Document Type : Original Article
Authors
1 Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
2 Gastroenterology and Hepatology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
3 Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
4 Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
Abstract
Introduction: Apelin is a cardioprotective peptide, and opium addiction is prevalent in some regions; both are implicated in cardiovascular disease pathogenesis. However, their interaction in the context of coronary artery disease (CAD) is not fully understood. This study evaluated the relationship between opium addiction and serum apelin concentration in patients with stable angina.
Methods: We enrolled 228 participants in this cross-sectional study and assigned to four matched groups: non-addicts, addicts, angina non-addicts, and angina addicts (57 per group). Opium addiction was confirmed based on DSM-IV criteria. We measured serum apelin concentrations using a specific ELISA kit and gathered demographic, cardiovascular risk factor, and angiographic data from the participants.
Results: The prevalence of hyperlipidemia, diabetes, family history of CAD, and smoking was significantly higher in the angina groups compared to the healthy groups (all p<0.01). Serum apelin levels differed significantly among the four groups (p=0.027). Apelin was significantly higher in Healthy non-addicts compared to Angina non-addicts (p=0.012), and interestingly, higher in Angina addicts compared to Angina non-addicts (p=0.013). No significant correlation was found between apelin levels and the number of diseased coronary vessels, age, or blood pressure.
Conclusion: The findings suggest a complex relationship between opium addiction and the apelin system in CAD. The relative elevation of apelin in addicted angina patients could speculatively be interpreted as a possible compensatory‑like pattern, but this remains a hypothesis that requires direct experimental testing. Other non‑compensatory explanations, such as altered apelin clearance or receptor signaling, are equally plausible.
Highlights
Masoome Kahnooji (Google Scholar)
Hamidreza Nasri (Google Scholar)
Beydolah Shahouzehi (Google Scholar)
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