Key result
Higher admission nesfatin-1 linked to ~19% lower odds of angiographic no-reflow during STEMI PCI.
Why the study?
No-reflow is a poor prognostic indicator in STEMI patients undergoing pPCI, and the relationship between admission serum nesfatin-1, no-reflow, and coronary artery disease complexity was unknown.
Does admission serum nesfatin-1 level predict angiographic no-reflow and correlate with CAD complexity in STEMI patients undergoing pPCI?
Observational (n=252)
Does admission serum nesfatin-1 level predict angiographic no-reflow and correlate with CAD complexity in STEMI patients undergoing pPCI?
Effect estimate: OR 0.81 (95% CI 0.708-0.936)
p-value: p=0.004
Lower admission serum nesfatin-1 levels independently predict angiographic no-reflow and correlate with greater CAD complexity in STEMI patients undergoing primary PCI.
May aid no-reflow risk stratification in STEMI; hypothesis-generating and requires validation before clinical use.
BACKGROUND: Nesfatin-1 is a novel peptide possessing pleiotropic metabolic effects. No-reflow phenomenon (NR) is a poor prognostic indicator occurring in around 30% of all patients undergoing primary percutaneous coronary interventions (pPCI). Inflammation and complexity of coronary artery disease (CAD) play pivotal roles in the pathogenesis of NR. In this study, we investigated the relationship between admission serum nesfatin-1 level, NR and complexity of CAD assessed by SYNTAX-1 (SS-1) and SYNTAX-2 (SS-2) scores in patients with ST-segment elevation myocardial infarction (STEMI) undergoing pPCI. METHODS: A total of 174 STEMI patients who underwent pPCI were included in the study and divided into NR (n = 36) and normal flow (n = 138) groups. Serum nesfatin-1 was measured by enzyme-linked immunosorbent assay. Seventy-eight consecutive age-, gender- and co-morbidity-matched patients undergoing coronary angiography with < 50% stenosis comprised the control group. RESULTS: Nesfatin-1 levels were significantly lower in the NR group compared to the normal flow and control groups (10.8 ± 6.6 ng/mL vs. 34.9 ± 24 ng/mL vs. 43.6 ± 23.2 ng/mL, respectively, p < 0.001). Nesfatin-1 was significantly and inversely correlated with SS-1 and SS-2 scores (r = -0.709 and r = -0.655, respectively, both p < 0.001). Multivariate logistic regression analysis showed that nesfatin-1 [odds ratio (OR) = 0.81, 95% confidence interval (CI) = 0.708-0.936, p = 0.004] and glomerular filtration rate (OR = 0.94, 95% CI = 0.892-0.989, p = 0.018) were independently associated with NR. In the receiver operating characteristic analysis, nesfatin-1 < 15.21 ng/mL predicted NR with 78.4% sensitivity and 72.2% specificity (area under the curve = 0.809, 95% CI = 0.701-0.918, p < 0.001). CONCLUSIONS: Admission nesfatin-1 level is a potent predictor of NR in STEMI patients undergoing pPCI. Additionally, nesfatin-1 has a robust and negative correlation with the complexity of CAD.
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Sivri et al. (2020) conducted an observational in ST-Segment Elevation Myocardial Infarction (n=252). Admission serum nesfatin-1 level was evaluated on Angiographic no-reflow (OR 0.81, 95% CI 0.708-0.936, p=0.004). Lower admission serum nesfatin-1 levels independently predicted angiographic no-reflow in STEMI patients undergoing primary PCI (OR 0.81; 95% CI 0.708-0.936; p=0.004).
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