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Phagocyte activation in coronary artery disease
G Ricevuti1, A Mazzone, I Mazzucchelli
1Department of Internal Medicine, University of Pavia, IRCCS S. Matteo Hospital, Italy.
Insights
Granulocytes (PMNs) contribute to heart damage in coronary artery disease (CAD). Their aggregation and CD11b/CD18 expression increase, while superoxide release decreases, particularly during angioplasty.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathophysiology
Background:
- Granulocytes (polymorphonuclear cells, PMNs) are implicated in myocardial ischemia and injury.
- These cells release mediators that contribute to tissue damage.
- Understanding PMN function is crucial in coronary artery disease (CAD).
Purpose of the Study:
- To evaluate granulocyte function in patients with CAD.
- To assess changes in PMN activity during coronary angioplasty (PTCA).
Main Methods:
- Studied 20 patients with CAD, comparing PMN activity in the coronary sinus and aorta.
- Analyzed PMN aggregation, leukotriene C4 release, superoxide production, and CD11b/CD18 integrin expression.
- Assessed superoxide release post-stimulation with phorbol-myristate-acetate (PMA) during PTCA.
Main Results:
- PMN aggregating activity was significantly higher in the coronary sinus than the aorta (P < 0.01).
- Smokers showed lower leukotriene C4 release (P < 0.025).
- PMN superoxide production decreased more in the coronary sinus than aorta during PTCA (P < 0.05).
- CD11b/CD18 integrin expression was significantly increased in CAD patients compared to controls (P < 0.01) and correlated with aggregation (r = 0.87, P < 0.001).
Conclusions:
- Granulocytes play a significant role in the pathophysiology of myocardial ischemia in CAD.
- Increased PMN aggregation and CD11b/CD18 expression, coupled with altered superoxide release, highlight their involvement.
- These findings underscore the potential of targeting granulocyte function in managing CAD.
Abstract:
Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Granulocytes can release a variety of molecules mediating tissue injury which act synergistically with other molecules and cells. The aim of our investigation was to evaluate the granulocyte function in patients affected by coronary artery disease (CAD) and during coronary angioplasty (PTCA). We studied 20 patients suffering from CAD. The PMN's aggregating activity was greater in the coronary sinus than in the aorta (P < 0.01). The increase in aggregating activity was evident in patients who were smokers: their cells release significantly lower quantities of leukotriene C4 (P < 0.025). In the 20 patients who underwent coronary angioplasty we analyzed superoxide release after stimulation with phorbol-myristate-acetate (PMA). The results showed a greater decrease of PMN's superoxide production in the coronary sinus than in the aorta (P < 0.05). In all patients affected by CAD we evaluated the PMN's expression of CD11b/CD18 membrane integrins. In these patients the increase in expression of CD11b/CD18 was statistically significant in comparison with the controls (P < 0.01). This increase in expression correlates with a higher aggregation (r = 0.87, P < 0.001). The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in the pathophysiology of myocardial injury due to regional ischemia and reperfusion is an area of intense investigation. This paper presents studies carried out in vivo which have been instrumental in demonstrating the role of granulocytes as mediators of myocardial ischemia.