scholarly journals Chronic obstructive pulmonary disease is an independent predictor of death but not atherosclerotic events in patients with myocardial infarction: analysis of the Valsartan in Acute Myocardial Infarction Trial (VALIANT)

2009 ◽  
Vol 11 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Nathaniel M. Hawkins ◽  
Zhen Huang ◽  
Karen S. Pieper ◽  
Scott D. Solomon ◽  
Lars Kober ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chronic Obstructive Pulmonary Disease ◽  
Acute Myocardial Infarction ◽  
Pulmonary Disease ◽  
Independent Predictor ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Oxygen therapy in suspected acute myocardial infarction and concurrent normoxemic chronic obstructive pulmonary disease: a prespecified subgroup analysis from the DETO2X-AMI trial

2019 ◽  
Vol 9 (8) ◽  
pp. 984-992 ◽  
Author(s):  
Pontus Andell ◽  
Stefan James ◽  
Ollie Östlund ◽  
Troels Yndigegn ◽  
David Sparv ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chronic Obstructive Pulmonary Disease ◽  
Acute Myocardial Infarction ◽  
Pulmonary Disease ◽  
Subgroup Analysis ◽  
Oxygen Therapy ◽  
Ambient Air ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Suspected Acute Myocardial Infarction

Background: The DETermination of the role of Oxygen in suspected Acute Myocardial Infarction (DETO2X-AMI) trial did not find any benefit of oxygen therapy compared to ambient air in normoxemic patients with suspected acute myocardial infarction. Patients with chronic obstructive pulmonary disease may both benefit and be harmed by supplemental oxygen. Thus we evaluated the effect of routine oxygen therapy compared to ambient air in normoxemic chronic obstructive pulmonary disease patients with suspected acute myocardial infarction. Methods and results: A total of 6629 patients with suspected acute myocardial infarction were randomly assigned in the DETO2X-AMI trial to oxygen or ambient air. In the oxygen group ( n=3311) and the ambient air group ( n=3318), 155 and 141 patients, respectively, had chronic obstructive pulmonary disease (prevalence of 4.5%). Patients with chronic obstructive pulmonary disease were older, had more comorbid conditions and experienced a twofold higher risk of death at one year (chronic obstructive pulmonary disease: 32/296 (10.8%) vs. non-chronic obstructive pulmonary disease: 302/6333 (4.8%)). Oxygen therapy compared to ambient air was not associated with improved outcomes at 365 days (chronic obstructive pulmonary disease: all-cause mortality hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.50–1.99, Pinteraction=0.96); cardiovascular death HR 0.80, 95% CI 0.32–2.04, Pinteraction=0.59); rehospitalisation with acute myocardial infarction or death HR 1.27, 95% CI 0.71–2.28, Pinteraction=0.46); hospitalisation for heart failure or death HR 1.08, 95% CI 0.61–1.91, Pinteraction=0.77]); there were no significant treatment-by-chronic obstructive pulmonary disease interactions. Conclusions: Although chronic obstructive pulmonary disease patients had twice the mortality rate compared to non-chronic obstructive pulmonary disease patients, this prespecified subgroup analysis from the DETO2X-AMI trial on oxygen therapy versus ambient air in normoxemic chronic obstructive pulmonary disease patients with suspected acute myocardial infarction revealed no evidence for benefit of routine oxygen therapy consistent with the main trial’s findings. Clinical Trials Registration: NCT02290080

scholarly journals Identification of Common Mechanisms and Key Genes in the Chronic Obstructive Pulmonary Disease and Acute Myocardial Infarction

2021 ◽  
Author(s):  
Fengshou Chen ◽  
Haijia Hou ◽  
Bing Tang
Keyword(s):  
Myocardial Infarction ◽  
Chronic Obstructive Pulmonary Disease ◽  
Acute Myocardial Infarction ◽  
Pulmonary Disease ◽  
Signaling Pathway ◽  
Chronic Obstructive ◽  
Biological Processes ◽  
Hub Genes ◽  
Obstructive Pulmonary Disease ◽  
The Relationship

Abstract Background: Chronic obstructive pulmonary disease (COPD) and acute myocardial infarction (AMI) have a strong association. We aimed to study the relationships between COPD and AMI, and reveal potential therapeutic targets and biomarkers. Materials and methods: The dataset GSE38974 and GSE60993 were downloaded from the Gene Expression Omnibus (GEO) database to analyze the intersections among differentially expressed genes (DEGs). Common DEGs were identified and performed functional enrichment analyses. The hub genes were obtained based on the protein-protein interaction (PPI) network by cytoHubba in Cytoscape software. The receiver operator characteristic (ROC) curve analysis was applied to identify the diagnosis efficacy of hub genes. The relationship between hub genes and these two diseases in the CTD database were validated. Finally, the transcription factors (TFs) corresponding to hub genes were also analyzed. Results: In our study, sixty-five common DEGs were obtained in COPD and AMI. GO enrichment analysis indicated that inflammation or apoptotic biological processes are significant enriched biological processes. Common DEGs were mostly enriched in pathways including apoptosis, HIF-1 signaling pathway, TNF signaling pathway, and cytokine-cytokine receptor interaction. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes. Furthermore, we found that the expression of hub genes was significantly associated with a diagnosis efficacy of COPD and AMI. We also validated the relationship between the hub genes and these two diseases in the CTD database. We also found that ELK1, ETV4, STAT3 and TFAP2A were significant TFs, which interacted with the hub genes. Conclusion: In conclusion, our study revealed the communal DEGs and related mechanisms between the pathophysiology of COPD and AMI. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes that are associated with COPD and AMI. Our study provides new ideas and evidence for further exploration of the mechanisms and treatment of COPD and AMI.

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