What is cardiovascular disease (CVD)?

Cardiovascular disease (CVD) refers to a group of disorders that affect the heart and blood vessels, leading to impaired function and increased risk of adverse cardiovascular events such as heart attack, stroke, and heart failure. Cardiovascular disease encompasses a wide range of conditions, including coronary artery disease, hypertension (high blood pressure), heart failure, arrhythmias, peripheral artery disease, and congenital heart defects, among others.


The pathogenesis of cardiovascular disease involves complex interactions between genetic, environmental, and lifestyle factors. Common mechanisms underlying cardiovascular disease include inflammation, endothelial dysfunction, oxidative stress, and atherosclerosis (the buildup of plaque in the arteries). These processes can lead to narrowing or blockage of blood vessels, reduced blood flow to the heart and other organs, and ultimately, tissue damage and dysfunction.


What is the relationship between CVD and oxidative stress?

The relationship between cardiovascular disease (CVD) and oxidative stress is significant, with oxidative stress playing a central role in the development, progression, and complications of various cardiovascular conditions. Here’s how oxidative stress is related to cardiovascular disease:


  • Atherosclerosis: Oxidative stress is a key contributor to the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries. Reactive oxygen species (ROS) generated within the blood vessel walls can oxidize low-density lipoprotein (LDL) cholesterol, leading to the formation of oxidized LDL (oxLDL). OxLDL is highly pro-inflammatory and promotes endothelial dysfunction, smooth muscle cell proliferation, and foam cell formation, all of which contribute to the progression of atherosclerosis.


  • Endothelial Dysfunction: Oxidative stress can impair the function of endothelial cells, which line the inner surface of blood vessels and regulate vascular tone and permeability. Excessive ROS production disrupts the balance of endothelium-derived vasodilators (e.g., nitric oxide) and vasoconstrictors, leading to endothelial dysfunction and impaired vasodilation. Endothelial dysfunction is a hallmark of early-stage cardiovascular disease and contributes to hypertension, atherosclerosis, and thrombosis.


  • Hypertension: Oxidative stress plays a role in the pathogenesis of hypertension (high blood pressure) by promoting vasoconstriction, sodium retention, and remodeling of blood vessels. ROS can activate signaling pathways involved in smooth muscle cell contraction and proliferation, leading to increased vascular resistance and elevated blood pressure. Additionally, oxidative stress contributes to endothelial dysfunction, further impairing vascular function and exacerbating hypertension.


  • Myocardial Remodeling: In conditions such as heart failure and myocardial infarction (heart attack), oxidative stress contributes to maladaptive remodeling of the heart muscle. ROS generated during ischemia-reperfusion injury promote cardiomyocyte death, fibrosis, and inflammation, leading to impaired contractility and heart failure. Chronic oxidative stress in the myocardium also contributes to arrhythmias, electrical instability, and mitochondrial dysfunction.


  • Thrombosis and Platelet Activation: Oxidative stress promotes platelet activation and aggregation, leading to thrombus formation and acute cardiovascular events such as myocardial infarction and stroke. ROS can stimulate platelet adhesion to injured endothelium, activate platelet signaling pathways, and enhance thromboxane production, all of which contribute to thrombus formation and vascular occlusion.


  • Inflammation: Oxidative stress is intimately linked with inflammation, and both processes are closely intertwined in the pathogenesis of cardiovascular disease. ROS activate pro-inflammatory signaling pathways and promote the expression of adhesion molecules, cytokines, and chemokines, leading to immune cell recruitment, endothelial activation, and plaque destabilization.


Overall, oxidative stress plays a critical role in the pathophysiology of cardiovascular disease by promoting endothelial dysfunction, atherosclerosis, hypertension, myocardial remodeling, thrombosis, and inflammation.