Persistence of the altered polymorphonuclear leukocyte rheological and metabolic variables after 12 months in juvenile myocardial infarction.
Acute myocardial infarction (AMI) is associated with an elevated polymorphonuclear leukocyte (PMN) count and a PMN rheological impairment. In this study we evaluated two major rheological aspects (membrane fluidity and cytosolic Ca2+ concentration) in a group of young adults with AMI. We enrolled 41 AMI patients (39 men and 2 women; mean age 41.0 +/- 4.0 years), who were examined 5-10 days after AMI (T1) and 12 months later (T2). The membrane fluidity was obtained labelling granulocytes with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) and considering the degree of fluorescence polarization, inversely correlated to the membrane lipid fluidity. The cytosolic Ca2+ content was obtained marking PMN cells with the fluorescent probe Fura-2AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. Both parameters were evaluated at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) at the concentration of 4.5 muM, prolonged for 5 and 15 minutes. At T1 the PMN membrane fluidity and cytosolic Ca2+ content in AMI patients were respectively decreased and increased in comparison with control group. At T2 the membrane fluidity was not any more different from control subjects, but there was also a further increase in cytosolic Ca2+ content. In vitro, PMN activation caused no significant variation of these parameters in the control group, while in AMI patients membrane fluidity significantly decreased and cytosolic Ca2+ content increased not only during the initial stage, but also after 12 months. The long-term functional alteration of PMN cells observed in young adults with AMI confirms the role of these cells in the inflammatory response following AMI. In the light of these data, the use of molecules able to modulate granulocyte activity, such as calcium channel blockers or pentoxifylline, should be reconsidered in myocardial infarction, together with the usual pharmacological treatment.
Lo Presti
Rosalia
R
Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università degli Studi di Palermo, Italy.
Tozzi Ciancarelli
Maria Giuliana
MG
Hoffmann
Enrico
E
Incalcaterra
Egle
E
Canino
Baldassare
B
Montana
Maria
M
D'Amico
Teresa
T
Catania
Anna
A
Caimi
Gregorio
G
D000328:Adult; D017668:Age of Onset; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D002118:Calcium / Q000032:analysis*; D002462:Cell Membrane / Q000502:physiology*; D003600:Cytosol / Q000737:chemistry; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D008297:Male; D008560:Membrane Fluidity; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D009504:Neutrophils / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology
D000806:Angiotensin-Converting Enzyme Inhibitors; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D002118:Calcium