© 2019 Elsevier Inc. Amplified innate leukocytes (neutrophils and monocytes/macrophages) are associated with advanced ischemic and non-ischemic heart failure (HF). Intensified neutrophilic leukocytosis (neutrophilia) and sustained activation of neutrophils is the predominant factor that determines over activated inflammation in acute HF and the outcome of long-term chronic HF. After heart attack, the first wave of innate responsive and short-lived neutrophils is essential for the initiation of inflammation, resolution of inflammation, and cardiac repair, however uncontrolled and long-term activation of neutrophils leads to collateral damage of myocardium. In the presented review, we highlighted the interactive and integrative role of neutrophil phenotypes in cellular and molecular events of ischemic HF. In addition, we discussed the current, nonimmune, immune, and novel paradigms of neutrophils in HF associated with differential factors with a specific interest in non-resolving inflammation and resolution physiology.