scholarly journals Circulating Monocyte Subsets Are Associated With Extent of Myocardial Injury but Not With Type of Myocardial Infarction

2021 ◽  
Vol 8 ◽  
Author(s):  
Noushin Askari ◽  
Christoph Lipps ◽  
Sandra Voss ◽  
Nora Staubach ◽  
Dimitri Grün ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Stable Coronary Artery Disease ◽  
Inflammatory Cells ◽  
Monocyte Subsets ◽  
Coronary Syndrome ◽  
Monocyte Subpopulations ◽  
Artery Disease ◽  
Classical Monocytes ◽  
Intermediate Monocytes

Inflammation is a hallmark of the period after a myocardial infarction (MI) that is either promoted or resolved by distinct subtypes of circulating inflammatory cells. The three main monocyte subpopulations play different roles inflammation. This study examined whether the type of MI (type 1 or type 2) or the extent of myocardial injury is associated with differences in monocyte subpopulations. For this purpose, peripheral whole blood from patients with a suspected MI was used for flow cytometric measurements of the monocyte subpopulations, and myocardial injury was classified by cardiac troponin levels in serum. In patients with acute coronary syndrome (n = 82, 62.2% male) similar proportions of the monocyte subsets were associated with the two types of MI, whereas total monocyte counts were increased in patients with substantial myocardial injury vs. those with minor injury (p = 0.045). This was accompanied by a higher proportion of intermediate (p = 0.045) and classical monocytes (p = 0.059); no difference was found for non-classical monocytes (p = 0.772). In patients with chronic coronary syndrome (n = 144, 66.5% male), an independent association with myocardial injury was also observed for classical monocytes (p = 0.01) and intermediate monocytes (p = 0.08). In conclusion, changes in monocyte subpopulation counts, particularly for classical and intermediate monocytes, were related to the extent of myocardial injury in acute and stable coronary artery disease but not to the type of MI.

Circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with monocyte subsets in patients with stable coronary artery disease

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
KA Krychtiuk ◽  
M Lenz ◽  
P Hohensinner ◽  
K Distelmaier ◽  
L Schrutka ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Statin Treatment ◽  
Lipid Lowering ◽  
Monocyte Subsets ◽  
Proprotein Convertase ◽  
Artery Disease ◽  
Circulating Levels ◽  
Classical Monocytes

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWF Background and aims Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14 + CD16++; NCM). Results Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.

scholarly journals Neutrophil Phenotypes in Coronary Artery Disease

2020 ◽  
Vol 9 (5) ◽  
pp. 1602
Author(s):  
Patrick Maréchal ◽  
Julien Tridetti ◽  
Mai-Linh Nguyen ◽  
Odile Wéra ◽  
Zheshen Jiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Stable Coronary Artery Disease ◽  
St Elevation Myocardial Infarction ◽  
Multivariable Logistic Regression Analysis ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Artery Disease

Clinical evidence indicates that innate immune cells may contribute to acute coronary syndrome (ACS). Our prospective study aimed at investigating the association of neutrophil phenotypes with ACS. 108 patients were categorized into chronic stable coronary artery disease (n = 37), unstable angina (UA) (n = 19), Non-ST-Elevation Myocardial Infarction (NSTEMI) (n = 25), and ST-Elevation Myocardial Infarction (STEMI) (n = 27). At the time of inclusion, blood neutrophil subpopulations were analysed by flow cytometry. Differential blood cell count and plasma levels of neutrophilic soluble markers were recorded at admission and, for half of patients, at six-month follow-up. STEMI and NSTEMI patients displayed higher neutrophil count and neutrophil-to-lymphocyte ratio than stable and UA patients (p < 0.0001), which normalized at six-month post-MI. Atypical low-density neutrophils were detected in the blood of the four patient groups. STEMI patients were characterized by elevated percentages of band cells compared to the other patients (p = 0.019). Multivariable logistic regression analysis revealed that plasma levels of total myeloperoxidase was associated with STEMI compared to stable (OR: 1.434; 95% CI: 1.119–1.837; P < 0.0001), UA (1.47; 1.146–1.886; p = 0.002), and NSTEMI (1.213; 1.1–1.134; p = 0.0001) patients, while increased neutrophil side scatter (SSC) signal intensity was associated with NSTEMI compared to stable patients (3.828; 1.033–14.184; p = 0.045). Hence, changes in neutrophil phenotype are concomitant to ACS.

scholarly journals Neutrophil extracellular traps and monocyte subsets at the culprit lesion site of myocardial infarction patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Andreas Mangold ◽  
Thomas M. Hofbauer ◽  
Anna S. Ondracek ◽  
Tyler Artner ◽  
Thomas Scherz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Neutrophil Extracellular Traps ◽  
Lesion Site ◽  
Monocyte Subsets ◽  
Culprit Lesion ◽  
Extracellular Traps ◽  
Classical Monocytes ◽  
Intermediate Monocytes ◽  
Cx3cr1 Expression

Abstract Neutrophils release their chromatin into the extracellular space upon activation. These web-like structures are called neutrophil extracellular traps (NETs) and have potent prothrombotic and proinflammatory properties. In ST-elevation myocardial infarction (STEMI), NETs correlate with increased infarct size. The interplay of neutrophils and monocytes impacts cardiac remodeling. Monocyte subsets are classified as classical, intermediate and non-classical monocytes. In the present study, in vitro stimulation with NETs led to an increase of intermediate monocytes and reduced expression of CX3CR1 in all subsets. Intermediate monocytes have been associated with poor outcome, while non-classical CX3CR1-positive monocytes could have reparative function after STEMI. We characterized monocyte subsets and NET markers at the culprit lesion site of STEMI patients (n = 91). NET surrogate markers were increased and correlated with larger infarct size and with fewer non-classical monocytes. Intermediate and especially non-classical monocytes were increased at the culprit site compared to the femoral site. Low CX3CR1 expression of monocytes correlated with high NET markers and increased infarct size. In this translational system, causality cannot be proven. However, our data suggest that NETs interfere with monocytic differentiation and receptor expression, presumably promoting a subset shift at the culprit lesion site. Reduced monocyte CX3CR1 expression may compromise myocardial salvage.

Abstract 15930: Circulating Levels of Proprotein Convertase Subtilisin/kexin Type 9 (pcsk9) are Associated With Monocyte Subsets in Patients With Stable Coronary Artery Disease

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Konstantin Krychtiuk ◽  
Max Lenz ◽  
Philipp Hohensinner ◽  
Klaus Distelmaier ◽  
Lore Schrutka ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Statin Treatment ◽  
Lipid Lowering ◽  
Monocyte Subsets ◽  
Proprotein Convertase ◽  
Artery Disease ◽  
Circulating Levels ◽  
Classical Monocytes

Introduction: Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis. Circulating monocytes can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods: We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14+CD16++; NCM). Results: Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n=55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p=0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R=0.29; p=0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p=0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p=0.05). Conversely, patients with PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p=0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions: We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.

CXCR4 positive and angiogenic monocytes in myocardial infarction

2013 ◽  
Vol 109 (02) ◽  
pp. 255-262 ◽  
Author(s):  
Benjamin Wrigley ◽  
Silvia Montoro-Garcia ◽  
Gregory Lip ◽  
Eduard Shantsila ◽  
Luke Tapp
Keyword(s):  
Myocardial Infarction ◽  
Stable Coronary Artery Disease ◽  
Scavenger Receptor ◽  
Tissue Type ◽  
Monocyte Subsets ◽  
Angiogenic Potential ◽  
Type Plasminogen Activator ◽  
Artery Disease ◽  
Stable Cad

SummaryLimited data are available on the role of monocytes in cardiac repair. In the present study, we evaluated the dynamic alterations of monocytes with reparative and angiogenic potential in patients with myocardial infarction(MI). Reparative CXCR4+ monocytes, and CD34+ and KDR+ monocytes with angiogenic potential derived from individual monocyte subsets were quantified by flow cytometry in patients with ST-elevation MI (n=50) and stable coronary artery disease (CAD, n=40). Parameters were measured on days 1, 3, 7 and 30 post MI. Monocyte subsets were defined as CD14++CD16–CCR2+ (‘classical’, Mon1), CD14++CD16+CCR2+ (‘intermediate’, Mon2), CD14+CD16++CCR2– (‘non-classical’, Mon3). Plasma levels of inflammatory cytokines, fibrinolytic factors and microparticles (MPs) were assessed on day 1. CXCR4+ and KDR+ monocytes were increased following MI, being more prominently associated with Mon2 (median[IQR] of CXCR4+ Mon2 60[25–126] per μl in STEMI vs. 27[21–41] per μl in stable CAD). The counts of CXCR4+ Mon2 in STEMI significantly reduced by day 30 of follow-up (27[18–47], p<0.001). Expression of the pro-reparative scavenger receptor CD163 on Mon3 was reduced in acute MI (p=0.008), and on other subsets later during the follow-up with lowest levels at day 3 post-MI (p<0.001 for Mon1, p=0.02 for Mon2). CD204 expression on Mon1 correlated with tissue type plasminogen activator levels (r=0.46, p=0.001). Interleukin(IL)6 levels correlated with counts of Mon2-derived CXCR4+ and KDR+ cells. Interleukin-1β correlated with KDR+ Mon2 counts. IL10 correlated with CXCR4+ Mon2 levels. Low count of CXCR4+ Mon2 and low CD163 expression by Mon2 were associated with higher ejection fraction six-weeks after MI. In conclusion, the Mon2 subset has the most prominent role in the observed changes in reparative monocytes in MI. The association of reparative monocytes with inflammatory/fibrinolytic markers indicates a complex interplay of these cells in the post-MI state.Note: The review process for this paper was fully handled by Prof. Christian Weber, Editor in Chief.

scholarly journals Management of multivessel coronary artery disease in patients with non-ST-elevation myocardial infarction: a complex path to precision medicine

2020 ◽  
Vol 11 ◽  
pp. 204062232093852
Author(s):  
Angus A. W. Baumann ◽  
Aashka Mishra ◽  
Matthew I. Worthley ◽  
Adam J. Nelson ◽  
Peter J. Psaltis
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
St Elevation Myocardial Infarction ◽  
Complete Revascularization ◽  
Multivessel Coronary Artery Disease ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Artery Disease

Recent analyses suggest the incidence of acute coronary syndrome is declining in high- and middle-income countries. Despite this, overall rates of non-ST-elevation myocardial infarction (NSTEMI) continue to rise. Furthermore, NSTEMI is a greater contributor to mortality after hospital discharge than ST-elevation myocardial infarction (STEMI). Patients with NSTEMI are often older, comorbid and have a high likelihood of multivessel coronary artery disease (MVD), which is associated with worse clinical outcomes. Currently, optimal treatment strategies for MVD in NSTEMI are less well established than for STEMI or stable coronary artery disease. Specifically, in relation to percutaneous coronary intervention (PCI) there is a paucity of randomized, prospective data comparing multivessel and culprit lesion-only PCI. Given the heterogeneous pathological basis for NSTEMI with MVD, an approach of complete revascularization may not be appropriate or necessary in all patients. Recognizing this, this review summarizes the limited evidence base for the interventional management of non-culprit disease in NSTEMI by comparing culprit-only and multivessel PCI strategies. We then explore how a personalized, precise approach to investigation, therapy and follow up may be achieved based on patient-, disease- and lesion-specific factors.

scholarly journals The Effect of Pharmacological Preconditioning with Nicorandil before Elective Coronary Stenting on the Long-Term Prognosis of Patients with Stable Coronary Artery Disease

2020 ◽  
Vol 16 (2) ◽  
pp. 191-198
Author(s):  
G. N. Soboleva ◽  
R. V. Gostishchev ◽  
A. N. Rogoza ◽  
T. I. Kotkina ◽  
A. N. Samko ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Events ◽  
Myocardial Injury ◽  
Stable Coronary Artery Disease ◽  
Secondary Endpoint ◽  
Control Group ◽  
Creatine Kinase Mb ◽  
Artery Disease

Aim. To study nicorandil prescription effects before elective percutaneous coronary intervention (PCI) to prevent myocardial injury and 4a type acute myocardial infarction (MI, primary endpoint) and cardiovascular events (CVE) in the first year after PCI (secondary endpoint) in patients with stable coronary artery disease.Material and methods. 182 patients with stable coronary artery disease were included into the study and were randomized into two groups: nicorandil treatment group (n=90) and a control group with a standard medical treatment (n=92). Nicorandil was prescribed orally: 2 days before PCI – 30 mg/day; on the day of PCI – 20 mg 2 hours before intervention and 10 mg 6-12 hours after PCI; over the next 30 days – 30 mg/day. High sensitivity troponin I (hs-Tr) and creatine kinase-MB tests were carried out before PCI, 24 and 72 hours after the intervention; the 4a type MI was diagnosed according to the 4th Universal Definition. Non-fatal myocardial infarction, nonfatal stroke, death from cardiovascular diseases, repeat revascularization (PCI, coronary artery bypass surgery due to aggravation), hospital admissions for angina pectoris recurrence (without interventions) and death from any causes were considered as cardiovascular events. Data on adverse outcomes were collected over the hospital stay, and then 30, 180 and 365 days after the hospital discharge.Results. 4a type MI was diagnosed in 14 patients (8%), in women – 12% and in men – 6%. There was a significant decrease in the incidence of type 4a MI in the nicorandil group (n=3; 3%) compared with the control group (n=11; 12%; p=0.05). Secondary endpoint was recorded in 21% of patients. The relationship was found between 4a type MI and the incidence of CVE the next year after the PCI (p=0.01). In patients with type 4a MI CVE odd ratio increases 5.8 times with confidence interval from 1.5426 to 21.6024. According to the logistic regression analysis the significant relationship between hs-Tr growth 24 hours after the PCI and CVE incidence next year after the PCI was found with cutting value 389.8 pg/ml, AUC=0.641 (p=0.04).Сonclusion. Peroral nicorandil 30 mg/day 2 days before PCI, 20 mg 2 hours before surgery and 10 mg 6-12 hours after PCI, and 30 mg/day next 30 days after PCI decreases the risk of intraoperative myocardial injury and CVE in the next year after PCI.

scholarly journals Focal ST-segment elevation without coronary occlusion: myocardial infarction with no obstructive coronary atherosclerosis associated with COVID-19—a case report

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Casey Meizinger ◽  
Bruce Klugherz
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Respiratory Failure ◽  
Coronary Atherosclerosis ◽  
Myocardial Injury ◽  
Cardiovascular Complications ◽  
St Segment Elevation ◽  
St Segment ◽  
Hypoxic Respiratory Failure ◽  
Artery Disease

Abstract Background While it is understood that coronavirus disease 2019 (COVID-19) is primarily complicated by respiratory failure, more data are emerging on the cardiovascular complications of this disease. A subset of COVID-19 patients present with ST-elevations on electrocardiogram (ECG) yet normal coronary angiography, a presentation that can fit criteria for myocardial infarction with no obstructive coronary atherosclerosis (MINOCA). There is little known about non-coronary myocardial injury observed in patients with COVID-19, and we present a case that should encourage further conversation and study of this clinical challenge. Case summary An 86-year-old man presented to our institution with acute hypoxic respiratory failure and an ECG showing anteroseptal ST-segment elevation concerning for myocardial infarction. Mechanic ventilation was initiated prior to presentation, and emergent transthoracic echocardiography reported an ejection fraction of 50–55%, with no significant regional wall motion abnormalities. Next, emergent coronary angiography was performed, and no significant coronary artery disease was detected. The patient tested positive for COVID-19. Despite supportive management in the intensive care unit, the patient passed away. Discussion We present a case of COVID-19 that is likely associated with MINOCA. It is crucial to understand that in COVID-19 patients with signs of myocardial infarction, not all myocardial injury is due to obstructive coronary artery disease. In the case of COVID-19 pathophysiology, it is important to consider the cardiovascular effects of hypoxic respiratory failure, potential myocarditis, and significant systemic inflammation. Continued surveillance and research on the cardiovascular complications of COVID-19 is essential to further elucidate management and prognosis.

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