The article reviews the role of leukocytes in cardiovascular diseases, particularly atherosclerosis, myocardial infarction (MI), and heart failure. Atherosclerosis, a chronic inflammatory process involving lipid-rich lesions in the vascular wall, can lead to MI and congestive heart failure. Leukocytes, including macrophages, neutrophils, and monocytes, play crucial roles at various stages of these diseases. Macrophages, the most abundant leukocytes in atherosclerotic lesions, can contribute to both atherogenesis and atheroprotection. Monocytes, which can differentiate into macrophages, are key players in the inflammatory response to atherosclerosis and MI. Neutrophils and mast cells also contribute to inflammation and lesion growth. After MI, leukocytes rapidly accumulate in the myocardium, with neutrophils and inflammatory monocytes being the first responders. These cells can be both protective and harmful, depending on their duration and type. The article highlights the complex interactions between leukocytes and other cells, as well as the systemic effects of MI, such as increased leukocyte recruitment and accelerated atherosclerosis. Understanding these mechanisms is essential for developing targeted therapies to manage cardiovascular diseases.The article reviews the role of leukocytes in cardiovascular diseases, particularly atherosclerosis, myocardial infarction (MI), and heart failure. Atherosclerosis, a chronic inflammatory process involving lipid-rich lesions in the vascular wall, can lead to MI and congestive heart failure. Leukocytes, including macrophages, neutrophils, and monocytes, play crucial roles at various stages of these diseases. Macrophages, the most abundant leukocytes in atherosclerotic lesions, can contribute to both atherogenesis and atheroprotection. Monocytes, which can differentiate into macrophages, are key players in the inflammatory response to atherosclerosis and MI. Neutrophils and mast cells also contribute to inflammation and lesion growth. After MI, leukocytes rapidly accumulate in the myocardium, with neutrophils and inflammatory monocytes being the first responders. These cells can be both protective and harmful, depending on their duration and type. The article highlights the complex interactions between leukocytes and other cells, as well as the systemic effects of MI, such as increased leukocyte recruitment and accelerated atherosclerosis. Understanding these mechanisms is essential for developing targeted therapies to manage cardiovascular diseases.