Author + information
- Received March 20, 2001
- Revision received August 7, 2001
- Accepted August 27, 2001
- Published online December 1, 2001.
- Antonino Mazzone, MD*,* (, )
- Chiara Cusa, MD*,
- Iolanda Mazzucchelli, BSc*,
- Monia Vezzoli, MD*,
- Elena Ottini, MD*,
- Roberta Pacifici, BSc†,
- Piergiorgio Zuccaro, MD† and
- Colomba Falcone, MD‡
- ↵*Reprint requests and correspondence: Dr. Antonino Mazzone, Chief of Internal Medicine and Oncology, Hospital of Legnano, Via Candiani 2, 20025 Legnano, Milano, Italy
The aim of the study was to examine the inflammatory cytokines in patients with myocardial ischemia to evaluate whether silent ischemia patients exibit any particular cytokine pattern.
Silent myocardial ischemia is frequently observed in patients with coronary artery disease. Various endogenous mechanisms control a patient’s perceived intensity of pain. Among them, the inflammatory process and the related cytokine production are known to modulate the threshold for activating the primary afferent nociceptors.
Seventy-eight patients with reproducible exercise-induced myocardial ischemia were studied: 34 symptomatic patients, with rest and/or stress angina; 44 asymptomatic patients, with no symptoms during daily life activities or during positive exercise stress test. Venous blood samples were taken from all patients to evaluate the expression of CD11b receptors both on neutrophils and monocytes. Frozen plasma samples (at −80°C) were used to quantify the anti-inflammatory (interleukin-4 and -10, transforming growth factor-β) and the proinflammatory cytokines (tumor necrosis factor-α, interferon-γ, interleukin-1β and -6).
In asymptomatic patients lower CD11b receptor expression and higher concentration of anti-inflammatory cytokines were observed. Proinflammatory cytokine production was similar in the two groups.
The data suggest that an “anti-inflammatory pattern” of cytokine production correlates with silent ischemia and that the immune and inflammatory system activation may be crucial for angina symptoms.
☆ This work was supported by grant 03/99 from IRCCS, S. Matteo Hospital, Pavia, Italy.
- Received March 20, 2001.
- Revision received August 7, 2001.
- Accepted August 27, 2001.
- American College of Cardiology