Clinical study: myocardial ischemia
Increased production of inflammatory cytokines in patients with silent myocardial ischemia

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Abstract

OBJECTIVES

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.

BACKGROUND

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.

METHODS

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).

RESULTS

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.

CONCLUSIONS

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.

Abbreviations

CAD
coronary artery disease
CGRP
calcitonin gene-related peptide
ECG
electrocardiogram or electrocardiographic
IFN-γ
interferon-gamma
IL
interleukin
MAb
monoclonal antibodies
MESF
molecules of equivalent soluble fluorescein
MI
myocardial infarction
NF-κB
nuclear factor-κB
PBR
peripheral benzodiazepine receptor
SP
substance P
TGF-β
transforming growth factor-beta
TNF-α
tumor necrosis factor-alpha

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This work was supported by grant 03/99 from IRCCS, S. Matteo Hospital, Pavia, Italy.