CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Toshio Imanishi, MD, PhD*,
Hiroto Tsujioka, MD and
Takashi Akasaka, MD, PhD
* Wakayama Medical University, Cardiovascular Medicine, 811-1 Kimiidera, Wakayama 641-8510, Japan (Email: t-imani{at}wakayama-med.ac.jp).
We are grateful to Drs. Kavsak and Jaffe for their valuable comments and suggestions to our study (1). They pose a question regarding the kinetics of monocyte chemoattractant protein (MCP)-1 release. They found no time-dependent increase in MCP-1 measurement during the first 12 h after the onset of symptoms in 216 patients with acute coronary syndromes (2). On the contrary, Matsumori et al. (3) have demonstrated that plasma MCP-1 levels in 23 patients with acute myocardial infarction (MI) increase as early as 3 h after the onset of chest pain and reach their maximum at 24 h, with further gradual decline. We have no idea about the MCP-1 kinetics, because we did not examine the measurement of circulating MCP-1 in this study (1). Further studies will be needed on this important subject. In addition, in contrast to a previous experimental study (4)—which shows that Ly-6Clo (CD14+CD16+ analogs) monocytes were found to be critical for myocardial healing via myofibroblasts accumulation, angiogenesis, and deposition of collagen—this study (1) did not show any significant effect of CD14+CD16+ monocytes on myocardial salvage followed by reperfused MI. However, we could not exclude the possibility that it might potentially be the result of a short period of observation (7 days after reperfusion).
We completely agree with Drs. Kavsak and and Jaffe's supposition that data in a more diverse group, including those with smaller events diagnosed with cardiac troponin, would be important to see whether difference exist between those groups. We also agree with their idea that data about monocyte subgroups would possibly determine the optical timing of intervention in patients with MI without ST-segment elevation (5). Well-designed prospective trials would highlight the effect of circulating distinct monocyte subsets on the optimal timing of intervention in patients for non–ST-segment elevation MI.
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References
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1. Tsujioka H, Imanishi T, Ikejima H, et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction J Am Coll Cardiol 2009;54:130-138.[Abstract/Free Full Text]2. Kavsak PA, Ko DT, Newman AM, et al. Risk stratification for heart failure and death in an acute coronary syndrome using inflammatory cytokines and N-terminal pro-brain natriuretic peptide Clin Chem 2007;53:2112-2118.[Abstract/Free Full Text] 3. Matsumori A, Furukawa Y, Hashimoto T, et al. Plasma levels of the monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 are elevated in patients with acute myocardial infarction J Mol Cell Cardiol 1997;29:419-423.[CrossRef][Web of Science][Medline] 4. Nahrendorf M, Swirski FK, Aikawa E, et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions J Exp Med 2007;204:3037-3047.[Abstract/Free Full Text] 5. Mehta SR, Granger CB, Boden WE, et al. Early versus delayed invasive intervention in acute coronary syndromes N Engl J Med 2009;360:2165-2175.[CrossRef][Medline]
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