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Platelet function and platelet-leukocyte adhesion in symptomatic coronary heart disease. Effects of intravenous
M Gawaz1, A Reininger, F J Neumann
11. Medizinische Klinik, Technischen Universität München, Germany.
Insights
Platelet activation and adhesion to leukocytes are elevated in coronary heart disease patients. Intravenous magnesium (Mg2+) effectively reduces these markers, suggesting a therapeutic role for magnesium in managing cardiovascular conditions.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Background:
- Platelet activation, indicated by P-selectin expression, and platelet-leukocyte adhesion are implicated in symptomatic coronary heart disease (CHD).
- Understanding the role of magnesium (Mg2+) in modulating platelet function is crucial for cardiovascular health.
Purpose of the Study:
- To investigate alterations in platelet function in patients with symptomatic coronary heart disease.
- To evaluate the ex vivo and in vitro effects of magnesium (Mg2+) on platelet activation and platelet-leukocyte adhesion.
Main Methods:
- Assessed spontaneous and ADP-induced P-selectin expression and platelet-leukocyte adhesion in CHD patients and controls.
- Administered intravenous Mg2+ and measured its ex vivo effects on platelet markers.
- Conducted in vitro experiments using whole blood, isolated neutrophils, and platelet membranes to determine Mg2+ dose-dependency and mechanism of inhibition.
Main Results:
- Symptomatic CHD patients exhibited significantly increased spontaneous and ADP-induced P-selectin expression and platelet-leukocyte adhesion compared to controls.
- Intravenous Mg2+ administration significantly reduced ex vivo P-selectin expression and platelet-leukocyte adhesion.
- In vitro, Mg2+ dose-dependently inhibited platelet adhesion to neutrophils, with maximal effects observed at 4 mM, and also inhibited adhesion of isolated platelet membranes.
Conclusions:
- Platelet function is demonstrably altered in symptomatic coronary heart disease.
- Intravenous Mg2+ administration can effectively modulate platelet activation and platelet-leukocyte adhesion, indicating potential therapeutic benefits in CHD.
Abstract:
Spontaneous P-selectin surface expression on platelets and platelet-leukocyte adhesion was increased in patients with symptomatic coronary heart disease (n = 12) compared to normal controls (n = 10) (p < 0.05). ADP-induced P-selectin expression and platelet-leukocyte adhesion was also enhanced in the patient group (p < 0.05). Administration of intravenous Mg2+ significantly reduced both platelet surface expression of P-selectin and platelet-leukocyte adhesion ex vivo (p < 0.02). The effect of extracellular Mg2+ was evaluated in in vitro experiments. Both in whole blood and in isolated neutrophil suspension Mg2+ inhibited platelet adhesion to neutrophils dose dependently with half maximal effects at 4 mM. Moreover, Mg2+ inhibited adhesion of isolated platelet membranes to neutrophils. We conclude that platelet function is altered in symptomatic coronary heart disease and can be modulated by administration of intravenous Mg2+.