Abstract 13261: Relationship Between Circulating CD34+ and CD146+ Cells and Change in Infarct Size in Patients With Acute Coronary Syndrome

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Damien Montange ◽  
Siamak Davani ◽  
Ségolène Gambert ◽  
Marie-France Seronde ◽  
Francois Schiele ◽  
...  

Background: The presence of CD34+ and CD146+ cells in the peripheral blood in response to myocardial ischemia has been advocated as a marker of an organism’s regenerative capacity by late and early progenitor cells respectively. The aim of this study was to evaluate the relationship between circulating CD34+ and CD146+ levels and the change in infarct size, as assessed by magnetic resonance imaging (MRI) in patients (pts) with acute coronary syndrome (ACS including ST and non ST elevation myocardial infarction). Methods: Patients <75 years old, admitted with a first ACS within 12 hours of onset of symptoms were enrolled. Peripheral blood samples for cytofluorimetric analysis of CD34+ and CD146+ cells level were drawn at day 0. Initial infarct size was evaluated from peak troponin I levels determined from 5 blood samples over the first 72 hours. MRI measurements of infarct size were performed at day 5 and at 6 months follow-up. Results: In total, 34 patients aged 57±10 years were included. Mean ejection fraction was 62±11%. Log-transformed number of CD 34+ and CD146+ were significantly correlated with the relative change in infarct size between day 5 and 6 month follow-up (p=0.01, r=-0;41 and p=0.001, r=-0.52 respectively) (Figure) Conclusion: The highest CD34+ and CD146+ cell levels were associated with the greatest relative reduction in infarct size 6 months after ACS. These results support the hypothesis that these cells could be considered as a marker of regenerative capacity in patients with acute coronary syndromes.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Takashima ◽  
S Usui ◽  
S Matsuura ◽  
C Goten ◽  
O Inoue ◽  
...  

Abstract Background In our previous 5-year cohort study, we demonstrated that low gene expression of nerve growth factor receptor (NGFR) in peripheral leucocytes in acute coronary syndrome (ACS) predicted repetitive coronary interventions at the de novo lesions. An NGFR-positive cell has been demonstrated to reside in bone marrow (BM) stromal fraction and to be increased in peripheral blood mononuclear cell (MNCs) fraction in patients with ischemic heart disease. Purpose To investigate whether the BM-NGFR+ cell is associated with arterial remodeling and the relationship between the levels of peripheral NGFR+ cells after ACS and coronary plaque progression in an experimental and prospective clinical study. Methods and results In an experimental study, 8-week-old C57B6/J wild type male mice were subjected to irradiation with 9.6 Gy and transplantation with BM (BMT) isolated from GFP-transgenic NGFR wild type (WT) or knock-out (KO) mice at day 1. Four weeks after BMT, the right carotid artery was ligated for 4 weeks. Induced neointimal area was increased (p&lt;0.05), where cells under apoptosis were decreased (p&lt;0.05) in NGFR-KO-BMT group compared to WT-BMT group (n=4). NGFR+ cells were not detected in wild type sham-operated artery, whereas in the ligated artery in WT-BMT group NGFR+ cells assembled in the developed neointima and exclusively presented double positive with GFP, but absent in NGFR-KO-BMT group (p&lt;0.05, n=4). In a clinical study, thirty patients with ACS who underwent primary percutaneous coronary intervention (PCI) were enrolled. The peripheral blood sample was collected on days 0, 3 and 7, and 9 months follow-up and the number of NGFR+MNCs were measured by flowcytometric analysis. The plaque volume at non-targeted coronary lesion (non-TL:&gt;5 mm proximal or distal to the implanted stents) were quantitatively analysed using gray-scale intravascular ultrasound (IVUS) and Q-IVUS™ software at the acute phase and 9 months follow-up. The number of NGFR+MNCs in peripheral blood was 1.5-fold increased at day 3 (0.064±0.056%) compared to day 0 (0.042±0.030%) (p&lt;0.05). The change in normalized total plaque volume (TAVN) at non-TL at 9 months was negatively correlated with the number of NGFR+MNCs at day 0 (r=−0.51), day 3 (r=−0.51) and 9 months (r=−0.59) after ACS (p&lt;0.05). Multiple regression analysis showed that NGFR+MNCs at day 0 (β=−0.48, p=0.01) and CRP (β=−0.53, P&lt;0.01) are independent factors associating with TAVN change at non-TL at 9 months, regardless of LDL-cholesterol control level. ROC analysis revealed that NGFR+MNCs &lt;0.049 at day 0 predicted the increase of TAVN with AUC 0.78; sensitivity 0.82 and specificity 0.67. Conclusions Bone marrow-derived peripheral NGFR+ cells negatively regulate arterial remodeling through appropriate apoptosis of neointimal cells and the peripheral level of NGFR+ cells in ACS predicts plaque progression at the non-targeted lesion. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): KAKENHI


QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Sherif Farouk Ibrahim ◽  
Ashraf Elsayed Elagmy ◽  
Abdelrhman Gamal Abdelsabour

Abstract Background Sepsis is heterogenous with regard to factors such as causal microorganism, patient predisposition, co-morbidity and response to therapy, a key element and unifying feature is the manifestation of cardiovascular dysfunction. Elevated concentrations of cardiac troponin I (cTnI) are frequently observed in patients with severe sepsis and septic shock even in the absence of an acute coronary syndrome (ACS). Objective To evaluate the prognostic value of (cTnI) with echocardiography assessment in septic patients. Patients and Methods This study was conducted at the intensive care units of Ain Shams university hospitals. 20 patients of both sexes with age ranging from 18 to 70 years diagnosed with sepsis admitted to Intensive care unit were included in prospective observational study. Results Baseline cTnI had a significant positive correlation with follow up troponine (p = 0.0016). Baseline EF had a significant negative correlation with follow up troponine (p = 0.036). Using ROC-curve analysis, troponin level at a cutoff point (&gt;1.9) predicted patients with mortality, with good (87%) accuracy, sensitivity= 90% and specificity= 90% (p &lt; 0.01). Conclusion Elevated concentrations of cardiac troponin I (cTnI) are frequently observed in patients with sepsis and septic shock even in the absence of an acute coronary syndrome.


2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
V.J. Van Den Berg ◽  
V.A.W.M. Umans ◽  
K.M. Akkerhuis ◽  
R.M. Oemrawsingh ◽  
F.W. Asselbergs ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Farhan Raza ◽  
Mohamad Alkhouli ◽  
Paul Sandhu ◽  
Reema Bhatt ◽  
Alfred A. Bove

Background. Elevated cardiac troponin in acute stroke in absence of acute coronary syndrome (ACS) has unclear long-term outcomes.Methods. Retrospective analysis of 566 patients admitted to Temple University Hospital from 2008 to 2010 for acute stroke was performed. Patients were included if cardiac troponin I was measured and had no evidence of ACS and an echocardiogram was performed. Of 200 patients who met the criteria, baseline characteristics, electrocardiograms, and major adverse cardiovascular events (MACE) were reviewed. Patients were characterized into two groups with normal and elevated troponins. Primary end point was nonfatal myocardial infarction during follow-up period after discharge. The secondary end points were MACE and death from any cause.Results. For 200 patients, 17 patients had positive troponins. Baseline characteristics were as follows: age63.1±13.8, 64% African Americans, 78% with hypertension, and 22% with previous CVA. During mean follow-up of 20.1 months, 7 patients (41.2%) in elevated troponin and 6 (3.3%) patients in normal troponin group had nonfatal myocardial infarction (P=0.0001). MACE (41.2% versus 14.2%,P=0.01) and death from any cause (41.2% versus 14.5%,P=0.017) were significant in the positive troponin group.Conclusions. Elevated cardiac troponin in patients with acute stroke and no evidence of ACS is strong predictor of long-term cardiac outcomes.


2021 ◽  
Vol 18 (6) ◽  
pp. 147916412110474
Author(s):  
Cindya P Iswandi ◽  
Victor J van den Berg ◽  
Suat Simsek ◽  
Daan van Velzen ◽  
Edwin Ten Boekel ◽  
...  

Purpose Insulin-like growth factor-1 (IGF-1) has been associated with both protective and detrimental effects on the development of ischemic heart disease. The relationship between IGF-1 levels and major adverse cardiovascular events (MACE) in acute coronary syndrome (ACS) patients remains unclear. This study aimed to investigate the relationship between IGF-1 admission levels in hyperglycemic ACS patients and: (1) MACE over a 5 years follow-up, (2) type 2 diabetes at discharge, and (3) post-ACS myocardial infarct size and dysfunction. Methods This was a post hoc analysis of the BIOMArCS-2 randomized controlled trial. From July 2008 to February 2012, 276 ACS patients with admission plasma glucose level between 140 and 288 mg/dL were included. Records of the composite of all-cause mortality and recurrent non-fatal myocardial infarction were obtained during 5 years follow-up. Venous blood samples were collected on admission. IGF-1 was measured batchwise after study completion. Oral glucose tolerance test was performed to diagnose type 2 diabetes, whereas infarct size and left ventricular function were assessed by myocardial perfusion scintigraphy (MPS) imaging, 6 weeks post-ACS. Results Cumulative incidence of MACE was 24% at 5 years follow-up. IGF-1 was not independently associated with MACE (HR:1.00 (95%CI:0.99–1.00), p = 0.29). Seventy-eight patients (28%) had type 2 diabetes at discharge, and the highest quartile of IGF-1 levels was associated with the lowest incidence of diabetes (HR:0.40 (95%CI:0.17–0.95), p = 0.037). IGF-1 levels were not associated with post-ACS myocardial infarct size and dysfunction. Conclusions IGF-1 carries potential for predicting type 2 diabetes, rather than long-term cardiovascular outcomes and post-ACS myocardial infarct size and dysfunction, in hyperglycemic ACS patients.


2018 ◽  
Vol 56 (11) ◽  
pp. 1954-1961 ◽  
Author(s):  
Alfredo Bardají ◽  
Gil Bonet ◽  
Anna Carrasquer ◽  
Maribel González-del Hoyo ◽  
Fernando Domínguez ◽  
...  

Abstract Background: Detectable troponin below the 99th percentile may reflect an underlying cardiac abnormality which might entail prognostic consequences. This study aimed to investigate the prognosis of patients admitted to an emergency department (ED) with detectable troponin below the 99th percentile reference limit who did not present with an acute coronary syndrome (ACS). Methods: We analysed the clinical data of all consecutive patients admitted to the ED during the years 2012 and 2013 in whom cardiac troponin was requested by the attending clinician (cTnI Ultra Siemens, Advia Centaur). Patients with troponin below the 99th percentile of the reference population (40 ng/L) and who did not have a diagnosis of ACS were selected, and their mortality was evaluated in a 2-year follow-up. Results: A total of 2501 patients had a troponin level below the reference limit, with 43.9% of those showing detectable levels (>6 ng/L and <40 ng/L). Patients with detectable levels were elderly and had a higher prevalence of cardiovascular history and more comorbidities. The total mortality in the 2-year follow-up was 12.4% in patients with detectable troponin and 4.5% in patients with undetectable troponin (p<0.001). In the Cox multivariate regression analysis, the detectable troponin was an independent marker of mortality at 2 years (HR 1.62, 95% CI 1.07–2.45, p=0.021). Conclusions: Detectable troponin I below the 99th percentile is associated with higher mortality risk at 2-year follow-up in patients admitted to the ED who did not present with ACS.


2008 ◽  
Vol 54 (4) ◽  
pp. 723-728 ◽  
Author(s):  
Fred S Apple ◽  
Stephen W Smith ◽  
Lesly A Pearce ◽  
Ranka Ler ◽  
MaryAnn M Murakami

Abstract Background: We determined the diagnostic accuracy of the Advia Centaur TnI-Ultra assay for detecting myocardial infarction (MI) and assessing risk of adverse events in patients presenting with ischemic symptoms suggestive of acute coronary syndrome. Methods: We measured cardiac troponin I (cTnI) on admission and 6–24 h after admission (follow-up) in plasma specimens from 371 consecutive patients. The end point was the first of cardiac event or death within 60 days. We estimated survival curves using the Kaplan-Meier method and compared groups with the log rank statistic. Results: MI was established in 49 patients (13%). Clinical sensitivities and specificities for MI based on the 99th percentile (0.04 μg/L) were 74% and 84%, respectively, on admission and 94% and 81% at follow-up. ROC curves showed significantly higher accuracy for MI in the follow-up specimen compared with admission (P = 0.001). Overall there were 2 cardiac deaths, 1 noncardiac death, 49 MIs, 7 coronary artery bypass grafts, and 36 percutaneous coronary interventions in 59 patients during follow-up. The event rate in those with cTnI &lt;0.006 μg/L was significantly lower than in groups with cTnI 0.006–0.04 μg/L, &gt;0.04–0.10 μg/L, or &gt;0.10 μg/L (2.8% vs 11.1%, 24.1%, 55.1%, respectively; P &lt;0.0001). Relative risks for the increasing cTnI cutoff groups were 3.9 (95% CI 1.2–13), 8.9 (2.4–34), and 25 (7.3–82) after adjustment for age, diabetes, history of hypertension, previous MI, and estimated glomerular filtration rate. Conclusions: The TnI-Ultra assay is a sensitive, early diagnostic biomarker for MI and an independent predictor of adverse events at any measurable cTnI in patients with symptoms of acute coronary syndrome.


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