HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Ravkilde, J. Search for Related Content PubMed PubMed Citation Articles by Ravkilde, J. Related Collections Proteomics and Protein Markers

Risk Stratification in Acute Coronary Syndrome Using Cardiac Troponin I

¹ Department of Cardiology, Aalborg University Hospital, Hobrovej 18-22, DK-9100 Aalborg, Denmark, Fax 45-9932-2361, E-mail ravkilde@dadlnet.dk

The interest in risk stratification of patients with acute coronary syndrome (ACS), i.e., acute myocardial infarction (MI) and unstable angina pectoris (AP), has increased considerably within recent years because of improved knowledge of pathology, progress in immunoassays of already existing biochemical markers, introduction of new biochemical markers [especially cardiac troponin I (cTnI) and T (cTnT)], and new methods of treatments.

Coronary artery disease may present clinically as stable AP or ACS. In cases of stable AP, myocardial ischemia commonly results from increases in myocardial oxygen demand that outstrip the ability of stenosed coronary arteries to increase oxygen delivery (1). In ACS, the accepted cause of acute MI is a plaque disruption, or fissuring, leading to coronary thrombosis with or without vasospasm, and thereby intermittent or persistent coronary occlusion. In patients with unstable AP, pathological postmortem investigations have documented that unstable AP leading to MI or cardiac death frequently is preceded by microinfarctions (2). This is important because patients with non-Q-wave MI tend to have smaller infarcts on presentation and rarely have total occlusion of the infarct-related vessel; it therefore is considered a relatively unstable condition associated with a lower initial mortality but a higher risk of later MI or cardiac death (3).

On the basis of the above considerations, many large-scale trials divide the patients with ACS into patients with ST-segment elevation and non-ST-segment elevation. If the patient presents with signs of evolving acute MI, i.e., an electrocardiogram (ECG) with unequivocal ST-segment elevation, then the patient in most cases is subjected to thrombolysis or primary percutaneous transluminal coronary angioplasty. However, evaluation of patients with non-ST-segment elevation is a key issue today because new treatments are focused to a great extent on this group, i.e., low-molecular weight heparins, platelet glycoprotein IIb/IIIa antagonist, direct thrombin inhibitors, . . . [Full Text of this Article]

References

The following articles in journals at HighWire Press have cited this article:

				M. Panteghini Acute Coronary Syndrome: Biochemical Strategies in the Troponin Era Chest, October 1, 2002; 122(4): 1428 - 1435. [Abstract] [Full Text] [PDF]