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Patients with acute coronary syndromes express enhanced CD40 ligand/CD154 on platelets
C D Garlichs1, S Eskafi, D Raaz
1Medical Clinic II, Friedrich-Alexander University Erlangen-Nürnberg, Ostliche Stadmauerstrasser 29, 91054 Erlangen, Germany. christoph.garlichs@rzmail.uni-erlangen.de
Insights
Platelet CD40L/CD154 and soluble CD40L/CD154 are elevated in acute coronary syndromes like myocardial infarction and unstable angina. These findings suggest CD40-CD40L/CD154 interactions contribute to the development of these inflammatory cardiovascular conditions.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Platelet Biology
Background:
- Acute coronary syndromes (ACS) involve inflammatory processes.
- The role of CD40 ligand (CD40L/CD154) in platelet activation and inflammation within ACS is not fully understood.
Purpose of the Study:
- To investigate the expression of CD40L/CD154 on platelets and its soluble form in patients with ACS.
- To determine if CD40L/CD154 plays a role in the inflammatory pathway of ACS.
Main Methods:
- Observational study conducted in a university hospital.
- Analysis of platelet CD40L/CD154 expression and serum soluble CD40L/CD154 concentrations.
- Inclusion of patients with acute myocardial infarction, unstable angina, stable angina, and healthy controls.
Main Results:
- Elevated platelet CD40L/CD154 expression and soluble CD40L/CD154 concentrations were observed in patients with acute myocardial infarction and unstable angina compared to controls and stable angina patients.
- A decrease in platelet CD40L/CD154 expression was noted at six-month follow-up in patients with unstable angina and acute myocardial infarction.
- Increased platelet CD40L/CD154 expression correlated with angina recurrence and need for repeat coronary angioplasty in unstable angina patients.
Conclusions:
- Both platelet-bound and soluble CD40L/CD154 are significantly increased in acute myocardial infarction and unstable angina.
- CD40-CD40L/CD154 interactions are implicated in the pathogenesis of acute coronary syndromes.
Objective:
To investigate whether CD40L/CD154 on platelets and soluble CD40L/CD154 may play a role in the inflammatory process of acute coronary syndromes.
Design And Setting:
Observational study in a university hospital.
Patients:
15 patients with acute myocardial infarction, 25 patients with unstable angina, 15 patients with stable angina, and 12 controls.
Main Outcome Measures:
CD40L/CD154 on platelets, P-selectin/CD62P on platelets, soluble CD40L/CD154 serum concentrations.
Results:
Mean (SD) CD40L/CD154 expression on platelets was 6.2 (2.8) MFI (mean fluorescence intensity) in the infarct group, 11 (3.3) MFI in the unstable angina group (p < 0.001 v infarction), 3.6 (0.9) MFI in the stable angina group (p < 0.01 v infarction; p < 0.001 v unstable angina), and 3.2 (1.0) MFI in the controls (p < 0.01 v infarction; p < 0.001 v unstable angina; NS v stable angina). Soluble CD40L/CD154 concentration was 5.2 (1.1) ng/ml in the infarct group, 4.2 (0.7) ng/ml in the unstable angina group (p < 0.001 v infarction), 2.9 (1.0) ng/ml in stable angina group (p < 0.001 v infarction and unstable angina), and 3.0 (0.5) ng/ml in the controls (p < 0.001 v infarction and unstable angina; NS v stable angina). At a six months follow up, there was lower expression of CD40L/CD154 on platelets in patients with unstable angina (12.3 (3.6) v 3.8 (1.2) MFI, p < 0.0001) and acute myocardial infarction (6.2 (2.8) v 3.5 (0.8) MFI, p < 0.01) compared with their admission values six months earlier. Patients with unstable angina who needed redo coronary angioplasty (PTCA) or who had recurrence of angina were characterised by increased CD40L/CD154 expression on platelets compared with the remainder of the study group (recurrence of angina: 12.7 (3.2) v 9.7 (1.6) MFI, p < 0.05; re-do PTCA: 14.3 (4.2) v 10.3 (2.1) MFI, p < 0.05).
Conclusions:
Both CD40L/CD154 on platelets and soluble CD40L/CD154 are raised in patients with unstable angina and myocardial infarction. These findings suggest that CD40-CD40L/CD154 interactions may play a pathogenic role in triggering and propagation of acute coronary syndromes.