total hospital costs, insurance payments (hospital revenue) dropped $1077 for private payers and $1199 for Medicare/Medicaid. A decrease in hospital charges ($70,430+/-$74,033 vs. $53,514+/-$23,378, P=0.059), diagnosis related group relative weight (3.7479+/-2.6731 vs. 2.9729+/-0.8545, P=0.017) and outlier payments with hospital revenue>$100,000 (7.7% vs. 0%, P=0.022) all contributed to decreasing STEMI hospitalization revenue. One-year post-discharge financial follow-up revealed similar results: Insurance payments: $49,959+/-$53,741 vs. $35,937+/-$23,125, P=0.044; Total hospital costs: $39,974+/-$37,434 vs. $26,778+/-$15,561, P=0.007; Net Income: $9984 vs. $9159, P=0.855.
Conclusions:
All of the financial benefits of reducing door-to-balloon time in STEMI go to payers both during initial hospitalization and after one-year follow-up.ClinicalTrials.gov ID: NCT00800163

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Background:
In Brazil, heart failure leads to approximately 25,000 deaths per year. Abnormal calcium handling is a hallmark of heart failure and changes in genes encoding for proteins involved in the re-uptake of calcium might harbor mutations leading to inherited cardiomyopathies. Phospholamban (PLN) plays a prime role in cardiac contractility and relaxation and mutations in the gene encoding PLN have been associated with dilated cardiomyopathy. In this study, our objective was to determine the presence of the -36A>C alteration in PLN gene in a Brazilian population of individuals with HF and to test whether this alteration is associated with heart failure or with a worse prognosis of patients with HF.
Methods:
We genotyped a cohort of 881 patients with HF and 1259 individuals from a cohort of individuals from the general population for the alteration -36A>C in the PLN gene. Allele and genotype frequencies were compared between groups (patients and control). In addition, frequencies or mean values of different phenotypes associated with cardiovascular disease were compared between genotypic groups. Finally, patients were prospectively followed-up for death incidence and genotypes for the -36A>C were compared regarding mortality incidence in HF patients.
Results:
No significant association was found between the study polymorphism and HF in our population. In addition, no association between PLN -36A>C polymorphism and demographic, clinical and functional characteristics and mortality incidence in this sample of HF patients was observed.
Conclusion:
Our data do not support a role for the PLN -36A>C alteration in modulating the heart failure phenotype, including its clinical course, in humans.

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Background:
We assessed the degree to which differences in guideline-based medical therapy for acute myocardial infarction (AMI) contribute to the higher mortality associated with kidney disease.
Methods:
In the PREMIER registry, we evaluated patients from 19 US centers surviving AMI. Cox regression evaluated the association between estimated glomerular filtration rate (GFR) and time to death over two years, adjusting for demographic and clinical variables. The contribution of variation in guideline-based medical therapy to differences in mortality was then assessed by evaluating the incremental change in the hazard ratios after further adjustment for therapy.
Results:
Of 2426 patients, 26% had GFR ? 90, 44% had GFR = 60- < 90, 22% had GFR = 30- < 60, and 8% had GFR < 30 ml/min/1.73 m2. Greater degrees of renal dysfunction were associated with greater 2-year mortality and lower rates of guideline-based therapy among eligible patients. For patients with severely decreased GFR, adjustment for differences in guideline-based therapy did not significantly attenuate the relationship with mortality (HR 3.82, 95% CI 2.39–6.11 partially adjusted; HR = 3.90, 95% CI 2.42–6.28 after adjustment for treatment differences).
Conclusion:
Higher mortality associated with reduced GFR after AMI is not accounted for by differences in treatment factors, underscoring the need for novel therapies specifically targeting the pathophysiological abnormalities associated with kidney dysfunction to improve survival.

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