Inflammation

Inflammation can be classified into acute and chronic types. Acute inflammation is the body’s natural defense response—a self-protective mechanism activated when foreign pathogens invade. Redness, swelling, heat, and pain are all typical signs of acute inflammation. In contrast, chronic inflammation results in prolonged exposure of tissue cells to inflammatory mediators, which over time can cause damage to body tissues. Many modern chronic diseases are closely linked to chronic inflammation.

Atherosclerosis

Inflammation is a primary cause of atherosclerosis. Inflammatory factors can damage the inner walls of arteries and oxidize lipoproteins, leading to the accumulation of fatty plaques. Initially, the buildup of fatty plaques beneath the endothelium causes the outer wall of the artery to expand outward, allowing blood flow to remain relatively normal despite a distorted vessel structure. However, as plaque accumulation continues and the artery can no longer expand outward, the plaques begin to protrude into the lumen, narrowing the vessel and leading to atherosclerosis. When a plaque ruptures, it can trigger the formation of a blood clot, which may block the artery and result in conditions such as angina, myocardial infarction, or stroke.

Chronic inflammation is associated with a wide range of diseases
Asthma	Cancer
Neurodegenerative diseases (e.g., Parkinson’s disease)	Alzheimer′s disease
Autoimmune disease	Arthritis
Diabetes	Cardiovascular disease
IBD	Depression

The important information provided by Atherosclerosis Progression-META^® is as follows

• Assessment of Vascular Wall IntegrityEndothelial cell dysfunction can easily lead to vascular diseases and contribute to the development of atherosclerosis. In patients with hypertension and cardiovascular disease, endothelial cell damage is commonly observed.
• Balancing the concentration of free radicals in the bloodstream helps protect the vascular wall from oxidative damage and prevents the development of atherosclerosis. Oxidized low-density lipoprotein (oxLDL) triggers inflammatory responses, causes cellular damage, and leads to endothelial dysfunction. This process attracts monocytes to migrate toward the endothelium, where they differentiate into macrophages that engulf oxLDL. Macrophages filled with oxLDL eventually become foam cells, and the accumulation of these foam cells along with fibrotic changes marks the beginning of atherosclerosis.
• Microalbumin in urine is considered an important marker of endothelial damage. Its levels significantly increase during cardiovascular injury or inflammation and can reflect systemic endothelial dysfunction throughout the vascular system.
• C-reactive protein, CRP is currently the most commonly used inflammatory marker and is an independent risk factor for assessing cardiovascular disease. Unlike other risk factors such as age, cholesterol levels, diabetes, or family history, CRP is not influenced by these variables, making it a reliable predictor of cardiovascular events.
• Myeloperoxidase (MPO) promotes lipid peroxidation, which in turn contributes to the development of atherosclerosis and cardiovascular disease. Therefore, it can serve as a novel biomarker for predicting cardiovascular risk.
• Lipoprotein-associated phospholipase A2 (LP-PLA2) hydrolyzes oxidized phospholipids on LDL particles, triggering inflammatory responses and accelerating the formation and accumulation of foam cells. This process contributes to the development of atherosclerosis, ultimately leading to cardiovascular disease.
• Troponin T is a type of myofibrillar protein released from cardiac muscle and is used to diagnose myocardial infarction and assess the severity of ischemic myocardial injury.