Dataset Information

Does Higher Spending Improve Survival Outcomes for Myocardial Infarction? Examining the Cost-Outcomes Relationship Using Time-Varying Covariates.

ABSTRACT:

Objectives

Previous patient-level acute myocardial infarction (AMI) research has found higher hospital spending to be associated with improved survival; however, survivor-treatment selection bias traditionally has been overlooked. The purpose of this study was to examine the AMI cost-outcome relationship, taking into account this form of bias.

Data sources

Hospital Discharge Abstract data tracked costs for AMI hospitalizations. Ontario Vital Statistics data tracked patient mortality.

Study design

A standard Cox survival model was compared to an extended Cox model using hospital costs as a time-varying covariate to examine the impact of cost on 1-year survival in a cohort of 30,939 first-time AMI patients in Ontario, Canada, from 2007 to 2010.

Principal findings

Higher patient-level AMI spending decreased the hazard of dying (Standard Model: log-cost hazard ratio: 0.513, 95 percent CI: 0.479-0.549; Extended Model: log-cost hazard ratio: 0.700, 95 percent CI: 0.645-0.758); however, the protective effect was overestimated by 62 percent when survivor-treatment bias was overlooked. In the extended model, a 10 percent increase in spending was associated with a 3.6 percent decrease in hazard of death.

Conclusion

The findings of this study suggest that if survivor-treatment bias is overlooked, future research may materially overstate the protective effect of patient-level spending on outcomes.

SUBMITTER: Cohen D

PROVIDER: S-EPMC4600363 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Publications

Does Higher Spending Improve Survival Outcomes for Myocardial Infarction? Examining the Cost-Outcomes Relationship Using Time-Varying Covariates.

Cohen Deborah D Manuel Douglas G DG Tugwell Peter P Sanmartin Claudia C Ramsay Tim T

Health services research 20150209 5

<h4>Objectives</h4>Previous patient-level acute myocardial infarction (AMI) research has found higher hospital spending to be associated with improved survival; however, survivor-treatment selection bias traditionally has been overlooked. The purpose of this study was to examine the AMI cost-outcome relationship, taking into account this form of bias.<h4>Data sources</h4>Hospital Discharge Abstract data tracked costs for AMI hospitalizations. Ontario Vital Statistics data tracked patient mortali ...[more]

PMID: 25664611

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Project description:Aim:The acute phase of myocardial infarction (MI) is accompanied by edema contributing to tissue damage and disease outcome. Here, we aimed to identify the mechanism whereby vascular endothelial growth factor (VEGF)-A induces myocardial edema in the acute phase of MI to eventually promote development of therapeutics to specifically suppress VEGFA-regulated vascular permeability while preserving collateral vessel formation. Methods and Results:VEGFA regulates vascular permeability and edema by activation of VEGF receptor-2 (VEGFR2), leading to induction of several signaling pathways including the cytoplasmic tyrosine kinase c-Src. The activated c-Src in turn phosphorylates vascular endothelial (VE)-cadherin, leading to dissociation of endothelial adherens junctions. A particular tyrosine at position 949 in mouse VEGFR2 has been shown to be required for activation of c-Src. Wild-type mice and mice with phenylalanine replacing tyrosine (Y) 949 in VEGFR2 (Vegfr2 Y949F/Y949F ) were challenged with MI through permanent ligation of the left anterior descending coronary artery. The infarct size was similar in wild-type and mutant mice, but left ventricular wall edema and fibrinogen deposition, indicative of vascular leakage, were reduced in the Vegfr2 Y949F/Y949F strain. When challenged with large infarcts, the Vegfr2 Y949F/Y949F mice survived significantly better than the wild-type strain. Moreover, neutrophil infiltration and levels of myeloperoxidase were low in the infarcted Vegfr2 Y949F/Y949F hearts, correlating with improved survival. In vivo tyrosine phosphorylation of VE-cadherin at Y685, implicated in regulation of vascular permeability, was induced by circulating VEGFA in the wild-type but remained at baseline levels in the Vegfr2 Y949F/Y949F hearts. Conclusion:Suppression of VEGFA/VEGFR2-regulated vascular permeability leads to diminished edema without affecting vascular density correlating with improved myocardial parameters and survival after MI.

Dataset Information

Does Higher Spending Improve Survival Outcomes for Myocardial Infarction? Examining the Cost-Outcomes Relationship Using Time-Varying Covariates.

Objectives

Data sources

Study design

Principal findings

Conclusion

Publications

Does Higher Spending Improve Survival Outcomes for Myocardial Infarction? Examining the Cost-Outcomes Relationship Using Time-Varying Covariates.

Similar Datasets

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