Open AccessActivation of leukocytes and of the kallikrein‐kinin system in patients with unstable angina pectoris
Author(s) -
Hoffmeister Hans Martin,
Beyer Martin E.,
Engel Zwetana,
Heller Wolfgang
Publication year - 1994
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960170106
Subject(s) - medicine , bradykinin , kinin , kallikrein , unstable angina , endocrinology , myocardial infarction , angina , pathophysiology , elastase , cardiology , enzyme , biochemistry , chemistry , receptor
We investigated the leucocyte‐elastase and the activity of the kallikrein system including kinin precursors and plasma inhibition levels in 14 patients with unstable angina pectoris (normal or only slightly elevated creatine kinase levels; no transmural myocardial infarction) and compared them with 10 controls. Leucocyte‐elastase levels and activity of the kallikrein system were significantly elevated in unstable angina pectoris. The bradykinin precursor high‐molecular‐weight kininogen was markedly decreased to 79 ± 16% indicating kinin generation. Except for a slight decrease in the beta factor Xlla inhibition, we observed no abnormalities in the plasma kallikrein inhibition or in the antithrombin III levels in patients with unstable angina pectoris. The findings indicate a significant activation of the plasma kallikrein‐kinin system, which is not associated with a considerable reduction in the plasma inhibitor levels. Kinin generation might influence vascular tone and leucocyte function and thus be involved in the pathophysiologic alterations occurring in patients with recurrent angina at rest.