Macrophages and atherosclerotic plaque stability

Low-density lipoprotein receptor gene therapy using helper-dependent adenovirus produces long-term protection against atherosclerosis in a mouse model of familial hypercholesterolemia

“…Medium-sized atherosclerotic vessels such as the coronary arteries are susceptible to acute occlusion as a result of plaque rupture and thrombosis, events that are thought to occur much more commonly in vulnerable-looking lesions. [20][21][22][23] We found that, in addition to a marked inhibition of atherosclerotic lesion …”

Coinfection with Mycoplasma Pneumoniae and Chlamydia Pneumoniae in ruptured plaques associated with acute myocardial infarction

“…The mean number of lymphocytes per field was calculated and divided by 0.36 mm 2 (area of the microscopic field), providing the mean number of lymphocytes per mm 2 . In the plaque, all lymphocytes were counted and divided by the area of the plaque in mm 2 .…”

“…However, the cause of this inflammation still remains unclear 1,2 . Oxidized low-density lipoproteins (LDL) 3,4 , tissue factor 5 , and other factors have been considered important in the development of rupture and thrombosis of the plaque 6,7 .…”

Comparison between Adventitial and Intimal Inflammation of Ruptured and Nonruptured Atherosclerotic Plaques in Human Coronary Arteries

“…Many reports [3][4][5][6][7][8] have attributed to inflammation in the cap and shoulder of the atherosclerotic lesion a fundamental pathogenetic role in plaque disruption and consequent acute thrombotic complications; otherwise, microvessels in atherosclerotic plaques have been considered to favor the influx of inflammatory cells into them 9,10 . Few pathological studies have addressed the involvement of inflammation in the media or adventitia 11,12 in the development of atherosclerosis and arterial remodelling.…”