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) All Versions of this Article: clinchem.2008.117572v1 55/1/9    most recent 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 PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lindahl, B. Search for Related Content PubMed PubMed Citation Articles by Lindahl, B.

Multimarker Approach for Diagnosis of Acute Myocardial Infarction: Better Answers Need Better Questions

Uppsala Clinical Research Center and Department of Cardiology, University Hospital, Uppsala, Sweden

Address correspondence to the author at: Uppsala Clinical Research Center and Department of Cardiology, University Hospital, S-751 85 Uppsala, Sweden, Fax +46 18 506638, E-mail bertil.lindahl@ucr.uu.se

The first 20% of the full text of this article appears below.

Chest pain is the presenting complaint in approximately 5% of all emergency department visits, making chest pain the second most common reason for seeking acute medical care (1). The prevalence of acute myocardial infarction (AMI) in this emergency department population with chest pain ranges from 5% to 15%. Reliable exclusion or confirmation of AMI within the first few hours after presentation still constitutes a diagnostic challenge. Earlier confirmation (rule-in) than is obtainable currently would permit earlier start of appropriate treatment, and earlier exclusion (rule-out) would facilitate early discharge of patients for whom further in-hospital evaluation or treatment is unnecessary.

Myocardial infarction is defined as myocardial necrosis of ischemic origin (2). AMI is not a homogenous condition, however. It ranges from minor infarctions with necrosis of less than 1 g of the myocardium to large infarctions of more than one-third of the left ventricular mass. Furthermore, although by definition the cause of the necrosis is ischemia, the causes of the ischemia can range from plaque rupture with an overlying coronary-flow–obstructing thrombosis (type I infarction) to supply/demand imbalance without a thrombotic component (type II, secondary infarction) to iatrogenic causes, e.g., associated with percutaneous coronary intervention or coronary artery bypass grafting procedures (type IV and V infarctions). Thus, the challenge to find biochemical markers useful for diagnosis of AMI remains fundamentally important.

Presently, the only biochemical markers used for diagnosis of AMI are markers of myocardial necrosis. According to current international guidelines, the diagnosis of AMI requires demonstration of an increase of a specific marker of myocardial injury, e.g., cardiac troponin I or T. Although an increase of cardiac troponin is highly specific for myocardial injury, it tells nothing . . . [Full Text of this Article]

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

				T. Reichlin, W. Hochholzer, S. Bassetti, S. Steuer, C. Stelzig, S. Hartwiger, S. Biedert, N. Schaub, C. Buerge, M. Potocki, et al. Early Diagnosis of Myocardial Infarction with Sensitive Cardiac Troponin Assays N. Engl. J. Med., August 27, 2009; 361(9): 858 - 867. [Abstract] [Full Text] [PDF]