What is a heart attack?

Myocardial infarction, commonly known as a heart attack, occurs when there is a sudden blockage of blood flow to a part of the heart muscle, leading to tissue damage or death (infarction) of the affected area. This typically happens due to the obstruction of one or more coronary arteries, which supply oxygen-rich blood to the heart muscle (myocardium).


The most common cause of myocardial infarction is the formation of a blood clot (thrombus) within a coronary artery, usually as a result of the rupture or erosion of an atherosclerotic plaque—a buildup of cholesterol, fatty deposits, and other substances on the inner walls of the arteries. When a plaque ruptures, it exposes the underlying tissue to blood, triggering the formation of a clot that can partially or completely block the artery, thereby reducing or cutting off blood flow to a portion of the heart.


The lack of oxygen and nutrients delivered by the blood deprives the affected part of the heart muscle of its vital supply, leading to ischemia (inadequate blood supply) and subsequent damage or death of the myocardial cells. If blood flow is not restored promptly, irreversible damage can occur, resulting in permanent impairment of heart function or even death.


What is the relationship between heart attack and oxidative stress?

The relationship between myocardial infarction (MI), commonly known as a heart attack, and oxidative stress involves complex interactions between various factors that contribute to tissue damage, inflammation, and the progression of cardiovascular disease. Here’s how oxidative stress may be related to myocardial infarction:


  • Reactive Oxygen Species (ROS) Production: Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense mechanisms in the body. During myocardial infarction, ischemia (inadequate blood supply) and reperfusion (restoration of blood flow) to the heart muscle lead to the generation of ROS within the cardiac tissues. Ischemia-induced hypoxia and the subsequent reoxygenation during reperfusion can trigger the production of ROS by various mechanisms, including mitochondrial dysfunction, activation of xanthine oxidase, and recruitment of inflammatory cells, among others.


  • Oxidative Damage to Cardiac Tissues: Oxidative stress can cause direct damage to the cells and tissues of the heart, including the myocardium (heart muscle), endothelial cells (lining the blood vessels), and cardiac fibroblasts (supporting connective tissue). ROS can oxidize lipids, proteins, and DNA within the cardiac cells, leading to cellular dysfunction, apoptosis (cell death), and tissue injury. Oxidative damage to the myocardium can exacerbate myocardial ischemia, impair cardiac contractility, and promote adverse remodeling of the heart, contributing to the progression of heart failure and other complications following myocardial infarction.


  • Inflammatory Response and Tissue Injury: Oxidative stress in the heart can trigger an inflammatory response and tissue injury, leading to further damage and dysfunction of cardiac tissues. ROS can activate inflammatory pathways, stimulate the release of pro-inflammatory cytokines and chemokines, and recruit immune cells to the site of injury, amplifying the inflammatory response and exacerbating tissue damage. Chronic inflammation and oxidative stress in the myocardium are implicated in the pathogenesis of atherosclerosis, plaque rupture, and myocardial infarction, as well as in the development of complications such as ventricular remodeling, arrhythmias, and heart failure.


  • Impaired Antioxidant Defense Mechanisms: The heart possesses antioxidant defense mechanisms to neutralize ROS and maintain redox homeostasis. However, in conditions of chronic oxidative stress or inadequate antioxidant protection, these defense mechanisms may be overwhelmed, leading to increased susceptibility to oxidative damage and myocardial infarction. Aging, genetic factors, lifestyle choices (such as smoking, poor diet, and sedentary behavior), and underlying medical conditions (such as diabetes, hypertension, or hyperlipidemia) can impair antioxidant enzyme activity, diminish levels of cellular antioxidants, or disrupt redox signaling pathways, further exacerbating oxidative stress and cardiovascular risk.


Overall, oxidative stress plays a critical role in the pathogenesis of myocardial infarction by promoting tissue damage, inflammation, and adverse remodeling of the heart.