Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction:a possible role for left ventricular remodeling

Maekawa, Yuichiro; Anzai, Toshihisa; Yoshikawa, Tsutomu; Asakura, Yasushi; Takahashi, Toshiyuki; Ishikawa, Shiro; Mitamura, Hideo; Ogawa, Satoshi

doi:10.1016/s0735-1097(01)01721-1

Cited by 275 publications

(196 citation statements)

References 19 publications

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“…The concordant nature of the results likely reflects the strong effector role of monocytes in mediating inflammation. Not surprisingly, these molecular studies also mirror a number of prior clinical investigations demonstrating a simple association between peripheral monocyte count and subclinical atherosclerosis, post-myocardial infarction ventricular remodeling and in-stent restenosis (Chapman et al 2004, Fukuda et al 2004, Maekawa et al 2002. Though we have simply summarized the findings reported by the studies in Table 1, it will be useful in the future to perform a more systematic and complete analysis of all the primary data.…”

Section: Concordance Of Transcriptional Studies Of Human Atherosclerosupporting

confidence: 56%

Genomic Analysis of Circulating Cells: A Window Into Atherosclerosis

Kang

Patino

Matoba

et al. 2006

Trends in Cardiovascular Medicine

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Translational studies using genomic techniques in cardiovascular diseases are still in their infancy. Access to disease-associated cardiovascular tissues from patients has been a major impediment to progress in contrast to the diagnostic advances made by oncologists using gene expression on readily available tumor samples. Nonetheless, progress is being made for atherosclerosis by carefully designed experiments using diseased tissue or surrogate specimens. This review details the rationale and findings of a study using freshly isolated blood mononuclear cells from patients undergoing carotid endarterectomy due to atherosclerotic stenosis and from matched normal subjects. Using this cardiovascular tissue surrogate, the mRNA levels of the Finkel-Biskis-Jinkins osteosarcoma (FOS) gene in circulating monocytes were found to correlate with atherosclerosis severity in patients, and with HMG CoA reductase inhibitor (statin) therapy in normal subjects. The major finding of this investigation is discussed in relation to observations from other human atherosclerosis gene expression studies. These distinct studies converge to demonstrate the unequivocal importance of inflammation in atherosclerosis. Although the clinical utility of the specific findings remains open, the identification of similar genes by different investigations serves to validate their reports. They also provide us with insights into pathogenesis that may impact future translational applications. Diagnostic markers of inflammation and atherosclerosisBased on our current understanding of atherosclerosis, the pathogenesis of this leading cause of morbidity and mortality in westernized societies is best described by chronic vascular inflammation that starts early in life and exacerbates with aging (Glass and Witztum 2001, Hansson 2005). Multiple hereditary and environmental factors contribute to the initiation and progression of this disease (Lusis 2000). However, some well established clinical risk factors such as low density lipoprotein (LDL) and the metabolic syndrome (including obesity and insulin-resistance, diabetes) and basic factors such as angiotensin II all appear to promote oxidative stress and inflammation (Daugherty and Cassis 2004, Glass and Witztum 2001, Libby 2002. Though a number of molecules linked to inflammation have been proposed for use as atherosclerosis markers, C-reactive protein (CRP) has gained prominence because of its association with increased cardiovascular risk in clinical trials (Jain and Ridker 2005). Revealing insights into statins' mechanism of action, the recent clinical trial PROVE IT-TIMI 22 separated the cholesterol lowering and anti-inflammatory effects of statin therapy by demonstrating the independent and additive predictive values of serum cholesterol and CRP levels on cardiovascular events, respectively (Jain andRidker 2005, Ridker et al. 2005). A question that follows such fundamental observations is whether there exist other predictive markers that have equal or greater sensitivity and specificity. Th...

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Section: Concordance Of Transcriptional Studies Of Human Atherosclerosupporting

confidence: 56%

Genomic Analysis of Circulating Cells: A Window Into Atherosclerosis

Kang

Patino

Matoba

et al. 2006

Trends in Cardiovascular Medicine

View full text Add to dashboard Cite

show abstract

“…Exacerbated and prolonged inflammation may impede the healing process, as it was shown in infarcted mice with atherosclerosis that displayed adverse cardiac remodeling and blood monocytosis (38). Accordingly, elevated blood monocyte counts in patients after MI negatively correlate with ejection fraction (39). Along these lines, humans and mice with heart failure also display a blood leukocytosis (3,40,41).…”

Section: Monocytes/macrophages In the Post-mi Phasementioning

confidence: 95%

Monocytes and macrophages in cardiac injury and repair

Sager¹,

Kessler²,

Schunkert³

2017

J. Thorac. Dis.

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“…Recently, clinical research has focused on the predictive effects of blood cell-related biomarkers on admission and their usefulness in modifying the clinical approach of no-reflow phenomenon in patients with acute myocardial infarction (AMI). Recent investigations have suggested that monocytes may be involved in the pathogenesis of coronary artery disease [3] and high total monocyte count is a strong predictor of high risk of myocardial infarction (MI) [4]. Previous studies have shown that interactions between monocytes and platelets probably play an important role in the pathogenesis of coronary microvascular obstruction [5].…”

Section: Introductionmentioning

confidence: 99%

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

et al. 2016

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A b s t r a c t Background:The no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction. Aim:To assess the relation between admission monocyte count and angiographic no-reflow after pPCI. Methods:A total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades ≤ 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI. Conclusions:Monocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.

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Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction:a possible role for left ventricular remodeling

Abstract: Peripheral monocytosis is associated with LV dysfunction and LV aneurysm, suggesting a possible role of monocytes in the development of LV remodeling after reperfused AMI.

Cited by 275 publications

References 19 publications

Genomic Analysis of Circulating Cells: A Window Into Atherosclerosis

Genomic Analysis of Circulating Cells: A Window Into Atherosclerosis

Monocytes and macrophages in cardiac injury and repair

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

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