Neutrophil-to-lymphocyte ratio predicts coronary artery lesion severity and long-term cardiovascular mortality in patients with unstable angina pectoris.

OBJECTIVES: Neutrophil-to-lymphocyte ratio (NLR), one of the composite biomarker of systemic inflammatory status, was proved promising in predicting clinical outcomes of acute coronary syndrome (ACS). However, there were no evidences that NLR was directly relative to the clinical outcomes of unstable angina pectoris (UAP). Therefore, this study was aimed to detect whether NLR could predict the coronary artery lesion severity (indicated as SYNTAX score) and clinical outcomes (especially long-term cardiovascular mortality) in patients with. METHODS: In the single-centre retrospective study, 4110 patients with UAP were enrolled and divided into two groups according to their primary NLR values and followed up at a median time duration of 36 months. The differences of SYNTAX score and cardiovascular mortality between groups were analysed, and the predictive value of NLR was determined. RESULTS: NLR was positively and linearly correlated with SYNTAX score (r = 0.270). Diabetes (p = 0.049), lymphocyte (p = 0.004), NLR (p = 0.002) and SYNTAX score (p < 0.001) were independent predictors of long-term cardiovascular mortality in patients with UAP. Kaplan-Meier analysis revealed higher occurrence of cardiovascular mortality when NLR > 2.38 (p = 0.015). Receiver operating characteristic (ROC) analysis showed that NLR = 2.76 is an effective cut point for predicting cardiovascular mortality (69.2% sensitivity, 64.8% specificity). CONCLUSIONS: NLR value was positively related to the severity of coronary artery lesion and proved to be an independent predictor of cardiovascular mortality in patients with UAP. This study would contribute to therapy and prognosis optimisation of UAP.

Involvement of enhanced expression of classical complement C1q in atherosclerosis progression and plaque instability: C1q as an indicator of clinical outcome.

Activation of the classical complement pathway plays a major role in regulating atherosclerosis progression, and it is believed to have both proatherogenic and atheroprotective effects. This study focused on C1q, the first protein in the classical pathway, and examined its potentialities of plaque progression and instability and its relationship with clinical outcomes. To assess the localization and quantity of C1q expression in various stages of atherosclerosis, immunohistochemistry, western blotting, and real-time polymerase chain reaction (PCR) were performed using abdominal aortas from eight autopsy cases. C1q immunoreactivity in relation to plaque instability and clinical outcomes was also examined using directional coronary atherectomy (DCA) samples from 19 patients with acute coronary syndromes (ACS) and 18 patients with stable angina pectoris (SAP) and coronary aspirated specimens from 38 patients with acute myocardial infarction. C1q immunoreactivity was localized in the extracellular matrix, necrotic cores, macrophages and smooth muscle cells in atherosclerotic lesions. Western blotting and real-time PCR illustrated that C1q protein and mRNA expression was significantly higher in advanced lesions than in early lesions. Immunohistochemical analysis using DCA specimens revealed that C1q expression was significantly higher in ACS plaques than in SAP plaques. Finally, immunohistochemical analysis using thrombus aspiration specimens demonstrated that histopathological C1q in aspirated coronary materials could be an indicator of poor medical condition. Our results indicated that C1q is significantly involved in atherosclerosis progression and plaque instability, and it could be considered as one of the indicators of cardiovascular outcomes.

Impact of clinical presentations on lipid core plaque assessed by near-infrared spectroscopy intravascular ultrasound.

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) studies have demonstrated that lipid core plaque (LCP) is frequently observed in the culprit segment of myocardial infarction (MI). However, little is known about the impact of clinical presentations such as chronic coronary syndrome (CCS) and acute coronary syndrome (ACS) including unstable angina (UA), non ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI) on LCP. The present prospective single-center registry included a total of 178 patients who underwent percutaneous coronary intervention under NIRS-IVUS guidance. Patients were divided into CCS and ACS groups, and ACS patients were further sub-divided into the 3 groups according to the clinical presentation. The primary endpoint was coronary LCP in the target lesion assessed by NIRS-IVUS with maximal lipid core burden index over any 4 mm segment (maxLCBI4mm). The study population included 124 and 54 patients with CCS and ACS. MaxLCBI4mm in the target lesion was significantly higher in the ACS group than in the CCS group (503 [284-672] vs. 406 [250-557], p = 0.046). Among ACS patients, MaxLCBI4mm in the target lesion was also significantly different in those with UA (n = 18), NSTEMI (n = 21), and STEMI (n = 15) (288 [162-524] vs. 518 [358-745] vs. 646 [394-848], p = 0.021). In conclusion, LCP assessed by NIRS-IVUS, a surrogate of coronary plaque vulnerability, was significantly different according to the clinical presentations such as CCS, UA, NSTEMI, and STEMI.

Extracellular ubiquitin levels are increased in coronary heart disease and associated with the severity of the disease.

Aim: This study aimed to evaluate concentration of plasma extracellular ubiquitin (UB) in coronary heart disease (CHD) patients and its correlation with the disease severity.Methods: Levels of UB and stromal cell-derived factor-1a (SDF-1a) were measured in 60 healthy controls and 67 CHD cases. Coronary atherosclerosis was assessed with Gensini scoring system. Spearman correlation was used to evaluate the correlation between UB and low-density lipoprotein cholesterol (LDL-C), C-reactive protein (CRP), creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) or SDF-1a. The receiver-operating characteristic (ROC) curve was established to assess the predictive value of UB.Results: Plasma UB levels were significantly higher in CHD patients than in controls (p < .0001), and the levels in those with acute myocardial infarction (AMI) were higher than stable angina pectoris (SAP) and unstable angina pectoris (UAP) groups (both p < .01). UB was also positively correlated with Gensini score, CRP, CK-MB and cTnI in CHD. ROC analysis of UB showed that the area under the curve (AUC) were 0.711 (95%CI, 0.623-0.799) and 0.778 (95%CI, 0.666-0.890) for CHD and acute coronary syndrome (ACS), respectively. Plasma SDF-1a levels were elevated in CHD patients but showed no significant correlation with UB concentration or the severity of the disease.Conclusion: Plasma UB concentration was increased in CHD and the change of UB levels may reflect the progression of CHD.

Suppression of long noncoding RNA NEAT1 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-378a-3p.

BACKGROUND/AIMS: lncRNA NEAT1 is involved in the development of many diseases. However, the function of lncRNA NEAT1 in myocardial infarction is unclear. Therefore, this experimental design based on lncRNA NEAT1 to explore the pathogenesis of myocardial infarction. METHODS: RT-qPCR was used to detect the expression of lncRNA NEAT1 and miR-378a-3p in peripheral blood and mouse cardiomyocytes of patients with myocardial infarction. MTT assay, flow cytometry, Caspase-3 kit and transwell assay were used to detect the effects of lncRNA NEAT1 and miR-378a-3p on cardiomyocyte proliferation, apoptosis and migration. Target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lncRNA NEAT1 and miR-378a-3p. Western blotting was used to detect the protein expression of Atg12 and related autophagy genes. RESULTS: lncRNA NEAT1 was highly expressed in peripheral blood and mouse cardiomyocytes of patients with myocardial infarction. Moreover, lncRNA NEAT1 significantly promoted cell proliferation and migration of cardiomyocytes. In addition, lncRNA NEAT1 inhibited miR-378a-3p expression, and miR-378a-3p inhibited Atg12 expression, while lncRNA NEAT1 regulated expression of Atg12 and related autophagic factors via miR-378a-3p. Knockout of microRNA-378-3p reversed the effects of NEAT1 silencing on cell damage. CONCLUSION: lncRNA NEAT1 can regulate the proliferation of cardiomyocytes by regulating miR-378-3p/Atg12 axis, thus accelerating the occurrence and development of cardiomyocytes.

CRAX: A simple cardiovascular risk assessment tool to predict risk of acute myocardial infarction or death.

BACKGROUND: Determining the risk of cardiovascular events is essential to optimize patient management. METHODS AND RESULTS: 5842 individuals underwent SPECT myocardial perfusion imaging (MPI) with 4.4 ± 1.2 years of follow-up. Models (the CRAX tool) were derived to predict the cumulative risk of death and acute myocardial infarction (AMI) at 1, 3, and 5 years using clinical and MPI variables. Predictors of AMI and death included age, number of hospitalizations in the 3 years preceding MPI, and left ventricular ejection fraction (LVEF). Additional predictors of death were the use of pharmacological stress, and global stress total perfusion deficit (sTPD), while transient ischemic dilation (TID), and ischemic total perfusion deficit (iTPD) change were predictive of AMI. CRAX predictions were significantly (P < .001) more accurate than clinical variables or MPI results alone, resulting in a significant net reclassification improvement (NRI, 7.5% for AMI, 14.5% death) compared to clinical variables alone. Accuracy for predicting major adverse cardiac events (MACE, comprising all-cause death, AMI, unstable angina, late revascularization) was comparable to that of AMI or death. CONCLUSIONS: CRAX is a risk assessment tool that predicts the risk of AMI, death, or MACE, and improves prediction compared to clinical variables or MPI results alone.

Plasma levels of receptor interacting protein kinase-3 correlated with coronary artery disease.

BACKGROUND: Necroptosis plays an important role in human atherosclerosis and atheroma development. Since receptor interacting protein kinase-3 (RIP3) acts as a key mediator of necroptosis, this study aimed to explore its relationship between plasma RIP3 levels and coronary artery disease (CAD) and discover a potential new biomarker for screening CAD subtypes and severity. METHODS: A total of 318 patients with CAD who had coronary angiography and 166 controls in Peking Union Medical College Hospital from September 2017 to January 2018 were enrolled in this study. Patients with CAD were divided into three subgroups: patients with stable coronary artery disease (SCAD), patients with unstable angina (UA), and patients with myocardial infarction (MI). The severity of atherosclerosis was determined by Gensini score (GSS). Logistic regression was used to determine the relationship between plasma RIP3 levels and CAD. The correlation between plasma RIP3 and GSS was calculated using multiple linear regression models. RESULTS: Overall, plasma RIP3 levels were significantly higher than serum RIP3 levels. Plasma RIP3 levels in patients with CAD were significantly higher than those in controls. Plasma RIP3 levels were strongly associated with CAD (odds ratio: 6.00, 95% confidence interval 3.04-11.81; P < 0.001). Plasma RIP3 levels increased linearly from controls to patients with SCAD, then patients with UA, and finally to patients with MI. We found a significantly positive correlation between proportion of cases of acute coronary syndrome in subjects and their plasma RIP3 level quartile. Plasma RIP3 levels were also associated with GSS (B 0.027; standard error 0.012; P < 0.05). CONCLUSIONS: Plasma RIP3 levels were independently associated with CAD. Plasma RIP3 levels could potentially supplement clinical assessment to screen CAD and determine CAD severity.

Association of plasma apolipoprotein CIII, high sensitivity C-reactive protein and tumor necrosis factor-α contributes to the clinical features of coronary heart disease in Li and Han ethnic groups in China.

BACKGROUND: Apolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China. METHODS: A cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal-Wallis or Wilcoxon-Mann-Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software. RESULTS: Compared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp(a) (P < 0.05, TC and Lp(a); P < 0.01, FBS, TG, LDL-C, apoB); and lower HDL-C and apoAI (P < 0.05). Plasma apoCIII, TNF-α and hs-CRP levels were higher in CHD individuals (16.77 ± 5.98 mg/dL vs. 10.91 ± 4.97 mg/dL; 17.23 ± 6.34 pg/mL vs. 9.49 ± 3.88 pg/mL; 9.55 ± 7.32 mg/L vs. 2.14 ± 1.56 mg/L; P < 0.01 vs. healthy participants). Identical patterns were obtained in the Li and Han groups (16.46 ± 6.08 mg/dL vs. 11.72 ± 5.16 mg/dL; 15.71 ± 5.52 pg/mL vs. 9.74 ± 4.31 pg/mL; 8.21 ± 7.09 mg/L vs. 2.15 ± 1.51 mg/L in Li people; 17.05 ± 5.90 mg/dL vs. 10.07 ± 4.63 mg/dL; 18.59 ± 6.73 pg/mL vs. 9.23 ± 3.38 pg/mL; 10.75 ± 7.44 mg/L vs. 2.12 ± 1.63 mg/L in Han people; P < 0.01). Paired comparisons of subgroups with stable angina, unstable angina, and acute myocardial infarction (AMI) revealed significant variation in plasma levels of apoCIII, TNF-α and hs-CRP (P < 0.01), but not among subgroups with mild, moderate and severe stenosis (P > 0.05). Plasma apoCIII, TNF-α and hs-CRP contributed to the development of CHD (OR = 2.554, 7.252, 6.035, P < 0.01) with paired correlations in CHD patients (apoCIII vs. TNF-α, r = 0.425; apoCIII vs. hs-CRP, r = 0.319; TNF-α vs. hs-CRP, r = 0.400, P < 0.01). CONCLUSIONS: Association among plasma apoCIII, hs-CRP and TNF-α interacts with unfavorable lipid profiles to contribute to the clinical features of CHD with stable angina, unstable angina, and AMI in the Li and Han ethnic groups in China.

Quantitative Extent of Atherosclerotic Plaque in the Major Epicardial Coronary Arteries in Patients with Fatal Coronary Heart Disease, in Coronary Endarterectomy Specimens, in Aorta-Coronary Saphenous Venous Conduits, and Means to Prevent the Plaques: A Review after Studying the Coronary Arteries for 50 Years.

This review tries to answer the following 15 questions: Is atherosclerosis a systemic or a regional disease? Is atherosclerosis in any particular region focal or diffuse? What is the quantity of atherosclerotic plaques in endarterectomy specimens of the right coronary artery in patients undergoing coronary artery bypass grafting (CABG) compared to that in the right coronary artery in patients with fatal coronary artery disease? How do the units used for measuring arterial narrowing by angiography compare to the units used for measuring arterial narrowing at necropsy? What do atherosclerotic plaques consist of in coronary arteries in patients with fatal coronary disease? What is the quantity of atherosclerotic plaque in bypassed -vs- non-bypassed native coronary arteries in patients dying early (<60 days) or late (>60 days) after coronary artery bypass grafting? What is the frequency of acute coronary lesions and multi-luminal channels at necropsy in patients with unstable angina pectoris, sudden coronary death, and acute myocardial infarction? What is the mechanism of luminal widening by angioplasty in the coronary arteries? What observations suggest that atherosclerotic plaques are the result at least in part of organization of thrombi? Is atherosclerosis a multifactoral or a unifactoral disease? What characteristics distinguish carnivores and herbivores? What are reasonable guidelines for whom to treat with lipid-altering agents? What is the rule of 5 and the rule of 7 in statin therapy? What is the effect of lipid lowering drug therapy on coronary luminal narrowing? What are some requisites for a healthy life?

Intermediate and nonclassical monocytes show heterogeneity in patients with different types of acute coronary syndrome.

This study was performed to gain further insight in the heterogeneity of monocytes in the different categories of acute coronary syndrome (ACS), especially between patients with unstable angina pectoris, ST-elevation myocardial infarction (STEMI), and non-ST-elevation myocardial infarction (NSTEMI). For this purpose, blood samples were collected in the acute phase from patients presenting with an ACS. These samples were examined with multiparameter flow cytometry to identify the different monocyte subsets and to analyze the expression of monocyte-associated molecules. Leukocytes, as well as an absolute number of monocytes, showed a clear and significant increase in patients with STEMI. This increase was seen in all subtypes of monocytes. The classical monocytes (CD14++CD16-) of patients with an NSTEMI had a significantly increased CD11b expression when compared to the control group, while these cells showed a decreased expression pattern in STEMI patients. This increased CD11b-expression was also seen in the intermediate monocytes of NSTEMI, while it was almost completely downregulated on the intermediate monocytes of STEMI. Finally, CX3CR1, which is almost exclusively expressed on intermediate and nonclassical monocytes, showed a significant decrease in expression in patients with STEMI. In conclusion, intermediate and nonclassical monocytes have a different immunophenotypic pattern in patients with STEMI versus NSTEMI. These differences reflect the pro-inflammatory state of the monocytes in NSTEMI and can be used as target molecules for novel therapeutic strategies to diminish the migration of proinflammatory monocytes into the myocardial tissue. © 2017 International Society for Advancement of Cytometry.

MMP1 and MMP3 gene polymorphisms in patients with acute coronary syndromes.

Matrix metalloproteinases (MMPs) are the group of proteolytic enzymes that break down the components of the connective tissue matrix leading to unstable atherosclerotic plaques. The aim of this study was to examine the association between MMP1-1607dupG (rs1799750) and MMP3-1171dupA (rs3025058) gene polymorphisms and acute coronary syndromes (ACS) in the form of unstable angina. This study included 197 patients with ACS in the form of unstable angina confirmed by coronary angiography (defined by >70% stenosis in at least one major coronary artery) and 144 healthy controls. There was no statistically significant difference in the distribution of the MMP1-1607dupG (rs1799750) polymorphism between patients with unstable angina and the control group. With regard to the MMP3-1171dupA (rs3025058) polymorphism, a significant increase in the frequency of the 6A/6A genotype among patients with unstable angina was detected. This association was confirmed in multivariate logistic regression analysis, where male sex and rs3025058 6A/6A genotype were significantly associated with an increased risk of ACS. © 2017 IUBMB Life, 69(11):850-855, 2017.

Unusually aggressive immature neo-intimal hyperplasia causing in-stent restenosis.

This image illustrates a very unusual pattern of early and aggressive immature neo-intimal hyperplasia in a 52-year-old man with unstable angina, two months after deployment of a drug-eluting stent in the proximal left anterior descending artery.

Prognostic value of CT-derived left atrial and left ventricular measures in patients with acute chest pain.

PURPOSE: To determine which left atrial (LA) and left ventricular (LV) parameters are associated with future major adverse cardiac event (MACE) and whether these measurements have independent prognostic value beyond risk factors and computed tomography (CT)-derived coronary artery disease measures. MATERIALS AND METHODS: This retrospective analysis was performed under an IRB waiver and in HIPAA compliance. Subjects underwent coronary CT angiography (CCTA) using a dual-source CT system for acute chest pain evaluation. LV mass, LV ejection fraction (EF), LV end-systolic volume (ESV) and LV end-diastolic volume (EDV), LA ESV and LA diameter, septal wall thickness and cardiac chamber diameters were measured. MACE was defined as cardiac death, non-fatal myocardial infarction, unstable angina, or late revascularization. The association between cardiac CT measures and the occurrence of MACE was quantified using Cox proportional hazard analysis. RESULTS: 225 subjects (age, 56.2±11.2; 140 males) were analyzed, of whom 42 (18.7%) experienced a MACE during a median follow-up of 13 months. LA diameter (HR:1.07, 95%CI:1.01-1.13permm) and LV mass (HR:1.05, 95%CI:1.00-1.10perg) remained significant prognostic factor of MACE after controlling for Framingham risk score. LA diameter and LV mass were also found to have prognostic value independent of each other. The other morphologic and functional cardiac measures were no significant prognostic factors for MACE. CONCLUSION: CT-derived LA diameter and LV mass are associated with future MACE in patients undergoing evaluation for chest pain, and portend independent prognostic value beyond traditional risk factors, coronary calcium score, and obstructive coronary artery disease.

A rare coronary anomaly consisting of a single right coronary ostium in an adult undergoing surgical coronary revascularization: a case report and review of the literature.

BACKGROUND: Coronary arteries originating from the right coronary ostium in the ascending aorta represent a very rare anatomic presentation. Also, the presence of a single coronary ostium is an extremely rare finding. CASE PRESENTATION: We present the case of a 74-year-old Albanian man from Kosovo. He had unstable angina due to critical triple vessel disease and a single coronary artery originating from a single ostium in the right sinus of Valsalva with an anomalous course of his left anterior descending artery anteriorly to the right ventricular outflow tract as a "T-vessel" from which originated the proximal and distal left anterior descending artery, the circumflex artery originating from the mid portion of the right coronary artery which had a normal course. He underwent successful coronary revascularization consisting of three vein grafts to the right coronary artery, first diagonal and obtuse marginal artery, and left internal mammary artery anastomosed to left anterior descending artery. CONCLUSIONS: We describe a proposed IID1 pattern. After a careful revision of the literature, only six cases have been reported with a similar anomalous coronary origin. Only two out of six patients underwent surgical coronary revascularization. In our case the aberrant vessel arising from his right coronary artery coursed anteriorly to the right ventricle and continued as a left anterior descending artery at its mid portion which then continued distally as the distal left anterior descending artery and proximally as a proximal left anterior descending artery, having the shape of a "T vessel". The "T-vessel" configuration has never been reported in the literature. The reported case with its specific presentation adds further information on this rare form of anomalous origin of the coronary arteries, representing a first report of a configuration that we name the "T-vessel" of the left anterior descending artery. Diagnosis of the coronary anatomy is very important for the invasive cardiologist and cardiac surgeon in cases with a single coronary ostium, such as our case, so that they can proceed with the invasive or surgical treatment when critical coronary artery disease is present.

Serum miRNA-499 and miRNA-210: A potential role in early diagnosis of acute coronary syndrome.

In clinical practice, there is still a need for novel biomarkers, which can reliably rule in or rule out acute coronary syndrome (ACS) immediately on admission. This is of particular interest in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) in whom diagnostic uncertainty is high. The aim of the present study is to evaluate the potential role of miRNA-499 and miRNA-210 as novel molecular biomarkers for early diagnosis of UA and NSTEMI suspected patients presented at the emergency unit. A total of 110 patients presenting to the intensive care unit (ICU) within 24 h of onset of chest pain suggestive of ACS were enrolled in the study. They included 37 UA, 48 NSTEMI and 25 noncardiac chest pain (NCCP) patients. Immediately at enrollment, blood samples were taken for estimation of serum miRNA-499 and miRNA-210 expression levels by real time PCR. miRNA-499 and miRNA-210 expression levels were significantly increased in UA and NSTEMI patients compared with NCCP patients (P < 0.001). Receiver operating characteristic (ROC) curve analysis revealed that the area under curve (AUC) of miR-499 for the diagnosis of UA and NSTEMI was 0.98 and 0.97, respectively; while the AUC of miRNA-210 was 0.84 and 0.90, respectively. The important finding of our study was that the AUC of miRNA-499 for the diagnosis of ACS patients with symptoms onset <3 h was 0.89, while the AUC of miRNA-210 was 0.86. Interestingly, combining miRNA-499 and miRNA-210 significantly improved the diagnostic value by increasing the AUC to 0.96, P < 0.001. In conclusion, serum miRNA-499 and miRNA-210 are associated with UA and NSTEMI and with those presenting within 3 h of symptom onset. Both miRNAs might be potentially novel biomarkers for accelerating the diagnosis of ACS patients in emergency unit. © 2016 IUBMB Life, 68(8):673-682, 2016.

Circulating fibrocytes as predictors of adverse events in unstable angina.

Half of the patients who present with unstable angina (UA) develop recurrent symptoms over the subsequent year. Identification of patients destined to develop such adverse events would be clinically valuable, but current tools do not allow for this discrimination. Fibrocytes are bone marrow-derived progenitor cells that co-express markers of leukocytes and fibroblasts and are released into the circulation in the context of tissue injury. We hypothesized that, in patients with UA, the number of circulating fibrocytes predicts subsequent adverse events. We enrolled 55 subjects with UA, 18 with chronic stable angina, and 22 controls and correlated their concentration of circulating fibrocytes to clinical events (recurrent angina, myocardial infarction, revascularization, or death) over the subsequent year. Subjects with UA had a >2-fold higher median concentration of both total and activated fibrocytes compared with subjects with chronic stable angina and controls. In UA subjects, the concentration of total fibrocytes identified those who developed recurrent angina requiring revascularization (time-dependent area under the curve 0.85) and was superior to risk stratification using thrombolysis in myocardial infarction risk score and N-terminal pro B-type natriuretic peptide levels (area under the curve, 0.53 and 0.56, respectively, P < 0.001). After multivariable adjustment for thrombolysis in myocardial infarction predicted death, MI, or recurrent ischemia, total fibrocyte level was associated with recurrent angina (hazard ratio, 1.016 per 10,000 cells/mL increase; 95% confidence interval, 1.007-1.024; P < 0.001). Circulating fibrocytes are elevated in patients with UA and successfully risk stratify them for adverse clinical outcomes. Fibrocytes may represent a novel biomarker of outcome in this population.