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J Am Coll Cardiol, 2008; 52:316, doi:10.1016/j.jacc.2008.03.056
© 2008 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

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David R. Holmes, Jr, MD*

* Mayo Clinic, Cardiovascular Diseases and Internal Medicine, 200 First Street, SW, Rochester, Minnesota 55905 (Email: holmes.david{at}mayo.edu).


We appreciate the comments from Drs. Roik and Opolski on our long-term observations in patients with cardiogenic shock who were enrolled in the GUSTO (Global Utilization of Streptokinase and Tissue-Type Plasminogen Activator for Occluded Coronary Arteries)-I trial (1). One of the important advantages of long-term datasets is that long-term data are available—along with the advantage comes the disadvantage that they are old data on patients followed up for a long time. That must be kept in mind because the GUSTO-I trial enrolled patients presenting with their index event between 1990 and 1993 from around the world, including Warsaw, Poland. Many things have changed since then in the field of acute myocardial infarction and cardiogenic shock. Just to name a few, we no longer use streptokinase; in fact, it is no longer even available in the U.S. for use during acute myocardial infarction. We now routinely use stents, sometimes even drug-eluting stents, and IIb/IIa inhibitors are now commonly given. Thus treatment strategies have changed dramatically.

The patients included in our long-term follow-up were all randomized because they had presented with acute infarction as part of the 41,021-patient cohort. We note that there are many subsets of patients with shock, but at the time of the initial GUSTO shock publication, this shock substudy was the largest in the literature. Undoubtedly some subsets have a worse prognosis than others, and work continues to optimize identification of higher-risk patients as well as to optimize their outcomes.

As previously documented in the GUSTO-I experience (2), 89% of these patients developed shock after admission using a definition of shock of "a systolic blood pressure <90 mm Hg for at least 1 h, not responsive to fluid administration, thought to be secondary to cardiac dysfunction, and associated with signs of hypoperfusion." The fact that the in-hospital mortality was 56% identifies that this indeed was a very-high-risk group of patients.

The most important points of our follow-up study are that: 1) we need better strategies for optimizing early outcomes of cardiogenic shock; and 2) as Drs. Hochman and Apolito pointed out in their accompanying editorial (3), after the initial storm, there is surprising calm.


    References
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 References
 
1. Singh M, White J, Hasdai D, et al. Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock: insights from the GUSTO-I trial J Am Coll Cardiol 2007;50:1752-1758.[Abstract/Free Full Text]

2. Holmes Jr. DR, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience J Am Coll Cardiol 1995;26:668-674.[Abstract]

3. Hochman JS, Apolito R. The calm after the storm J Am Coll Cardiol 2007;50:1759-1760.[Free Full Text]


Related Article

Long-Term Outcome Among Patients With ST-Segment Elevation Myocardial Infarction Complicated by Shock
Marek Roik and Grzegorz Opolski
J. Am. Coll. Cardiol. 2008 52: 315. [Full Text] [PDF]




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