ORIGINAL PAPER TNF-a, myocardial perfusion and function in patients with ST-segment elevation myocardial infarction and primary percutaneous coronary intervention Eva S. Kehmeier • Wolfgang Lepper • Martina Kropp • Christian Heiss • Ulrike Hendgen-Cotta • Jan Balzer • Mirja Neizel • Christian Meyer • Marc W. Merx • Pablo E. Verde • Christian Ohmann • Gerd Heusch • Malte Kelm • Tienush Rassaf Received: 25 January 2012 / Accepted: 19 April 2012 / Published online: 6 May 2012 Ó Springer-Verlag 2012 Abstract Aims To characterize the time course of tumor necrosis factor-a (TNF-a) serum levels along with myocardial per- fusion and contractile function in patients with ST-segment elevation myocardial infarction (STEMI) and successful primary percutaneous coronary intervention (PCI). Methods Serum levels of TNF-a, interleukin 6 (IL-6), and C-reactive protein (CRP) were measured in 42 patients with STEMI before, one and 6 days after successful PCI. Myocardial perfusion was assessed by contrast-enhanced echocardiography (ceEcho), contractile function by unen- hanced two-dimensional (2DE) and real-time three- dimensional echocardiography. In a subset of 18 patients, infarct size was quantified by late gadolinium enhancement cardiovascular magnetic resonance imaging (LGE-CMR) on day six. Results TNF-a serum levels were in the upper normal range within the first 12 h from symptom onset and increased continuously until day six, while IL-6 and CRP increased subsequently with a peak on day one after STEMI. Serum TNF-a on day one after PCI correlated with perfusion defects, wall motion abnormalities, and infarct size (ceEcho: r = 0.52, p = 0.005; 2DE: r = 0.56, p = 0.002; LGE-CMR: r = 0.83–0.86; p \ 0.0001). Using multiple regression linear analysis, infarct size on day six was predicted by serum TNF-a 1 day after PCI (p = 0.006, adjusted R 2 0.638). Conclusion Our data reflect the clinical significance of early TNF-a elevation in patients with STEMI and primary PCI (Controlled Clinical Trials number, NCT00529607). Keywords Contractile function Á Infarct size Á Myocardial perfusion Á PCI Á STEMI Á TNF-a Introduction Acute myocardial infarction is characterized by an inflammatory response with rapid formation and release of TNF-a [1–8] and initiation of the cytokine cascade via nuclear factor-kB. TNF-a facilitates the expression of IL-6, which itself is a key cytokine and promotes synthesis and secretion of acute phase proteins, including CRP. While TNF-a [9], IL-6 [10, 11] and CRP [12–14] have been E. S. Kehmeier and W. Lepper share first authorship. E. S. Kehmeier Á W. Lepper Á M. Kropp Á C. Heiss Á U. Hendgen-Cotta Á J. Balzer Á M. Neizel Á C. Meyer Á M. W. Merx Á M. Kelm Á T. Rassaf Division of Cardiology, Pulmonary Diseases and Vascular Medicine, Department of Medicine, University Hospital Aachen, 52074 Aachen, Germany Present Address: E. S. Kehmeier Á M. Kropp Á C. Heiss Á U. Hendgen-Cotta Á J. Balzer Á M. Neizel Á C. Meyer Á M. W. Merx Á M. Kelm Á T. Rassaf (&) Division of Cardiology, Pulmonary Diseases and Vascular Medicine, Department of Medicine, University Hospital Duesseldorf, Moorenstr. 5, 40225 Duesseldorf, Germany e-mail: Tienush.Rassaf@med.uni-duesseldorf.de Present Address: W. Lepper Division of Cardiology and Intensive Care, Department of Medicine, St Johannes Hospital, 47166 Duisburg, Germany P. E. Verde Á C. Ohmann Coordination Centre for Clinical Trials, Heinrich-Heine University, 40225 Duesseldorf, Germany G. Heusch Center of Internal Medicine, Institute for Pathophysiology, University of Essen Medical School, 45122 Essen, Germany 123 Clin Res Cardiol (2012) 101:815–827 DOI 10.1007/s00392-012-0465-x