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(Circulation. 2003;108:376.)
© 2003 American Heart Association, Inc.

Editorial

Plasminogen Activator Inhibitor-1 and the Calculus of Mortality After Myocardial Infarction

Douglas E. Vaughan, MD

From the Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to Douglas E. Vaughan, MD, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Room 383 PRB, 2220 Pierce Ave, Nashville, TN 37232-6300. E-mail doug.vaughan@vanderbilt.edu

Key Words: Editorials • myocardial infarction • mortality

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

There are numerous clinical factors that have been identified that are associated with an adverse outcome after acute myocardial infarction (MI). These factors include female gender, the presence of severe left ventricular dysfunction or congestive heart failure, a history of diabetes mellitus, age >70 years, infarct location (anterior versus inferior), and patency of the infarct-related artery. In this issue of Circulation, Collet and colleagues¹ describe a previously unrecognized relationship between acute increases in plasma levels of plasminogen activator inhibitor-1 (PAI-1) in patients hospitalized with acute ST-elevation MI and risk of mortality during a 1-month period.

See p 391

PAI-1 is the primary circulating inhibitor of tissue-type plasminogen activator and the urokinase-type plasminogen activator in plasma. Elevated plasma PAI-1 levels have been shown to be a predictor of recurrent MI² and have been identified as an independent predictor of cardiovascular risk.³ When one considers the many factors that regulate plasma PAI-1 levels, it is not completely surprising that acute increases in the levels of PAI-1 in plasma might reflect increased risk of mortality after acute MI. The PAI-1 that circulates in plasma is derived from the composite output of several different cellular synthetic sites, including the liver, the vascular endothelium, and visceral adipose tissue. There are a number of factors that are known to directly affect PAI-1 production, including metabolic factors such as glucose,⁴ insulin,⁵ and VLDL,⁶ neurohumoral factors including angiotensin II and aldosterone,^7,8 and inflammatory cytokines including tumor necrosis factor-⁹ and interleukin-1.¹⁰ The remarkable relationship described in this study . . . [Full Text of this Article]

Related Article:

Acute Release of Plasminogen Activator Inhibitor-1 in ST-Segment Elevation Myocardial Infarction Predicts Mortality

J.P. Collet, G. Montalescot, E. Vicaut, A. Ankri, F. Walylo, C. Lesty, R. Choussat, F. Beygui, M. Borentain, N. Vignolles, and D. Thomas
Circulation 2003 108: 391-394. [Abstract] [Full Text]

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