Increased subendothelial infiltration of the coronary arteries with monocytes/macrophages in patients with unstable angina Histological data on 14 autopsied patients

Sato, Takashi; Takebayashi, Shigeo; Kohchi, Kyoji

doi:10.1016/0021-9150(87)90198-5

Cited by 63 publications

(23 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It may also be that the late rise in CRP is partly an indirect consequence of reperfusion or revascularisation therapy. 38) Our results, together with the evidence of an inflammatory component documented in previous studies, [7][8][9][10][11][12][13][14][15]17) have important pathophysiologic implications regarding acute-phase response and C-reactive protein levels in patients with acute coronary syndromes. However, it is not known whether the elevated levels of acute-phase proteins are related to the type of inflammatory stimuli or to the intensity of the individual response.…”

Section: Discussionmentioning

confidence: 79%

“…A role for inflammation in unstable angina is suggested by histologic studies of unstable coronary plaques, [7][8][9][10] evidence of the systemic release of thromboxanes and leukotrienes, [11][12][13] and the presence of activated circulating leukocytes. 14,15) Furthermore, increased concentrations of plasma C-reactive protein, the prototypal acute-phase reactant, have been reported in some patients with unstable angina, 16,17) in patients with coronary artery disease and other types of angina, 18) and in 20 percent of patients who have an acute myocardial infarction within six hours after the onset of symptoms, before any elevation of myocardialenzyme levels in serum.…”

mentioning

confidence: 99%

See 1 more Smart Citation

<b>C-reactive Protein and Coronary Artery Disease</b>

et al. 2002

View full text Add to dashboard Cite

SUMMARYEvidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop to an acute clinical event by the induction of plaque rupture and therefore cause acute coronary syndromes.The aim of this study was to determine the serum levels of the circulating acute-phase reactant C-reactive protein (CRP), which is a sensitive indicator of inflammation, in patients with chronic stable coronary artery disease (CAD) and acute coronary syndromes (ACS).We studied 56 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age, 68.5±14.3 years, range, 40-86) with unstable angina (UA) or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64±12.7; range, 47-83, years) with signs and symptoms of clinically stable CAD. High-sensitivity-C-reactive protein (hs-CRP) levels were determined with a commercially available enzyme-linked immunoassay method.In patients with unstable angina and AMI before reperfusion therapy, CRP levels were not significantly different to those in patients with stable CAD (5.96±2.26 versus 4.35±2.6 mg/L; P=0.12), but tended to be higher in patients with unstable angina and AMI. Baseline CRP levels in the subgroup of patients with AMI (6.49±2.28 mg/L) were significantly higher than levels in patients with stable CAD (4.35±2.6 mg/L; P=0.02).CRP levels in patients with unstable angina and AMI were measured four times during a 72-hour period (0, 12, 24, and 72 hours). The lowest value was observed at baseline and differed significantly from values measured at any other time of the observation period (P<0. 001; 5.96±2.26; 9.5±9.04, 18.25±11.02; 20.25±10.61). CRP levels after 12, 24, and 72 hours were also significantly different to the initial values for patients with stable CAD (P<0.01). There was no correlation between CRP and creatine kinase (CK), CK-MB isoenzyme, or troponin I positivity as markers for the extent of the myocardial injury during the observation period.Baseline levels of serum CRP tended to be higher in patients with unstable angina or AMI but were not significantly different from levels in patients with chronic stable CAD. In the subgroup of patients with AMI, baseline CRP levels were significantly higher than the levels in patients with stable CAD. CRP as a marker of inflammation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 12 hours), supporting the hypothesis of an activation of inflammatory From

show abstract

Section: Discussionmentioning

confidence: 79%

mentioning

confidence: 99%

<b>C-reactive Protein and Coronary Artery Disease</b>

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Atherosclerosis is now considered to be a chronic inflammatory process due to arterial injury (1)(2)(3)(4)(5). Pathological studies have shown that there is invasion of macrophages and T-lymphocytes into atherosclerotic plaques, which suggests that both innate and acquired immunity are involved in the pathogenesis of atherosclerosis (5,6).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Expression of TLR2 (Toll-like Receptor 2) and TLR4 on Circulating Monocytes in Coronary Artery Disease

Ashida

Miyazaki

Takayama

et al. 2005

J Atheroscler Thromb

View full text Add to dashboard Cite

TLRs are receptors involved in the recognition of pathogens by the innate immune system, and TLR2 and TLR4 play important roles in the activation of monocytes. A total of 105 consecutive patients who underwent coronary angiography comprised of 46 with stable effort angina (SA), 41 with unstable angina (UA), and 18 with no significant CAD (CNT) were enrolled. The baseline expression levels of TLR2 and TLR4 on monocytes in peripheral blood mononuclear cells (PBMCs) were determined by flowcytometric analysis. Since TLR2 expression has been reported to be regulated by TLR4 signaling, we cultured PBMCs with or without lipopolysaccharide (LPS, 1 µ µ µ µ µg/ ml). At baseline, TLR4 levels (mean of fluorescence intensity ) in SA (145 ± ± ± ± ± 58, p < 0.05) and UA (164 ± ± ± ± ± 65, p < 0.01) were higher than those in CNT (107 ± ± ± ± ± 37). As for TLR2, levels were higher in UA (108 ± ± ± ± ± 36, p < 0.05) than in SA (94 ± ± ± ± ± 18) and CNT (87 ± ± ± ± ± 22). After stimulation with LPS, TLR2 levels increased in SA but decreased in UA. In conclusions, TLR4 levels increased in both SA and UA. Monocytes in UA were characterized by elevated TLR2 levels and unresponsiveness of the TLR2 levels to TLR4 stimulation. J Atheroscler Thromb, 2005; 12: 53-60.

show abstract

“…[21][22][23][24][25] Coronary atherosclerotic plaques contain abundant lymphoplasma cell and monocyte-macrophage infiltrates,26-29 which are found much more frequently to be markedly increased into the site of plaques in subendothelium and in perivascular nerves of unstable angina patients with fatal outcome than of patients with effort angina who died of noncardiac causes, even with the same degree of coronary luminal narrowing. [30][31][32] After in vitro exposure to immune or nonimmune stimuli, monocytes express tissue factor on their surfaces24,33-40 and can specifically activate blood clotting.…”

mentioning

confidence: 99%