European Heart Journal Advance Access originally published online on September 7, 2007
European Heart Journal 2007 28(21):2685; doi:10.1093/eurheartj/ehm368
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STEMI and NSTEMI are two distinct pathophysiological entities
Department of Medicine
Hadassah-Hebrew University Medical Center
Mt. Scopus
Jerusalem 97654
Israel
Hadassah Hebrew University Medical Center
Mt. Scopus
Jerusalem
Israel
Tel: +972 2 584 4520 Fax: +972 02 581 2754 E-mail address: drott{at}012.net.il
Montalescot et al.1 recently demonstrated that patients with STEMI and NSTEMI have similar in-hospital and long-term prognoses as well as similar independent correlates of outcome, despite very different in-hospital management. As per accepted guidelines, whereas most STEMI patients underwent emergent reperfusion treatment (e.g. primary PCI or thrombolysis), NSTEMI patients hardly ever received this kind of therapy.2 This different treatment strategies, however, are justified by evidence-based medicine as thrombolytic therapy in non-Q wave MI patients showed no benefit over standard therapy.3 The reason for the failure of intravenous thrombolytic therapy to improve clinical outcomes in the absence of AMI with ST-segment elevation is most likely related to the fact that in STEMI the culprit artery is usually occluded by a thrombus, whereas in NSTEMI the culprit artery is usually patent with a non-occlusive thrombus.
The development of STE vs. NSTE MI does not appear to be coincidental. We have demonstrated that most patients with recurrent MI episodes will have either repeated episodes of STEMI or NSTEMI but not both, suggesting predilection of some patients to repeated episodes of occlusive thrombi and others to repeated episodes of non-occlusive thrombi.4 Smoking cessation did not influence this finding.5 Individual differences in endogenous tissue plasminogen activator levels/activity as well as fibrinogen VII and PAI-1 levels, may explain these differences which suggest STEMI and NSTEMI are in fact different entities. Therefore, while we certainly agree with the authors that secondary prevention such as aggressive lipid lowering, antiplatelet therapy, etc. are critical with either type of MI, it is still important to consider STEMI and NSTEMI as distinct entities.
References
- Montalescot G, Dallongeville J, Van Belle E, Rouanet S, Baulac C, Degrandsart A, Vicaut E. STEMI and NSTEMI: are they so different? 1 year outcomes in acute myocardial infarction as defined by the ESC/ACC definition (the OPERA registry). Eur Heart J (2007) 28:1409–1417.
[Abstract/Free Full Text] - Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J, Levin TN, Pepine CJ, Schaeffer JW, Smith EE 3rd, Steward DE, Theroux P, Gibbons RJ, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Hiratzka LF, Jacobs AK, Smith SC Jr. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction. J Am Coll Cardiol (2002) 40:1366–1374.
[Free Full Text] - Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non–Q wave myocardial infarction: results of the TIMI IIIB trial. Thrombolysis In Myocardial Ischemia. Circulation (1994) 89:1545–1556.
[Abstract/Free Full Text] - Rott D, Weiss A, Chajek-Shaul T, Leibowitz D. ST deviation patterns in recurrent myocardial infarctions. Am J Cardiol (2006) 98:10–13.[CrossRef][Web of Science][Medline]
- Rott D, Salameh S, Weiss A, Chajek-Shaul T, Leibowitz D. Smoking cessation does not alter ST deviation pattern of recurrent myocardial infarctions. Int J Cardiol (2007) in press.
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