In recent years, numerous studies have validated the role of inflammation in the pathogenesis of atherosclerosis. Several of such studies have produced compelling evidence that inflammation participates in both, the initiation and perpetuation of the atherosclerotic process. Furthermore, epidemiological observations have found basal white blood cell (WBC) count is strongly associated with future cardiovascular disease (CVD), highlighting the participation of leukocytes in the pathogenesis of the ischemic damage that occurred during an acute coronary event, in particularly during the acute myocardial infarction (MI). Fundamentally, an acute MI triggers a systemic response to a necrotic insult characterized by leukocytosis and acute-phase protein synthesis. In this setting, elevated WBC count plays a central role in the reparative process that takes place to replace the necrotic tissue for collagen. In addition to be a proxy for the intensity of the peri-infarction inflammatory response, recent evidence has also shown that an elevated WBC counts, measured during the acute phase of MI, to be associated with adverse outcomes. This relationship holds true even when adjusting for classical prognostic variables some of which are surrogates for the extension of the infarctedarea. WBC count prognostic value in absence of necrosis marker elevation (like unstable angina), however, remains unclear and controversial. Additionally, and essentially due to its simplicity, cost-effectiveness and wide availability, WBC count has drawn the attention of researchers as a potential stratification tool in acute coronary syndromes (ACS). However, a formal comparison is needed between WBC count with other inflammatory markers such high-sensitive C-reactive protein to fully characterize its diagnostic accuracy.