Neutrophil infiltration of culprit lesions in acute coronary syndromes.
BACKGROUND
Neutrophils in unstable atherosclerotic lesions have not received much consideration, despite accumulating evidence suggesting a link between systemic inflammation and acute coronary syndromes.


RESULTS
Coronary artery segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI); 8 had a ruptured and 5 an eroded plaque. Patients (n=45) who had died of noncardiovascular diseases served as reference. Atherectomy specimens were obtained from 35 patients with stable angina pectoris (SAP) and from 32 patients with unstable angina pectoris (UAP). Antibodies against CD66b, elastase, myeloperoxidase, and CD11b identified neutrophils; CD10 identified neutral endopeptidase (NEP). CD66b-positive and NEP-positive neutrophils were counted and expressed as a number per square millimeter of tissue. All specimens with plaque rupture or erosion showed distinct neutrophil infiltration; the number did not differ between ruptured and eroded plaques. However, the number of NEP-positive neutrophils was significantly higher (P<0.0001) in ruptured plaques than in eroded plaques. UAP patients showed neutrophils in 14 of 32 culprit lesions; in SAP only 2 of 35 lesions contained neutrophils. The number of neutrophils and NEP-positive cells in patients with UAP was significantly higher (neutrophils, P<0.0005; NEP-positive cells, P<0.005) than in patients with SAP.


CONCLUSIONS
The observations suggest that neutrophil infiltration is actively associated with acute coronary events. The high number of NEP-positive neutrophils in ruptured plaques, compared with eroded plaques, may reflect differences in the underlying pathophysiological mechanisms.
Naruko
Takahiko
T
Department of Cardiology, Osaka City General Hospital, Osaka.
Ueda
Makiko
M
Haze
Kazuo
K
van der Wal
Allard C
AC
van der Loos
Chris M
CM
Itoh
Akira
A
Komatsu
Ryushi
R
Ikura
Yoshihiro
Y
Ogami
Masayuki
M
Shimada
Yoshihisa
Y
Ehara
Shoichi
S
Yoshiyama
Minoru
M
Takeuchi
Kazuhide
K
Yoshikawa
Junichi
J
Becker
Anton E
AE
D000208:Acute Disease; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000473:pathology; D000789:Angina, Unstable / Q000473:pathology; D000918:Antibody Specificity; D015703:Antigens, CD; D000951:Antigens, Neoplasm / Q000096:biosynthesis; D017225:Atherectomy, Coronary; D039481:CD11b Antigen / Q000096:biosynthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002452:Cell Count; D003324:Coronary Artery Disease / Q000473:pathology* / Q000601:surgery; D003331:Coronary Vessels / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology; D015260:Neprilysin / Q000096:biosynthesis; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology*; D009195:Peroxidase / Q000096:biosynthesis
D015703:Antigens, CD; D000951:Antigens, Neoplasm; D039481:CD11b Antigen; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D009195:Peroxidase; D015260:Neprilysin