LETTER TO THE EDITOR
Prognostic significance of immune activation after acute coronary syndromes
Johann Auer, MD,
Robert Berent, MD,
Elisabeth Lassnig, MD,
Thomas Weber, MD and
Bernd Eber, MD, FESC
Department of Cardiology and Intensive Care, General Hospital Wels, Grieskirchnerstraße 42A-4600 Wels, Austria, Europe, E-mail: johann.auer@khwels.at
We read with great interest the study by Maekawa et al. (1) in a recent issue of the Journal. The article reports that the peripheral peak monocyte count is associated with adverse cardiac outcome during a 33-month follow-up period. The authors could demonstrate that peripheral monocytosis represents an independent determinant of adverse cardiac outcome, including pump failure, left ventricular aneurysm, hospital readmission for heart failure, recurrent myocardial infarction and cardiac deaths, including sudden deaths.
Elevated C-reactive protein, as a marker of inflammation, measured early after the onset of acute ischemia (2), has been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI) (3,4). In acute coronary syndromes (ACS), the release of different cytokines activates cellular defense (5). Infiltration of neutrophils and monocytes/macrophages is detected in the myocardium after AMI. Macrophages activated by interferon gamma synthesize metalloproteinases and neopterin, a pteridine derivative and a byproduct of the guanosine triphosphate-biopterin pathway (6), that has been used as an immune marker (7). We (8) and others (9, 10) previously demonstrated that neopterin levels significantly increase in patients with ACS shortly after the onset of ischemic symptoms. In our study (8), there was no correlation between neopterin and creatine kinase (CK), CK-MB isoenzyme or troponin I as markers for the extent of the myocardial injury.
The prognostic significance of the degree of increased neopterin levels after ACS has not yet been evaluated (to our knowledge). The 25 patients with ACS (18 men, 7 women; mean age, 68.5 ± 14.3 years; range, 40 to 86 years) included in our study (8) were followed up for 22 (±3) months. Six patients (24%) had adverse cardiovascular events (defined as cardiovascular death, recurrent AMI, stroke, hospital readmission for heart failure) during follow-up. Neopterin levels measured 72 hours after the onset of symptoms of ACS were 7.13 (±2.34) nmol/l in patients without cardiovascular events, and 10.6 (±2.56) nmol/l in patients with adverse cardiovascular events during follow-up, respectively (p < 0.01).
Therefore, our data support and expand the results from Maekawa et al. (1) that the degree of inflammatory response and immune activation after ACS, in particular the monocyte/macrophage-mediated process, predicts adverse cardiovascular events during follow-up independent of the extent of the myocardial injury.
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References
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1. Maekawa Y, Anzai T, Yoshikawa T. Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction: a possible role for left ventricular remodeling. J Am Coll Cardiol. 2002;39:241–246[Abstract/Free Full Text]
2. Auer J, Berent R, Kirchgatterer A, Weber T, Eber B. C-reactive protein and fibrinolysis in acute myocardial infarction. Z Kardiol. 2000;89:893
3. Celik S, Baykan M, Erdol C. C-reactive protein as a risk factor for left ventricular thrombus in patients with acute myocardial infarction. Clin Cardiol. 2001;24:615–619[Medline]
4. Anzai T, Yoshikawa T, Shiraki H. C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction. Circulation. 1997;963:778–784
5. Cruickshank AM, Oldroyd KG, Cobbe SM, et al. Serum interleukin-6 levels in suspected myocardial infarction. Lancet. 1994;343:974[Medline]
6. Werner-Felmayer G, Werner ER, Fuchs D. Pteridine biosynthesis in human endothelial cells: impact on nitric oxide-mediated formation of cyclic GMP. J Biol Chem. 1993;268:1842–1846[Abstract/Free Full Text]
7. Huber C, Batchelor JR, Fuchs D, et al. Immune response-associated production of neopterin: release from macrophages primarily under control of interferon-gamma. J Exp Med. 1984;160:310–316[Abstract/Free Full Text]
8. Auer J, Berent R, Lassnig E, Eber B. Serum neopterin and activity of coronary artery disease. Heart Dis. 2001;3:297–301[CrossRef][Medline]
9. Schumacher M, Halwachs G, Tatzber F. Increased neopterin in patients with chronic and acute coronary syndromes. J Am Coll Cardiol. 1997;30:703–707[Abstract]
10. Gupta S, Fredricks S, Schwartzman RA. Serum neopterin in acute coronary syndromes. Lancet. 1997;349:1252[Medline]
This article has been cited by other articles:
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J. C. Kaski, P. Avanzas, and R. Arroyo-Espliguero
Neopterin--a forgotten biomarker
J. Am. Coll. Cardiol.,
September 17, 2003;
42(6):
1142 - 1143.
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