Abstract
Aim: To determine the discriminative potency of score to prognosticate poor clinical outcomes in ST-Segment Elevation Myocardial Infarction (STEMI) patients. Methods: From the entire population of STEMI (n=268), we enrolled 177 individuals with acute STEMI who underwent complete revascularization with primary Percutaneous Coronary Intervention (PCI). Clinical assessment, echocardiography, Doppler, and biomarkers’ measure were performed at baseline. Results: Combined endpoint (Major Cardiovascular Events - MACEs [composite of cardiovascular death, recurrent myocardial infarction, newly diagnosed Heart Failure] and hospitalization) was determined in 75 patients with acute STEMI population (40.6%). Newly onset heart failure (HF) was reported in 46 patients (26.0%), Cardiovascular (CV) death occurred in 12 patients (6.8%), MACEs were determined in 58 patients (32.8%), and recurrent hospitalization due to CV reasons was found in 17 (9.6%). The conventional risk predictive models were engineered by a combination of TIMI risk score +acute HF Killip class ≥ II + the levels of NT-pro brain natriuretic peptide > 300 pg / mL and troponin >0.05 ng/mL. We developed a new predictive model based on the presentation of T786С genotype of endothelial NO syntase gene (rs 2070744), А1166С in angiotensin-ІІ receptor-1 gene (rs5186) and serum levels of soluble suppressor tumorigenicity ≥35 pg/mL, vascular endothelial growth factor ≤172 pg/mL and macrophage inhibitory factor ≥2792.7 pg/mL. STEMI patients who had >5 score points demonstrated significantly worse prognosis than those who had ≤5 score points. Conclusion: Here we have reported that a new original predictive model is better than a conventional model in discriminative ability to predict combined clinical outcome in STEMI patients.
Highlights
Onset heart failure was reported in 46 patients (26.0%), CV death occurred in 12 patients (6.8%), MACEs were determined in 58 patients (32.8%), and recurrent hospitalization due to CV reasons was found in 17 (9.6%)
Patients who met combined clinical outcomes did not differ from those who had no clinical outcomes in average age, gender, CV risk factors, and hemodynamics except left atrial volume (P=0.021), left atrial dimension (P=0.045), and E/eratio (P=0.042)
Using Receiver Operating Characteristic (ROC) analysis, we found that circulating levels of Macrophage Inhibitory Factor-1 (MIF)≥2792.7 pg/mL, VEGF >123 pg/mL, suppressor tumorigenicity-2 (sST2) ≥35 pg/mL, as well as SYNTAX score > 32 points, and TIMI score > 6 points were optimal having balanced sensitivity and specificity to predict combined clinical endpoint (Fig. 3)
Summary
A wide range of evidence supports that microvascular inflammation and small coronary artery occlusion after PCI are the most probable reasons for postSTEMI cardiac remodeling and one-year mortality [4 - 6]. Several studies have assessed the combination of circulating biological markers (i.e., troponin T and -I, soluble Suppressor Tumorigenicity-2 (sST2), natriuretic peptides, galectin-3, metalloproteinases, growth / differential factor-15, proadrenomedullin, Macrophage Inhibitory Factor-1 (MIF), C-reactive protein, creatinine, lipid profile) with multiple markers risk score for STEMI prognostication [11 13]. Previous studies have unleashed that numerous genetic biomarkers (Single Nucleotide Polymorphism (SNP) in the promoter region of endothelial NO synthase, aldosterone synthase (CYP11B2), and angiotensin-II receptor-1 genes, SNP Val66Met in Brain-Derived Neurotrophic Factor BDNF gene, SNP Lys198Asn in endothelin [EDN]-1 gene, Vascular Endothelial Growth Factor (VEGF) gene) well corresponded to post-STEMI adverse cardiac remodeling, early stent thrombosis, restenosis, microvascular obstruction and noreflow phenomenon after PCI [14 - 18]
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