International Journal of Cardiology 171 (2014) e103
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Antibodies against biologicals and acute coronary syndromes Tommaso Gori ⁎, Thomas Munzel Department of Cardiology, University Medical Center Mainz, Mainz, Germany
a r t i c l e
i n f o
Article history: Received 24 September 2013 Accepted 8 December 2013 Available online 18 December 2013 Keywords: Acute coronary syndromes Hypersensitivity reactions Coronary thrombosis
We are grateful to Dr Kounis et al. for expanding the discussion to our clinical case [1,2]. We concur with their comment that the use of antibodies directed against specific proinflammatory cytokines (in this case, an anti-TNF antibody) has several implications beyond their specific effects. On the other side, inflammatory diseases such as those against which the so-called biologicals are typically employed have also shown to have an impact on cardiovascular outcomes: for instance rheumatoid arthritis and psoriasis have both been associated with increased cardiovascular morbidity and mortality, and this increased risk of cardiovascular events appears to be due to inappropriate
⁎ Corresponding author at: Department of Cardiology, University Medical Center, Langenbeckstr1, 55131 Mainz, Germany. Tel.: +49 6131 172829; fax: +49 6131 176428. E-mail address: [email protected] (T. Gori). 0167-5273/$ – see front matter © 2013 Elsevier Ireland. Ltd All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.012
secretion of proinflammatory cytokines such as TNF-alpha [3]. Therefore, the interaction between the risk provoked by the disease and the additional risks associated with its treatments, and the interaction between cytokines and the interaction between blood and vascular function [4], are complex. Further, there are a number of possible mechanisms through which biological drugs might elicit cardiovascular events. To date, only anecdotal evidence is available, and more formally collected evidence is required. To our knowledge, the first multicentric study testing the impact of another such agent on intermediate cardiovascular phenotypes such as endothelial function and vascular stiffness is currently under planning. Other than that, the information regarding the incidence (and mechanism) of acute coronary syndromes induced by treatment with biological drugs remains unfortunately very scarce. References [1] Gori T, Munzel T. A case of coronary hypersensitivity (Kounis) syndrome associated with mid-ventricular ballooning pattern, intracoronary thrombosis and troponin elevation. Int J Cardiol 2011;149(3):377–8. [2] Kounis NG, Soufras GD, Kounis GN. Antibodies against antibodies inducing Kounis syndrome. Int J Cardiol 2013. [3] Solomon DH, Curtis JR, Saag KG, et al. Cardiovascular risk in rheumatoid arthritis: comparing TNF-alpha blockade with nonbiologic DMARDs. Am J Med 2013;126(8):730 [e9-730 e17]. [4] Urschel K, Cicha I, Daniel WG, Garlichs CD. Shear stress patterns affect the secreted chemokine profile in endothelial cells. Clin Hemorheol Microcirc 2012;50(1–2):143–52.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Antibodies against biologicals and acute coronary syndromes Tommaso Gori ⁎, Thomas Munzel Department of Cardiology, University Medical Center Mainz, Mainz, Germany
a r t i c l e
i n f o
Article history: Received 24 September 2013 Accepted 8 December 2013 Available online 18 December 2013 Keywords: Acute coronary syndromes Hypersensitivity reactions Coronary thrombosis
We are grateful to Dr Kounis et al. for expanding the discussion to our clinical case [1,2]. We concur with their comment that the use of antibodies directed against specific proinflammatory cytokines (in this case, an anti-TNF antibody) has several implications beyond their specific effects. On the other side, inflammatory diseases such as those against which the so-called biologicals are typically employed have also shown to have an impact on cardiovascular outcomes: for instance rheumatoid arthritis and psoriasis have both been associated with increased cardiovascular morbidity and mortality, and this increased risk of cardiovascular events appears to be due to inappropriate
⁎ Corresponding author at: Department of Cardiology, University Medical Center, Langenbeckstr1, 55131 Mainz, Germany. Tel.: +49 6131 172829; fax: +49 6131 176428. E-mail address: [email protected] (T. Gori). 0167-5273/$ – see front matter © 2013 Elsevier Ireland. Ltd All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.012
secretion of proinflammatory cytokines such as TNF-alpha [3]. Therefore, the interaction between the risk provoked by the disease and the additional risks associated with its treatments, and the interaction between cytokines and the interaction between blood and vascular function [4], are complex. Further, there are a number of possible mechanisms through which biological drugs might elicit cardiovascular events. To date, only anecdotal evidence is available, and more formally collected evidence is required. To our knowledge, the first multicentric study testing the impact of another such agent on intermediate cardiovascular phenotypes such as endothelial function and vascular stiffness is currently under planning. Other than that, the information regarding the incidence (and mechanism) of acute coronary syndromes induced by treatment with biological drugs remains unfortunately very scarce. References [1] Gori T, Munzel T. A case of coronary hypersensitivity (Kounis) syndrome associated with mid-ventricular ballooning pattern, intracoronary thrombosis and troponin elevation. Int J Cardiol 2011;149(3):377–8. [2] Kounis NG, Soufras GD, Kounis GN. Antibodies against antibodies inducing Kounis syndrome. Int J Cardiol 2013. [3] Solomon DH, Curtis JR, Saag KG, et al. Cardiovascular risk in rheumatoid arthritis: comparing TNF-alpha blockade with nonbiologic DMARDs. Am J Med 2013;126(8):730 [e9-730 e17]. [4] Urschel K, Cicha I, Daniel WG, Garlichs CD. Shear stress patterns affect the secreted chemokine profile in endothelial cells. Clin Hemorheol Microcirc 2012;50(1–2):143–52.
