[Vascular Calcification - Pathological Mechanism and Clinical Application - . The significance of arterial calcification in unstable plaques].
Plaque rupture or erosion with subsequent thrombus formation is the principal mechanism underlying the sudden onset of acute coronary syndromes. Plaque inflammation and increased oxidative stress play important roles in the pathogenesis of plaque destabilization. Macrophages, T lymphocytes, and neutrophils are the dominant types of inflammatory cells at human coronary unstable plaques, such as ruptured plaques or eroded plaques. Calcification is a common finding in human atherosclerotic lesions, and arterial calcification is generally classified into calcification within an atherosclerotic plaque, and Mönckeberg's medial calcific sclerosis characterized by calcific deposits within the media of small and medium-sized muscular arteries. It has been reported that a spotty pattern of calcification is associated with coronary unstable ruptured plaques in patients with acute myocardial infarction. Patients undergoing hemodialysis (HD) have a high prevalence of arterial calcification and cardiovascular events. We recently demonstrated that plasma oxidized low density lipoprotein (LDL) levels significantly increased after a single HD session. This HD session-related increase in plasma oxidized LDL levels could contribute to the progression and acceleration of atherosclerosis and arterial calcification, leading to the development of cardiovascular events in HD patients.
Department of Pathology, Osaka City University Graduate School of Medicine, Japan.
Mayumi
M
Inaba
Makiko
M
Ueda
D000818:Animals; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology; D018450:Disease Progression; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood; D008264:Macrophages / Q000502:physiology; D051379:Mice; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000473:pathology / Q000502:physiology; D018384:Oxidative Stress; D058226:Plaque, Atherosclerotic / Q000209:etiology* / Q000473:pathology; D015995:Prevalence; D006435:Renal Dialysis / Q000009:adverse effects; D013601:T-Lymphocytes / Q000502:physiology; D061205:Vascular Calcification / Q000145:classification / Q000209:etiology* / Q000473:pathology
D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein