This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Marsden, P. A. Search for Related Content PubMed PubMed Citation Articles by Marsden, P. A. Related Collections Related Article

(Circulation Research. 2006;99:1152.)
© 2006 American Heart Association, Inc.

Editorials

Inflammation and Coagulation in the Cardiovascular System

The Contribution of Influenza

Philip A. Marsden

From the Division Nephrology, St. Michael’s Hospital and University of Toronto, Canada.

Correspondence to Philip A. Marsden, MD, Rm 7358, Medical Sciences Building, University of Toronto, 1 King’s College Circle, Ontario, Canada M5S 1A8. E-mail p.marsden@utoronto.ca

See related article, pages 1261–1269

Key Words: influenza • sepsis • virus • endothelial

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
We need to know more about the functional interplay between the coagulation or fibrinolytic pathways and acute inflammation in the vasculature, especially from the viewpoint of acute infections and sepsis. This is a concept that is relevant in both the macro- and microvasculature. An especially important clinical infection is influenza. The extent to which endemic or epidemic influenza elicits systemic inflammation and coagulation is an evolving story. In this issue of the journal, Keller et al provide a focused dissection of changes in coagulation and fibrinolysis parameters in a murine model of respiratory influenza.¹ Their findings give us reason to remind ourselves about the important pathways involved.

Traditional and nontraditional Framingham risk factors for accelerated atherosclerosis, such as genetic susceptibility alleles or lifestyle issues, provide a background for the acute and chronic infectious diseases that are superimposed on the daily lives of patients. How these exogenous pathogens contribute to disease progression has stimulated much discussion but limited insight. This may be because of, in part, the difficulties in studying these in vivo concepts in patients. Scholarly clinical epidemiology studies have provided support for the view that acute infections are chronologically associated with an acute but transient risk for stroke and myocardial infarction. Arguments continue for a contribution of intralesional pathogens. However, it is more increasingly appreciated that acute infections are associated with systemic inflammation that increases the risk for superimposed acute arterial vascular events.^2,3 Parallel concepts have emerged for the venous side of the circulation.^4,5 Smeeth et al report that . . . [Full Text of this Article]

Related Article:

Effects on Coagulation and Fibrinolysis Induced by Influenza in Mice With a Reduced Capacity to Generate Activated Protein C and a Deficiency in Plasminogen Activator Inhibitor Type 1

Tymen T. Keller, Koen F. van der Sluijs, Martijn D. de Kruif, Victor E. A. Gerdes, Joost C. M. Meijers, Sandrine Florquin, Tom van der Poll, Eric C. M. van Gorp, Dees P. M. Brandjes, Harry R. Büller, and Marcel Levi
Circ. Res. 2006 99: 1261-1269. [Abstract] [Full Text] [PDF]