Neutrophil Infiltration of Culprit Lesions in Acute Coronary Syndromes

Naruko, Takahiko; Ueda, Makiko; Haze, Kazuo; Wal, Allard C. van der; Loos, Chris M. van der; Itoh, Akira; Komatsu, Ryushi; Ikura, Yoshihiro; Ogami, Masayuki; Shimada, Yoshihisa; Ehara, Shoichi; Yoshiyama, Minoru; Takeuchi, Kazuhide; Yoshikawa, Junichi; Becker, Anton E.

doi:10.1161/01.cir.0000042674.89762.20

Cited by 586 publications

(429 citation statements)

References 24 publications

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“…28,29 These acute-injury responses may play important roles in many pathological conditions, including acute coronary syndromes, as demonstrated by experimental and autopsy histological studies that show neutrophil infiltration. 30,31 An intervention that attenuates the processes that lead to acute neutrophil recruitment might have far-reaching vasoprotective implications.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

et al. 2004

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Background-We have previously shown that estrogen (17␤-estradiol; E2) inhibits neointima formation and migration of leukocytes, particularly neutrophils, into rat carotid arteries after acute endoluminal injury. This study tested the hypothesis that E2 inhibits expression of adhesion molecules, chemokines, and proinflammatory cytokines in rat carotid arteries in the early hours after balloon injury, thus attenuating the stimulus for leukocyte entry and negatively modulating the injury response. Methods and Results-Ovariectomized (OVX) rats were randomly assigned to treatment with E2 or vehicle (V) and subjected to balloon injury of the right carotid artery. After 2, 6, and 24 hours, rats were euthanized, and both carotid arteries were processed for real-time reverse transcription-polymerase chain reaction (2 and 24 hours), ELISA (6 hours), or neutrophil chemotaxis assay (24 hours). Expression of mRNA for adhesion molecules (P-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1), chemoattractants (cytokine-induced neutrophil chemoattractant [CINC]-2␤ and monocyte chemoattractant protein [MCP]-1), and proinflammatory cytokines (interleukin [IL]-1 and IL-6) was markedly increased (2 to 5000 times) in injured arteries of OVXϩV rats at 2 hours and was reduced by 24 hours. E2 significantly attenuated expression of the proinflammatory mediators (by 60% to 80%) at 2 hours. ELISA confirmed injury-induced upregulation of neutrophil and monocyte/macrophage chemoattractants (CINC-2␣, MCP-1) in OVXϩV arteries and E2-induced inhibition of CINC-2␣ expression. E2 significantly (by 65%) inhibited neutrophil chemotactic activity of arterial homogenates. Conclusions-E2 attenuates the early vascular injury response, at least in part, by negatively modulating proinflammatory mediator expression and the resultant chemotactic activity of injured vessels for neutrophils.

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Section: Discussionmentioning

confidence: 99%

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

et al. 2004

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“…Inflammation is considered to play a substantial role in the pathophysiological process of cardiac remodeling and results in subsequent adverse events after AMI. Innate immune cells of the neutrophils and monocytes/macrophages are present in the development of atherosclerotic lesions,1, 2, 3 and their activation may contribute significantly to plaque instability 4, 5, 6. Acute myocardial ischemia induces a systemic immediate‐phase response of the immune system, leading to cytokine and chemokine production and to the recruitment of neutrophils and mononuclear cells in the infarcted region of the heart 7, 8…”

Section: Introductionmentioning

confidence: 99%

Prognostic Utility of Soluble TREM‐1 in Predicting Mortality and Cardiovascular Events in Patients With Acute Myocardial Infarction

Wang

Tang

Shen

et al. 2018

JAHA

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BackgroundTriggering receptor expressed on myeloid cells‐1 (TREM‐1) is thought to be critical for inflammatory signal amplification and involved in the development of atherosclerosis. TREM‐1 is significantly increased in patients with myocardial infarction. The aim of this study was to investigate the association between soluble TREM‐1 (sTREM‐1) and mortality and cardiovascular events in patients with acute myocardial infarction.Methods and ResultsWe included 838 consecutive patients with acute myocardial infarction from October 7, 2012 to December 5, 2014. Blood samples were collected from patients with acute myocardial infarction immediately after diagnosis. During follow‐up, 88 patients died, and 180 patients reached the combined end points of major adverse cardiovascular event (MACE). Patients with high sTREM‐1 (higher than the median) had increased risk of all‐cause mortality and MACE compared with those with low sTREM‐1 (log‐rank test, P<0.001). After adjustment for confounding risk factors by Cox regression analysis, high sTREM‐1 remained an independent predictor of all‐cause mortality (hazard ratio, 1.978; 95% confidence interval, 1.462–2.675; P<0.001) and MACE (hazard ratio, 2.413; 95% confidence interval, 2.022–2.879; P<0.001). After the addition of sTREM‐1 to the reference model, the C‐statistic for all‐cause mortality increased from 0.86 to 0.89, and the difference was 0.023 (95% confidence interval, 0.0009–0.0477), and the C‐statistic for MACE increased from 0.71 to 0.80, and the difference was 0.087 (95% confidence interval, 0.053–0.122). sTREM‐1 levels were consistently positively associated with risks of all‐cause mortality and MACE in various subpopulations, and there was no significant interaction among prespecified subgroups.Conclusions sTREM‐1 was significantly associated with all‐cause mortality and MACE, independent of established conventional risk factors in patients with acute myocardial infarction.

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“…35 Naruko et al found in their study that neutrophil infiltration holds an important role in the destabilization of the atherosclerotic plaque. 36 Cancer therapies such as tyrosine kinase inhibitors in patients with chronic myeloid leukemia represent an increased risk for cardiovascular events (10%). 37 Moslehi et al stated that noninvasive cardiovascular screening is necessary before the start of dasatinib therapy and for patients with cardiopulmonary symptoms receiving treatment.…”

Section: Risk Of Artery Catheterization In Patients With Essential Thmentioning

confidence: 99%

Noninvasive Assessment of Coronary Arteries in Patients with Hematologic Disorders

Lázár¹,

Oltean²,

Jáni³

et al. 2017

Journal of Interdisciplinary Medicine

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Hematological conditions and their treatments have an increased risk of cardiovascular events, and invasive interventions have a higher risk of periprocedural complications in this group of patients. The aim of this review was to evaluate the risk of invasive interventions in patients with hematologic disorders and to underline the role of noninvasive cardiovascular screening in patients with hematological disorders such as Hodgkin and non-Hodgkin lymphoma, anemia, hemophilia, thrombocythemia, polycythemia vera, and leukemia. Based on present knowledge in the field, our opinion is that the screening of patients with hematological diseases is very important to reduce the morbidity and mortality due to cardiovascular events. Noninvasive assessments are suitable for this purpose with a significantly lower risk compared to invasive interventions.

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Neutrophil Infiltration of Culprit Lesions in Acute Coronary Syndromes

Cited by 586 publications

References 24 publications

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

Prognostic Utility of Soluble TREM‐1 in Predicting Mortality and Cardiovascular Events in Patients With Acute Myocardial Infarction

Noninvasive Assessment of Coronary Arteries in Patients with Hematologic Disorders

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