TNF-α is a Novel Biomarker for Predicting Plaque Rupture in Patients with ST-Segment Elevation Myocardial Infarction

Abstract

Background and Aims Patients with plaque rupture (PR) present with different cardiovascular risks, clinical strategies, and outcomes from those with plaque erosion (PE). However, there are lack of noninvasive biomarkers to distinguish PE from PR. Methods A prospective analysis of 382 patients with ST-segment elevation myocardial infarction (STEMI) was conducted. Of these patients, 262 and 120 presented with PR and PE, respectively. An additional 83 patients diagnosed with stable angina pectoris were enrolled as control group. Peripheral blood monocytes were collected pre-percutaneous coronary intervention and used to evaluate the mRNA expression of IL-4 , IL-10 , IL-1β , and TNF-α in all patients. Results STEMI patients had higher IL-4 , IL-10 , IL-1β , and TNF-α expression than the control patients. The mRNA levels of IL-4 , IL-1β , and TNF-α were significantly higher in PR patients than PE; however, no significant difference was observed in IL-10 between PE and PR. The areas under the receiver-operating characteristic curves for IL-4 , IL-1β , and TNF-α for PR versus PE were 0.685, 0.747, and 0.895, respectively. At the cut-off value of 2.52, TNF-α demonstrated a sensitivity of 70.61% and specificity of 93.33% for discriminating PR from PE patients. When added to the model of established clinical risk factors, TNF-α significantly improved the predictive accuracy of PR. Multivariable logistic regression analysis indicated that TNF-α mRNA level was independently associated with PR (odds ratio, 3.09; 95% confidence interval, 2.29–4.16; p < 0.001). Conclusion The inflammatory response of peripheral blood mononuclear cells in patients with PR was higher than that in patients with PE. TNF-α may be a potential biomarker for predicting PR that could facilitate risk stratification and management in STEMI patients.

The abnormal level and prognostic potency of multiple inflammatory cytokines in PCI‐treated STEMI patients

“…20 Another study discloses the high level of TNFα, IL-10, IL-4, and IL-1β in STEMI patients compared with the controls. 19 Partially in line with the previous studies, this study displayed that TNFα, IL-8, IL-17A, and VCAM-1 level was elevated in STEMI patients compared to angina pectoris patients. The possible explanation was listed as follows: TNFα, IL-8, IL-17A, and VCAM-1 were all proinflammatory cytokines, which accelerated endothelial dysfunction and increased atherosclerotic plaque burden.…”

“…When vascular walls are exposed to a proinflammation environment, the recruitment and accumulation of leukocytes are enhanced, which further promotes endothelial injury and the formation of thrombosis 17 . Subsequently, considering the essential role of inflammation in the pathogenesis of STEMI, the previous studies notice the abnormal level of several inflammatory cytokines in STEMI patients 18–21 . For instance, one previous study observes that serum TNF‐α and IL‐6 are beyond the normal range in STEMI patients who undergo PCI treatment 20 .…”

“…For instance, one previous study observes that serum TNF‐α and IL‐6 are beyond the normal range in STEMI patients who undergo PCI treatment 20 . Another study discloses the high level of TNF‐α, IL‐10, IL‐4, and IL‐1β in STEMI patients compared with the controls 19 . Partially in line with the previous studies, this study displayed that TNF‐α, IL‐8, IL‐17A, and VCAM‐1 level was elevated in STEMI patients compared to angina pectoris patients.…”

“… 17 Subsequently, considering the essential role of inflammation in the pathogenesis of STEMI, the previous studies notice the abnormal level of several inflammatory cytokines in STEMI patients. 18 , 19 , 20 , 21 For instance, one previous study observes that serum TNF‐α and IL‐6 are beyond the normal range in STEMI patients who undergo PCI treatment. 20 Another study discloses the high level of TNF‐α, IL‐10, IL‐4, and IL‐1β in STEMI patients compared with the controls.…”

Uncovering the Genetic Link between Acute Myocardial Infarction and Ulcerative Colitis Co-Morbidity through a Systems Biology Approach

“…TNF acts as a pleiotropic cytokine, which directly induces the expression of inflammation-associated genes, induces cell death, and indirectly drives inflammation and immune responses [57]. Luo et al [58] have proposed TNF-α as a novel biomarker for predicting plaque rupture in patients with ST-elevation myocardial infarction. Thus, inhibition of TNF-α may decrease the inflammatory load of the body and stabilize plaques, particularly in people with multiple inflammatory diseases.…”