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Relation Between White Blood Cell Count and Infarct Size: What About Differential?
READERS’ COMMENTS Relation Between White Blood Cell Count and Infarct Size: What About Differential? In the very interesting report published in the Am J Cardiol 2013,1 it was found that in patients with anterior wall acute myocardial infarction, elevated white blood count on admission is a powerful independent predictor of infarct size measured with cardiac magnetic resonance imaging 30 days after primary percutaneous coronary intervention. A previous study has also shown2 that in patients with ST-segment elevation acute myocardial infarction undergoing percutaneous coronary intervention, elevated baseline white blood count is an independent predictor of infarct size, as assessed by peak creatinine phosphokinase level, and of 1-year cardiac mortality, noncardiac mortality, and major bleeding. These results suggest a key role for inflammation in coronary artery disease. However, differential count was not available in these studies, and therefore, assessing the relative impact of white blood count subpopulations on infarct size was not reported. Indeed, neutrophil/lymphocyte ratio >3.3 was found to be an independent predictor of impaired coronary flow after primary percutaneous coronary intervention and of in-hospital major adverse cardiac events in patients with STsegment elevation myocardial infarction.3 Previous studies have shown that eosinophils may play an important role in coronary occlusion by promoting thrombus growth.4 In this study, eosinophils were observed in 106 (64.2%) of 165 samples. In a genome-wide association study5 for sequence variants affecting eosinophil counts in blood, it was found that a nonsynonymous “single nucleotide polymorphism” at 12q24, in SH2B3, was associated significantly with myocardial infarction. Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. It is known that eosinophils are bone marrowederived granulocytic leukocytes and express H4 histamine receptors. These receptors facilitate eosinophil chemotaxis toward mast cells, which are the major producers of an array
of inflammatory soluble mediators. Soluble mediators secreted by mast cells and eosinophils modulate also reciprocal interactions between these 2 cells in the so-called allergic effector unit.6 Therefore, differential white blood count and especially eosinophils should be always considered in all relative studies concerning acute coronary syndromes. Eosinophils are essential for elucidation of the origin of inflammation because denote hypersensitivity inflammation.7 George D. Soufras, MD George Hahali, MD Nicholas G. Kounis, MD Patras, Greece 20 October 2013
1. Palmerini T, Brener SJ, Genereux P, Maehara A, Della Riva D, Mariani A, Witzenbichler B, Godlewski J, Parise H, Dambrink JH, Ochala A, Fahy M, Xu K, Gibson CM, Stone GW. Relation between white blood cell count and final infarct size in patients with ST-segment elevation acute myocardial infarction undergoing primary percutaneous coronary intervention (from the INFUSE AMI trial). Am J Cardiol 2013;112:1860e1866. 2. Palmerini T, Mehran R, Dangas G, Nikolsky E, Witzenbichler B, Guagliumi G, Dudek D, Genereux P, Caixeta A, Rabbani L, Weisz G, Parise H, Fahy M, Xu K, Brodie B, Lansky A, Stone GW. Impact of leukocyte count on mortality and bleeding in patients with myocardial infarction undergoing primary percutaneous coronary interventions: analysis from the Harmonizing Outcome with Revascularization and Stent in Acute Myocardial Infarction trial. Circulation 2011;123:2829e2837. 3. Akpek M, Kaya MG, Lam YY, Sahin O, Elcik D, Celik T, Ergin A, Gibson CM. Relation of neutrophil/lymphocyte ratio to coronary flow to in-hospital major adverse cardiac events in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. Am J Cardiol 2012;110:621e627. 4. Sakai T, Inoue S, Matsuyama TA, Takei M, Ota H, Katagiri T, Koboyashi Y. Eosinophils may be involved in thrombus growth in acute coronary syndrome. Int Heart J 2009;50:267e277. 5. Gudjartsson DF, Bjornsdottir US, Halapi E, Helgadottir A, Sulem P, Jonsdottir GM, Thorleifsson G, Helgadottir H, Steinthorsdottir V, Stefansson H, Williams C, Hui J, Beilby J, Warrington NM, James A, Palmer LJ, Koppelman GH, Heinzmann A, Krueger M, Boezen HM, Wheatley A, Altmuller J, Shin HD, Uh ST, Cheong HS, Jonsdottir B, Gislason D, Park CS, Rasmussen LM, Porsbjerg C, Hansen JW, Backer V, Werge T, Janson C, Jönsson UB, Ng MC, Chan J, So WY, Ma R, Shah SH, Granger CB, Quyyumi AA, Levey AI, Vaccarino V, Reilly MP, Rader DJ, Williams MJ, van Rij AM, Jones GT, Trabetti E, Malerba G, Pignatti PF, Boner A, Pescollderungg L, Girelli D,
Am J Cardiol 2014;113:412 0002-9149/13/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved.
Olivieri O, Martinelli N, Ludviksson BR, Ludviksdottir D, Eyjolfsson GI, Arnar D, Thorgeirsson G, Deichmann K, Thompson PJ, Wjst M, Hall IP, Postma DS, Gislason T, Gulcher J, Kong A, Jonsdottir I, Thorsteinsdottir U, Stefansson K. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat Genet 2009;41:342e347. 6. Minai-Fleminger Y, Levi-Schaffer F. Mast cells and eosinophils: the two key effector cells in allergic inflammation. Inflamm Res 2009;58: 631e638. 7. Biteker M. Current understanding of Kounis syndrome. Exp Rev Clin Immunol 2010;6: 777e788. http://dx.doi.org/10.1016/j.amjcard.2013.10.006
A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance We read the report entitled “A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance.”1 It showed the equation pulmonary artery systolic pressure/right ventricular outflow tract velocity time integral þ 3 correlated best with pulmonary vascular resistance. We have previously shown that in patients with congenital heart disease, right ventricular pre-ejection period/velocity time integral <0.4 s/m correlated with pulmonary vascular resistance <3 Wood unit (WU) m2 with 97% accuracy. Right ventricular pre-ejection period/velocity time integral between 0.4 and 0.6 s/m correlated with pulmonary vascular resistance WU m2 between 3 and 7.5 with 91% accuracy. Values >6 s/m correlated with PVR >7.5 WU m2 with 94% accuracy in children.2 Our formula is also simple to use, but it was not referenced in your report, so we are writing to inform you of it. Brad Robinson, MD Wilmington, Delaware Makram Ebeid, MD Jackson, Mississippi 28 October 2013
1. Opotowsky AR, Clair M, Afilalo J, Landzberg MJ, Waxman AB, Moko L, Maron BA, Vaidya A, Forfia PR. A simple echocardiographic method to estimate pulmonary vascular resistance. Am J Cardiol 2013;112:873e882. 2. Ebeid MR, Ferrer PL, Robinson B, Weatherby N, Gebland H. Doppler echocardiographic evaluation of pulmonary vascular resistance in children with congenital heart disease. J Am Soc Echocardiogr 1996;9:822e831. http://dx.doi.org/10.1016/j.amjcard.2013.11.001
www.ajconline.org
of inflammatory soluble mediators. Soluble mediators secreted by mast cells and eosinophils modulate also reciprocal interactions between these 2 cells in the so-called allergic effector unit.6 Therefore, differential white blood count and especially eosinophils should be always considered in all relative studies concerning acute coronary syndromes. Eosinophils are essential for elucidation of the origin of inflammation because denote hypersensitivity inflammation.7 George D. Soufras, MD George Hahali, MD Nicholas G. Kounis, MD Patras, Greece 20 October 2013
1. Palmerini T, Brener SJ, Genereux P, Maehara A, Della Riva D, Mariani A, Witzenbichler B, Godlewski J, Parise H, Dambrink JH, Ochala A, Fahy M, Xu K, Gibson CM, Stone GW. Relation between white blood cell count and final infarct size in patients with ST-segment elevation acute myocardial infarction undergoing primary percutaneous coronary intervention (from the INFUSE AMI trial). Am J Cardiol 2013;112:1860e1866. 2. Palmerini T, Mehran R, Dangas G, Nikolsky E, Witzenbichler B, Guagliumi G, Dudek D, Genereux P, Caixeta A, Rabbani L, Weisz G, Parise H, Fahy M, Xu K, Brodie B, Lansky A, Stone GW. Impact of leukocyte count on mortality and bleeding in patients with myocardial infarction undergoing primary percutaneous coronary interventions: analysis from the Harmonizing Outcome with Revascularization and Stent in Acute Myocardial Infarction trial. Circulation 2011;123:2829e2837. 3. Akpek M, Kaya MG, Lam YY, Sahin O, Elcik D, Celik T, Ergin A, Gibson CM. Relation of neutrophil/lymphocyte ratio to coronary flow to in-hospital major adverse cardiac events in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. Am J Cardiol 2012;110:621e627. 4. Sakai T, Inoue S, Matsuyama TA, Takei M, Ota H, Katagiri T, Koboyashi Y. Eosinophils may be involved in thrombus growth in acute coronary syndrome. Int Heart J 2009;50:267e277. 5. Gudjartsson DF, Bjornsdottir US, Halapi E, Helgadottir A, Sulem P, Jonsdottir GM, Thorleifsson G, Helgadottir H, Steinthorsdottir V, Stefansson H, Williams C, Hui J, Beilby J, Warrington NM, James A, Palmer LJ, Koppelman GH, Heinzmann A, Krueger M, Boezen HM, Wheatley A, Altmuller J, Shin HD, Uh ST, Cheong HS, Jonsdottir B, Gislason D, Park CS, Rasmussen LM, Porsbjerg C, Hansen JW, Backer V, Werge T, Janson C, Jönsson UB, Ng MC, Chan J, So WY, Ma R, Shah SH, Granger CB, Quyyumi AA, Levey AI, Vaccarino V, Reilly MP, Rader DJ, Williams MJ, van Rij AM, Jones GT, Trabetti E, Malerba G, Pignatti PF, Boner A, Pescollderungg L, Girelli D,
Am J Cardiol 2014;113:412 0002-9149/13/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved.
Olivieri O, Martinelli N, Ludviksson BR, Ludviksdottir D, Eyjolfsson GI, Arnar D, Thorgeirsson G, Deichmann K, Thompson PJ, Wjst M, Hall IP, Postma DS, Gislason T, Gulcher J, Kong A, Jonsdottir I, Thorsteinsdottir U, Stefansson K. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat Genet 2009;41:342e347. 6. Minai-Fleminger Y, Levi-Schaffer F. Mast cells and eosinophils: the two key effector cells in allergic inflammation. Inflamm Res 2009;58: 631e638. 7. Biteker M. Current understanding of Kounis syndrome. Exp Rev Clin Immunol 2010;6: 777e788. http://dx.doi.org/10.1016/j.amjcard.2013.10.006
A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance We read the report entitled “A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance.”1 It showed the equation pulmonary artery systolic pressure/right ventricular outflow tract velocity time integral þ 3 correlated best with pulmonary vascular resistance. We have previously shown that in patients with congenital heart disease, right ventricular pre-ejection period/velocity time integral <0.4 s/m correlated with pulmonary vascular resistance <3 Wood unit (WU) m2 with 97% accuracy. Right ventricular pre-ejection period/velocity time integral between 0.4 and 0.6 s/m correlated with pulmonary vascular resistance WU m2 between 3 and 7.5 with 91% accuracy. Values >6 s/m correlated with PVR >7.5 WU m2 with 94% accuracy in children.2 Our formula is also simple to use, but it was not referenced in your report, so we are writing to inform you of it. Brad Robinson, MD Wilmington, Delaware Makram Ebeid, MD Jackson, Mississippi 28 October 2013
1. Opotowsky AR, Clair M, Afilalo J, Landzberg MJ, Waxman AB, Moko L, Maron BA, Vaidya A, Forfia PR. A simple echocardiographic method to estimate pulmonary vascular resistance. Am J Cardiol 2013;112:873e882. 2. Ebeid MR, Ferrer PL, Robinson B, Weatherby N, Gebland H. Doppler echocardiographic evaluation of pulmonary vascular resistance in children with congenital heart disease. J Am Soc Echocardiogr 1996;9:822e831. http://dx.doi.org/10.1016/j.amjcard.2013.11.001
www.ajconline.org