**Abstract**

Atherosclerosis is the main cause of myocardial infarction. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This review will summarize the molecular and cellular links between inflammation and thrombosis in the context of myocardial infarction, which support the concept of a thrombo inflammatory state leading to the vessel obstruction and to the subsequent myocardial necrosis.

**Keywords:** thrombosis, inflammation, atherosclerosis

#### **1. Introduction**

Myocardial infarction is a form of coronary artery disease, in which the occlusion of the coronary artery induces ischemia of the subsequent territory and eventually leads to the destruction of up to a billion myocardic cells.

Atherosclerosis is the main cause of myocardial infarction. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction.

Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke [1].

As the human heart cannot regenerate, the acute myocardial infarction is associated with the destruction of large proportion of myocardium that will lead to the development of a collagen scar. This process is associated with an evident inflammatory reaction. This inflammatory reaction will lead to the chemotaxis of leukocytes that will be preferentially localized at the border of the necrotic myocardium. These leukocytes may lead to cytotoxic reactions that can increase the injured zone [2].
