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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Editorial Board Member: Gillery, Philippe / Kazmierczak, Steven / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Whitfield, John B.

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High plasma levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) and interleukin-8 (IL-8) characterize patients prone to ventricular fibrillation complicating myocardial infarction

Elif Elmas1 / Siegfried Lang2 / Carl Erik Dempfle3 / Thorsten Kälsch4 / Dieter Hannak5 / Tim Sueselbeck6 / Christian Wolpert7 / Martin Borggrefe8 / Martina Brueckmann9

11st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

21st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

31st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

41st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

5Institute of Clinical Chemistry, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

61st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

71st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

81st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

91st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany

Corresponding author: Elif Elmas, MD, 1st Department of Medicine, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany Phone: +49-621-383-2204, Fax: +49-621-383-3821,

Citation Information: Clinical Chemical Laboratory Medicine. Volume 45, Issue 10, Pages 1360–1365, ISSN (Online) 14374331, ISSN (Print) 14346621, DOI: 10.1515/CCLM.2007.286, October 2007

Publication History

Received:
2007-03-06
Accepted:
2007-06-19
Published Online:
2007-10-10

Abstract

Background: Atherosclerotic plaques prone to cause thrombotic complications and plaque rupture account for the majority of fatal myocardial infarctions (MI), which may be complicated by ventricular fibrillation (VF). Matrix-degrading metalloproteinases (MMPs) and their inhibitors (TIMPs) are expressed in atherosclerotic lesions and contribute to plaque vulnerability. Interleukin-8 (IL-8) is one of the predominant chemokines interacting with MMPs and TIMPs and the coagulation system. The aim of the present study was to assess potential differences of levels of MMP-9, TIMP-1 and IL-8 in postmyocardial infarction patients with or without VF complicating acute MI.

Methods: Blood samples were taken from 45 patients with VF complicating acute MI and from 88 patients without VF. All samples were collected during a symptom-free interval remote from the acute ischemic event with a median of 556 days. The markers of interest were TIMP-1, MMP-9 and IL-8.

Results: IL-8 and TIMP-1 levels were significantly higher among patients with VF than among patients without VF (p<0.001). In a logistic regression approach IL-8 was an independent indicator of patients prone to VF during MI (p=0.03). High levels of TIMP-1 (p=0.05), MMP-9 (p=0.03), the MMP-9/TIMP-1 ratio (p=0.049) and hypertension (p=0.02) were found to be indicators in patients with reinfarction or unstable angina pectoris during follow-up. Hypertension (p=0.02) and MMP-9 (p=0.03) were the only significant indicators characterizing patients undergoing coronary reinterventions, such as percutaneous coronary interventions and coronary bypass surgery.

Conclusions: Higher TIMP-1 and IL-8 levels are present in patients with VF complicating MI. High TIMP-levels may be related to the degree of fibrosis which is a substrate for electrical instability and may contribute to the occurrence of VF. Patients prone to develop VF during MI seem to have an increased proinflammatory condition compared to patients without VF.

Clin Chem Lab Med 2007;45:1360–5.

Keywords: inflammation; myocardial infarction; sudden cardiac death

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