European Heart Journal Advance Access originally published online on September 7, 2007
European Heart Journal 2007 28(21):2685-2686; doi:10.1093/eurheartj/ehm374
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STEMI and NSTEMI are two distinct pathophysiological entities: reply
Institut du Coeur
Bureau 2-236
Hôpital pitié-Salpètrière
47 Bld de l'hôpital
Paris 75013
France
Tel: +33 1 4216 3006/7 Fax: +33 1 4216 2931 E-mail address: gilles.montalescot{at}psl.ap-hop-paris.fr
We thank Dr Rott for his thoughtful analysis of our recently published OPERA study and we concur with him on the point that patients with STEMI and NSTEMI have different initial management almost exclusively related to the decision of emergent reperfusion which is provided more systematically to STEMI than NSTEMI patients and, we have clearly outlined this point in our paper. However, it does not mean that the two entities do not share the same pathophysiology. Indeed, risk factors, demographics, pathogenesis of plaque rupture, complications, prognosis, and secondary prevention are quite similar in STEMI and NSTEMI. By definition, occlusion of the culprit coronary artery is more frequently found in STEMI patients, but it does exist in a significant number of patients presenting with NSTEMI. Moreover, ST-elevation may be missed in patients with an occluded artery particularly when the culprit lesion is located in the circumflex artery. Not to mention patients with simultaneously multiple active plaques or occluded vessels, undetectable by the electrocardiogram but found with angiography or intracoronary ultrasounds. Even haemostasis factors such as PAI-1 or von Willebrand factor have been reported to be increased in both situations and cannot discriminate between the two syndromes and certainly not sustain that they are two distinct pathophysiological entities.1–4 So, in contrast to what Dr Rott suggests, the frontier is not that sharp between STEMI and NSTEMI. For now, we agree that immediate management is different when a patient presents with vs. without ST-elevation but everyone knows that ST-elevation is sometimes transitory transforming the case in a ‘non STEMI’ for the decision of reperfusion. The opposite is also true. Finally, ongoing randomized studies are examining the hypothesis that immediate reperfusion of NSTE-ACS is a better strategy than a delayed approach; if these studies are positive that will make the two entities even closer than what they already are.
References
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[Abstract/Free Full Text] - Collet JP, Montalescot G, Vicaut E, Ankri A, Walylo F, Lesty C, Choussat R, Beygui F, Borentain M, Vignolles N, Thomas D. Acute release of plasminogen activator inhibitor-1 in st-segment elevation myocardial infarction predicts mortality. Circulation (2003) 108:391–394.
[Abstract/Free Full Text] - Montalescot G, Philippe F, Ankri A, Vicaut E, Bearez E, Poulard JE, Carrie D, Flammang D, Dutoit A, Carayon A, Jardel C, Chevrot M, Bastard JP, Bigonzi F, Thomas D, for the French Investigators of the ESSENCE Trial. Early increase of von Willebrand factor predicts adverse outcome in unstable coronary artery disease: beneficial effects of enoxaparin. Circulation (1998) 98:294–299.
[Abstract/Free Full Text] - Ray KK, Morrow DA, Gibson CM, Murphy S, Antman EM, Braunwald E, for the ENTIRE-TIMI 23 Study Group. Predictors of the rise in vWF after ST elevation myocardial infarction: implications for treatment strategies and clinical outcome: An ENTIRE-TIMI 23 substudy. Eur Heart J (2005) 26:440–446.
[Abstract/Free Full Text]
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