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Published on: January 28, 2020
Postmortem Alteration of Purine Metabolism in Coronary Artery Disease
Phakchira Somtua1,2, Churdsak Jaikang1,2, Giatgong Konguthaithip1,2
1Department of Forensic Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Insights
Investigating blood purine metabolites in deceased individuals with coronary artery disease (CAD) revealed significant changes. Decreased xanthine levels may help predict CAD as a cause of death, even in advanced decomposition.
Area of Science:
- Biochemistry
- Forensic Pathology
- Cardiovascular Science
Background:
- Coronary Artery Disease (CAD) diagnosis postmortem is challenging without full autopsy.
- The purine pathway's role in postmortem changes related to CAD requires further investigation.
Purpose of the Study:
- To explore alterations in blood purine metabolite levels in deceased individuals with CAD.
- To identify potential biomarkers for CAD as a cause of death in postmortem settings.
Main Methods:
- Heart blood samples from 60 individuals (23 CAD, 37 controls) were analyzed.
- Proton nuclear magnetic resonance (NMR) spectroscopy was used to measure purine metabolites.
Main Results:
- Significant decreases in Guanosine triphosphate (GTP), nicotinamide adenine dinucleotide (NAD), and xanthine were observed in the CAD group.
- Significant increases in adenine and deoxyribose 5-phosphate were found in the CAD group compared to controls.
- Decreasing xanthine levels showed potential as a predictive marker for CAD cause of death (AUC = 0.7).
Conclusions:
- Postmortem physiological processes disrupt the purine pathway, altering metabolite levels compared to living individuals.
- Xanthine warrants further study as a potential biomarker for diagnosing CAD in cases of decomposition and skeletonization.
Abstract:
A new approach for assisting in the diagnosis of coronary artery disease (CAD) as a cause of death is essential in cases where complete autopsy examinations are not feasible. The purine pathway has been associated with CAD patients, but the understanding of this pathway in postmortem changes needs to be explored. This study investigated the levels of blood purine metabolites in CAD after death. Heart blood samples (n = 60) were collected and divided into CAD (n = 23) and control groups (n = 37). Purine metabolites were measured via proton nuclear magnetic resonance. Guanosine triphosphate (GTP), nicotinamide adenine dinucleotide (NAD), and xanthine levels significantly decreased (p < 0.05); conversely, adenine and deoxyribose 5-phosphate levels significantly increased (p < 0.05) in the CAD group compared to the control group. Decreasing xanthine levels may serve as a marker for predicting the cause of death in CAD (AUC = 0.7). Our findings suggest that the purine pathway was interrupted by physiological processes after death, causing the metabolism of the deceased to differ from that of the living. Additionally, xanthine levels should be studied further to better understand their relationship with CAD and used as a biomarker for CAD diagnosis under decomposition and skeletonization settings.
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