White blood count and infarct size, myocardial salvage and clinical outcomes: the role of differentials

Abstract

Evidence suggests that inflammation, both local and systemic, plays an important role in the pathogenesis of acute myocardial infarction [1]. There is also evidence that increased concentrations of inflammatory markers such as C-reactive protein interleukin-2 and tumor necrosis factor can identify patients at high risk of future ischemic events, suggesting that the intensity of the inflammatory response influences clinical outcome in acute coronary syndromes [2, 3]. Multiple studies have demonstrated also an association between elevated leucocyte count, which is a non-specific marker of inflammation, and the extent of coronary artery disease or increased short-term or long-term risk of death in patients with various manifestations of coronary artery disease [4, 5]. Other studies [6] have shown that total leucocyte count, but not C-reactive protein, predicts 1-year mortality in patients with acute coronary syndromes treated with percutaneous coronary intervention. Furthermore, recent studies have emphasized the usefulness of neutrophil to lymphocyte ratio in predicting short-and long-term mortality, thrombus formation, infarct related artery patency, TIMI flow grade after primary coronary angioplasty, impaired myocardial perfusion, ventricular arrhythmias and critical limb ischemia [7–9]. Indeed, in patients with non-ST-elevation myocardial infarction a ratio above 4.7 has been reported to be an independent predictor of short-term and long-term mortality [7] and 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 ST-segment elevation myocardial infarction [10]. In a recent issue of the Int J Cardiovasc Imaging [11] and additional very interesting paper was published which shows that in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction an elevated baseline white blood count is associated with less salvaged myocardium, larger infarct size and poorer clinical outcomes. All these papers and results really suggest a key role of 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 myocardial infarction was not reported. Total white blood count comprises several cell types such as monocytes, lymphocytes and eosinophils all of which are implicated in the development, progression and instability of atherosclerotic plaque. None of the above studies have focused attention on the presence of eosinophils and this was probably based on an older study which has suggested that total white blood count is a better correlate of long-term than differentials [12]. Eosinophils, however, play an important role in inflammation and can identify the etiology of inflammation since they denote hypersensitivity inflammation [13–15]. Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. These cells are also bone marrow-derived granulocytic leukocytes which express H4 histamine receptors in their surface. These receptors facilitate eosinophil chemotaxis toward mast cells which are the major producers of an array of inflammatory soluble mediators. These inflammatory mediators can induce the coronary hypersensitivity associated Kounis syndrome manifesting as vasospastic angina and/or acute myocardial N. G. Kounis (&) Medical Sciences, Patras Highest Institute of Education and Technology, Patras, Achaia, Greece e-mail: ngkounis@otenet.gr