(Circulation. 2001;103:2987.)
© 2001 American Heart Association, Inc.
Cardiovascular Drugs |
Fibrinolysis for Acute Myocardial Infarction
Current Status and New Horizons for Pharmacological Reperfusion, Part 2
From the University of Alberta, Edmonton, Alberta, Canada (P.W.A.), and Katholieke Universiteit Leuven, Leuven, Belgium (D.C.).
Correspondence to Paul W. Armstrong, MD, 2-51 Medical Sciences Bldg, University of Alberta, Edmonton, Alberta T6G 2H7, Canada. E-mail paul.armstrong@ualberta.ca
Key Words: fibrinolysis • myocardial infarction • drugs
 |
Introduction |
|---|
Ancillary therapy in association with fibrinolysis may be classified into 2 general categories. Additional therapies may be used to facilitate, enhance, and sustain coronary reperfusion, ie, conjunctive therapy, or to minimize the impact of the ischemic insult to the myocardium and/or consequences of reperfusion injury, ie, adjunctive therapy.
|
Ancillary Therapy |
|---|
Conjunctive Therapy
An important paradox associated with the use of fibrinolytic therapy is its procoagulant potential. The effect of fibrinolytic agents on platelets is complex, poorly understood, and controversial.1 Conflicting evidence exists concerning the capacity of fibrinolytic agents to activate as opposed to diminish platelet activation; this may relate, in part, to differences in protocol design and methodology for assessment of platelet function, the type of fibrinolytic agent used, and the time course over which the studies are conducted.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Regardless of this controversy, exposure of clot-bound thrombin, when unmasked, becomes an extraordinarily potent platelet agonist that mandates conjunctive antithrombin and antiplatelet therapy as an essential component of any fibrinolytic strategy.5 Activated platelets provide an abundant source of factor Xa on their surface and, through extrusion from their alpha-granules, emit plasminogen activator inhibitor-1,
2 antiplasmin, platelet factor IV, and a
variety of vasoconstrictor substances such as thromboxane
2 and
serotonin.1 6 7
The latter substances have been demonstrated to be biologically active
in humans. They have also been suggested as the mechanism for no reflow
after apparently successful primary angioplasty for thrombotic
coronary occlusion and, together with the hematologic
mediators, antagonize the prospects of successful
fibrinolysis.8
Conjunctive antithrombin therapy with unfractionated heparin is also
associated with platelet This article has been cited by other articles:
 |
|
 |
|
  D. A. Alter, D. T. Ko, A. Newman, and J. V. Tu Factors explaining the under-use of reperfusion therapy among ideal patients with ST-segment elevation myocardial infarction Eur. Heart J., July 1, 2006; 27(13): 1539 - 1549. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Ivanusa, P. W. Armstrong, D. Collen, and E. Antman Fibrinolytic Therapy: What Size to Fit All? * Response Circulation, December 23, 2003; 108 (25): e170 - e170. [Full Text] [PDF]
|
|
|
|
|
|
S. Savonitto, P.W. Armstrong, A.M. Lincoff, G. Jia, C.A. Sila, J. Booth, P. Terrosu, C. Cavallini, H.D. White, D. Ardissino, et al. Risk of intracranial haemorrhage with combined fibrinolytic and glycoprotein IIb/IIIa inhibitor therapy in acute myocardial infarction: Dichotomous response as a function of age in the GUSTO V trial Eur. Heart J., October 2, 2003; 24(20): 1807 - 1814. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. W. Armstrong, D. Collen, and E. Antman Fibrinolysis for Acute Myocardial Infarction: The Future Is Here and Now Circulation, May 27, 2003; 107(20): 2533 - 2537. [Full Text] [PDF]
|
|
|
|
|
|
M. Aschermann and P. Widimsky I have an acute myocardial infarction: open my coronary artery, stent it and keep full flow! Eur. Heart J., June 2, 2002; 23(12): 913 - 916. [Full Text] [PDF]
|
|