Systemic infections cause exaggerated local inflammation in atherosclerotic coronary arteries: clues to the triggering effect of acute infections on acute coronary syndromes.
Systemic infections can trigger heart attacks. We conducted an autopsy study to investigate the pathologic effect of systemic infections on coronary artery inflammation. We studied 14 atherosclerotic patients diagnosed with an acute systemic infection. Our control group (n=13) had atherosclerosis without infection. The groups were similar in luminal stenosis and age. Coronary artery sections were stained with H&E and markers for macrophages (CD68), T cells (CD3), and dendritic cells (S100). On pathologic examination, 5 infected patients had acute myocardial infarction with thrombosis. Macrophage density in plaques and in periadventitial fat was higher in the infected group (NS). The infected patients' adventitia had significantly more macrophages (1,577 +/- 1,872 vs 265 +/- 185 per mm(2); P=0.047). The macrophage density, similar in the control group's adventitia and plaque, was significantly greater in the infected group's adventitia than in the plaque. The adventitia and periadventitial fat of the infected group had more T cells than did samples from the control group (48.4 +/- 45.0 vs 14.1 +/- 6.3 per mm(2); P=0.002). The groups exhibited similar plaque T-cell density. The infected patients' plaques, but not the adventitia and periadventitial fat, had more dendritic cells than did the controls' (3.2 +/- 2.5 vs 0.3 +/- 0.5 per mm(2); P=0.022). To our knowledge, this is the 1st report to establish a connection between acute systemic infections and significant increases in inflammatory cells in the atherosclerotic coronary arteries of human beings. This offers a new therapeutic target for preventing heart attacks in high-risk patients.
Madjid
Mohammad
M
Atherosclerosis Research Laboratory, Texas Heart Institute at St. Luke's Episcopal Hospital, Houston, TX 77030, USA. Mohammad.Madjid@uth.tmc.edu
Vela
Deborah
D
Khalili-Tabrizi
Hessam
H
Casscells
S Ward
SW
Litovsky
Silvio
S
D000208:Acute Disease; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D016022:Case-Control Studies; D003238:Connective Tissue / Q000473:pathology; D003324:Coronary Artery Disease / Q000209:etiology / Q000473:pathology; D023921:Coronary Stenosis / Q000209:etiology / Q000473:pathology; D003328:Coronary Thrombosis / Q000209:etiology / Q000473:pathology; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D012107:Research Design; D012141:Respiratory Tract Infections / Q000150:complications* / Q000378:metabolism; D009418:S100 Proteins / Q000378:metabolism; D018805:Sepsis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D013577:Syndrome; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D014552:Urinary Tract Infections / Q000150:complications* / Q000378:metabolism; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D009418:S100 Proteins; C067980:CD68 antigen, human; D000097382:CD68 Molecule