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Updated: Aug 30, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
The role of inflammation markers in triggering acute coronary events
Mehmet Tokaç1, Ali Ozeren, Murad Aktan
1Cardiology Department, School of Medicine, Selcuk University, Konya, Turkey. mehmettokac@hotmail.com
Insights
Inflammatory markers like C-reactive protein (CRP) and interleukin-2 (IL-2) are implicated in acute coronary events. Their levels change during unstable angina and after percutaneous coronary intervention, affecting plaque instability.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biochemistry
Background:
- Plasma concentrations of inflammation markers show varied results in acute coronary syndromes.
- The primary vs. secondary alterations of these markers in response to acute coronary syndromes remain unclear.
Purpose of the Study:
- To investigate the effect of soluble cell adhesion molecules and inflammatory markers on coronary plaque instability.
- To analyze changes in specific markers during different stages of coronary artery disease and interventions.
Main Methods:
- Prospective study involving patients with stable angina pectoris (SAP), unstable angina pectoris (UAP), and post-percutaneous transluminal coronary angioplasty (PTCA).
- Blood samples collected at various time points: admission for SAP, within 6h and 12h for UAP, and pre-, 2h-, and 14h-post-PTCA.
- Enzyme-linked immunosorbent assay (ELISA) used to analyze soluble vascular cell adhesion molecule-1 (VCAM-1), endothelial selectin, interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), and C-reactive protein (CRP).
Main Results:
- C-reactive protein (CRP) serum levels increased, while interleukin-2 (IL-2) levels decreased in UAP and PTCA patients.
- Soluble vascular cell adhesion molecule-1 (VCAM-1) levels decreased post-PTCA but returned to baseline by 14 hours.
- Both CRP and IL-2 were found to be directly involved in triggering acute coronary events.
Conclusions:
- CRP and IL-2 play a direct role in the mechanisms triggering acute coronary events.
- Changes in inflammatory markers and cell adhesion molecules provide insights into coronary plaque instability.
- Further research is needed to clarify the precise roles and interactions of these markers in acute coronary syndromes.
Abstract:
Studies have shown disparate results in relation to the role of plasma concentrations of inflammation markers such as fibrinogen, cytokines, and cell adhesion molecules in acute coronary syndromes. The differentiation of primary versus secondary alterations of these markers in response to acute coronary syndromes is not clear. The aim of this study was to investigate the effect of soluble cell adhesion molecules and some inflammatory markers on coronary plaque instability. The prospective study consisted of 15 patients with stable angina pectoris (SAP), 16 with unstable angina pectoris (UAP), and 16 who had undergone percutaneous transluminal coronary angioplasty (PTCA). Blood samples were obtained from the SAP group on admission, from the UAP group at the early stage of pain onset within 6 h of pain, and again after 12 h of pain. Samples from the PTCA group were collected before, 2, 14 h after the procedure. Soluble vascular cell adhesion molecule-1 (VCAM-1), endothelial selectin, interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), and C-reactive protein (CRP) were analyzed by enzyme-linked immunosorbent assay. CRP serum levels gradually increased although IL-2 gradually decreased in patients with UAP and PTCA. In addition, VCAM-1 levels were sharply decreased after the PTCA procedure. However, this value returned back to the preprocedure levels 14 h after PTCA. Both CRP and IL-2 are directly involved in the triggering mechanisms of acute coronary events.
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