AI Summary & Key Takeaways
AI InsightAccording to our findings, the decreased U-II and NKB levels were related to complicated atherosclerotic events.
📌 3 Key Takeaways
Abstract
Objective: This aim of the study is to investigate whether there are possible plasma urotensin-II (U-II) and neurokinin B (NKB) level changes in patients with acute myocardial infarction (AMI) or not and plasma urotensin-II (U-II) and neurokinin B (NKB) level changes in patients with acute myocardial infarction (AMI) and stable coronary artery disease (CAD) and to evaluate whether there is any relationship between these changes and the pathogenesis of these diseases. Methods: This is a prospective case-control study. Three groups were formed from randomly admitted patients with AMI, stable CAD, and controls. Biochemical parameters and U-II and NKB levels were measured. Patients with congestive heart failure, chronic hepatic and renal failure, severe cardiac valve disease, and severe pulmonary hypertension were excluded from the study. The normality of the data was evaluated using the Kolmogorov-Smirnov test. We compared the three groups with one-way ANOVA and Tukey test (Kruskal-Wallis test and Mann-Whitney U test). Results: Compared with controls (n=31) and CAD patients (n=32), AMI patients (n=32) had lower U-II and NKB levels. In cases of stable CAD, U-II and NKB levels were similar. A positive correlation was found between U-II and NKB (r=0.720; p=0.000). U-II and NKB were poorly correlated with left ventricle ejection fraction but not with C-reactive protein. Conclusion: We found that U-II and NKB levels were lower in patients with AMİ in than those with CAD or the control group. According to our findings, the decreased U-II and NKB levels were related to complicated atherosclerotic events.