FLOW RESISTANCE OF INDIVIDUAL NEUTROPHILS IN CORONARY-ARTERY DISEASE - DECREASED PORE TRANSIT TIMES IN ACUTE MYOCARDIAL-INFARCTION

Citation
Rm. Bauersachs et al., FLOW RESISTANCE OF INDIVIDUAL NEUTROPHILS IN CORONARY-ARTERY DISEASE - DECREASED PORE TRANSIT TIMES IN ACUTE MYOCARDIAL-INFARCTION, HEART, 77(1), 1997, pp. 18-23
Citations number
42
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
HEARTACNP
ISSN journal
13556037
Volume
77
Issue
1
Year of publication
1997
Pages
18 - 23
Database
ISI
SICI code
1355-6037(1997)77:1<18:FROINI>2.0.ZU;2-1
Abstract
Objective-To investigate single neutrophil flow resistance in coronary artery disease, including myocardial infarction before initiation of reperfusion therapy. Design-Neutrophil flow resistance was measured in 93 subjects in five groups: (group 1) 28 patients within 12 hours aft er the onset of myocardial infarction, before reperfusion therapy; (gr oup 2) 18 with unstable angina; (group 3) 13 with stable angina; (grou p 4) 13 age matched patients without coronary disease, and (group 5) 2 1 healthy volunteers. Main parameters-Single neutrophil transit rimes through 8 mu m oligopore falters determined with a modified cell trans it analyser. Results-Leucocyte count (10(9)/1) was increased in corona ry disease, especially in myocardial infarction and unstable angina (m ean and 95% confidence intervals for groups 1 to 5: 12.6 (11.0 to 14.2 ), 11.3 (8.5 to 14.1), 8.5 (7.4 to 9.6), 8.0 (6.0 to 10.0), 7.0 (6.1 t o 7.9)). Polymorphonuclear granulocyte (PMN) flow resistance correlate d negatively with white blood cell (WBC) count and was significantly d ecreased in coronary artery disease (CAI), especially in myocardial in farction; mean transit times (ms) for groups 1 to 5 were: 13.6 (11.5 t o 15.4), 16.9 (13.9 to 19.0), 16.9 (12.8 to 21.0), 22.0 (19.6 to 24.4) , and 18.6 (15.7 to 21.5). Conclusion-Neutrophil flow resistance was d ecreased in CAD, especially in myocardial infarction before reperfusio n therapy. In contrast to previous findings in repel-fused myocardial infarction, the present study showed that stiffened PMNs were not yet present in the circulating Mood peal. Thus a pharmacological approach aimed at suppressing leucocyte activation before or during reperfusion therapy may be feasible.