Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction
N T Mulvihill1, J B Foley, R Murphy
1Royal City of Dublin Hospital Research and Education Institute, Department of Cardiology, St. James's Hospital, Ireland.
Insights
Inflammation markers, specifically soluble cell adhesion molecules (CAMs), remain elevated for six months after unstable angina (UA) and non-Q wave myocardial infarction (NQMI), then decrease. This indicates a sustained inflammatory response post-acute coronary events.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarkers
Background:
- Coronary plaque inflammation is central to acute coronary syndromes (ACS).
- Cell adhesion molecules (CAMs) are key inflammatory mediators in ACS.
- Soluble CAMs are elevated in unstable angina (UA) and non-Q wave myocardial infarction (NQMI).
Purpose of the Study:
- To quantify the inflammatory response up to one year post-UA and NQMI.
- To assess the expression of soluble cell adhesion molecules (CAMs) as inflammatory markers.
Main Methods:
- Serum samples collected from 91 UA/NQMI patients and 24 controls at baseline, 3, 6, and 12 months.
- Quantification of soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-selectin, and platelet-selectin using ELISA.
- Comparison of CAM levels between patient groups and controls.
Main Results:
- All four soluble CAMs were significantly elevated in UA and NQMI patients versus controls at presentation, 3, and 6 months.
- CAM levels in UA and NQMI patients decreased significantly between 6 and 12 months post-presentation.
- Study included 91 patients (56 UA, 35 NQMI) and 24 controls.
Conclusions:
- The inflammatory process, indicated by CAM expression, persists for up to six months after UA or NQMI.
- CAM levels gradually return towards control values in the subsequent six months.
- Sustained inflammation up to six months is a key feature following UA and NQMI.
Objectives:
This study was designed to document the inflammatory response up to one year after acute presentation with unstable angina (UA) and non-Q wave infarction (NQMI) as reflected by the expression of soluble cell adhesion molecules (CAMs).
Background:
Coronary plaque inflammation is a key component in the pathogenesis of acute coronary syndromes. Cell adhesion molecules are critical mediators of the inflammatory process. Soluble forms of these molecules are detectable in serum and are elevated acutely in patients with UA and NQMI.
Methods:
Patients presenting with UA and NQMI had serum samples taken at presentation and then after three, six and 12 months. A control group of similar age and gender distribution was used for comparison. Levels of soluble inter-cellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-selectin and platelet-selectin were measured using an ELISA technique.
Results:
We studied 91 patients (M/F = 73/18, mean age 62 +/- 11 years, 56 UA and 35 NQMI) and 24 controls (M/F = 18/6, mean age 56 +/- 12 years). Levels of all four soluble CAMs were significantly elevated in both UA and NQMI patients at presentation, three and six months in comparison with controls. Levels in UA and NQMI groups fell between six and 12 months after initial presentation.
Conclusions:
The results suggest that the inflammatory stimulus triggering expression of CAMs is sustained for up to six months after presentation with either UA or NQMI and then returns toward control values over the following six months.
Related Concept Videos
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
01:30Acute Coronary Syndrome III: Diagnostic Studies
01:29Angina III: Clinical Manifestations and Assessment
01:30Acute Coronary Syndrome I: Introduction
01:21Myocarditis I: Introduction
01:27Myocarditis II: Clinical Features and Diagnostic Tests