scholarly journals Rapid fall in circulating non-classical monocytes in ST elevation myocardial infarction patients correlates with cardiac injury

2021 ◽  
Author(s):  
Sarah A. Marsh ◽  
Catherine Park ◽  
Rachael E. Redgrave ◽  
Esha Singh ◽  
Lilia Draganova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Mouse Model ◽  
Cardiac Injury ◽  
List Type ◽  
Coronary Vasculature ◽  
Cardiac Ischaemia ◽  
Rapid Fall ◽  
Classical Monocytes ◽  
Intermediate Monocytes

AbstractObjectiveMyocardial infarction leads to a rapid innate immune response that is ultimately required for repair of damaged heart tissue. We therefore examined circulating monocyte dynamics immediately after reperfusion of the culprit coronary vessel in STEMI patients to determine whether this correlated with level of cardiac injury. A mouse model of cardiac ischaemia/reperfusion injury was subsequently used to establish the degree of monocyte margination to the coronary vasculature that could potentially contribute to the drop in circulating monocytes.Approach and ResultsWe retrospectively analysed blood samples from 51 STEMI patients to assess the number of non-classical (NC), classical and intermediate monocytes immediately following primary percutaneous coronary intervention. Classical and intermediate monocytes showed minimal change. On the other hand circulating numbers of NC monocytes fell by approximately 50% at 90 minutes post-reperfusion. This rapid decrease in NC monocytes was greatest in patients with the largest infarct size (p<0.05) and correlated inversely with left ventricular function (r=0.41, p=0.04). The early fall in NC monocytes post reperfusion was confirmed in a second prospective study of 13 STEMI patients. Furthermore, in a mouse cardiac ischaemia model, there was significant monocyte adhesion to coronary vessel endothelium at 2 hours post-reperfusion pointing to a specific and rapid vessel margination response to cardiac injury.ConclusionsRapid depletion of NC monocytes from the circulation in STEMI patients following coronary artery reperfusion correlates with the level of acute cardiac injury and involves rapid margination to the coronary vasculature.Graphical AbstractHighlights3-5 bullet points that summarize the major findings of the study.Circulating non classical monocytes show a rapid fall in STEMI patients within 90 minutes of re-opening the culprit coronary artery.The extent of the drop in non classical monocytes correlates with loss of cardiac function and increased infarct size.A mouse model of cardiac ischaemia and reperfusion shows rapid margination of monocytes to the coronary vasculature

scholarly journals Rapid fall in circulating non‐classical monocytes in ST elevation myocardial infarction patients correlates with cardiac injury

2021 ◽  
Vol 35 (5) ◽  
Author(s):  
Sarah A. Marsh ◽  
Catherine Park ◽  
Rachael E. Redgrave ◽  
Esha Singh ◽  
Lilia Draganova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Injury ◽  
St Elevation Myocardial Infarction ◽  
Rapid Fall ◽  
St Elevation ◽  
Classical Monocytes

scholarly journals Monocytes of Different Subsets in Complexes with Platelets in Patients with Myocardial Infarction

2018 ◽  
Vol 118 (11) ◽  
pp. 1969-1981 ◽  
Author(s):  
Marina Loguinova ◽  
Natalia Pinegina ◽  
Valeria Kogan ◽  
Murad Vagida ◽  
Anush Arakelyan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Annexin V ◽  
Published Data ◽  
Healthy Controls ◽  
New Information ◽  
Platelet Antigen ◽  
Classical Monocytes ◽  
Intermediate Monocytes

AbstractAcute myocardial infarction (AMI) is associated with activation of various cells, including platelets that form monocyte–platelet complexes (MPCs). Here, we analysed MPC in vivo and in vitro and investigated the abilities of different monocyte subclasses to form MPC, the characteristics of the cells involved in MPC formation and MPC changes in AMI. We identified MPC by co-staining for platelet antigen CD41a and monocyte antigens CD14 and CD16. Platelet activation was evaluated from expression of phosphatidylserine as revealed by annexin V. Our results confirm published data and provide new information regarding the patterns of MPC in AMI patients. We found that the patterns of platelet aggregation with monocytes were different in AMI patients and controls: (1) in AMI patients, MPC formed by intermediate monocytes carry more platelets whereas in healthy controls more platelets aggregated with classical monocytes; (2) the numbers of MPC in AMI patients, being already higher than in controls, were further increased if these patients suffered various in-hospital complications; (3) on the basis of the CD41a fluorescence of the antibody-stained MPC, some of the aggregates seem to consist of monocytes and platelet-derived extracellular vesicles (EVs); (4) aggregation of monocytes with platelet EV occurred in in vitro experiments; and (5) these experiments demonstrated that monocytes from AMI patients aggregate with both platelets and platelet EVs more efficiently than do monocytes from controls. MPC in AMI patients may play an important role in this pathology.

scholarly journals Relationship between dynamic changes in subpopulations of blood monocytes and the development of complications in patients with acute myocardial infarction

2020 ◽  
Vol 27 (4) ◽  
pp. 9-17
Author(s):  
T. V. Talayeva ◽  
O. M. Parkhomenko ◽  
I. V. Tretyak ◽  
O. V. Dovhan ◽  
O. V. Shumakov
Keyword(s):  
Myocardial Infarction ◽  
Absolute Number ◽  
Control Group ◽  
Blood Monocytes ◽  
The Absolute ◽  
Anti Inflammatory ◽  
Classical Monocytes ◽  
Intermediate Monocytes ◽  
Patrolling Monocytes

The aim – to determine the extent of different subpopulations of blood monocytes in acute myocardial infarction (AMI) with ST-segment elevation patients on day 1 and 7 and to evaluate the relationship between their content and the dynamics of changes and the risk of complications after AMI.Materials and methods. The composition of individual subpopulations of monocytes in the peripheral venous blood (and general clinical and biochemical blood tests) was evaluated in 50 pts with STEMI (who were admitted within 6 hours after the onset of the disease) at admission (before primary PCI) and on day 7. All patients received standard recommended therapy. Dynamic heart echocardiography was also performed on the 1st and 7th day. All patients were divided into 2 groups depending on the dynamical increase (1 group – 21 pts) or decrease (2 group – 29 pts) of classical monocytes (CD14hiCD16–) subpopulation during 7 days of follow-up. The control group included 15 healthy subjects with no signs of coronary heart disease and 23 pts with chronic coronary heart disease without AMI.Results and discussion. In subgroup 1, the percentage of the «classical» fraction of monocytes during the observation increased to 89.0±1.2 %, which was 4.2 % more than on the 1st day and 12.5 % more than in the control group (р<0.05), while the absolute amount of classic monocytes on day 7 increased by 48 % compared to initial value (р<0.01). The percentage of «intermediate» (CD14hiCD16+) blood monocytes in patients of this subgroup on the 1st day of hospitalization was 70 % higher than in the control group, and 42 % higher than in the 2nd subgroup of patients (р<0,001), however, on the 7th day it decreased by 30 % compared to baseline, although it remained by 8 % more than in the control group (the absolute number of «intermediate» monocytes did not change). The activation index (IA) of the «intermediate» monocytes on the first day did not differ between subgroups and was 40 % higher than in the control group (р<0.001). However, in the dynamics of observation, in patients of subgroup 1, this figure did not change, while in subgroup 2 IA decreased by 60 % (р<0.001). Despite the fact that the absolute number of anti-inflammatory («patrolling») (CD14+lowCD16++) monocytes did not change until the 7th day of observation (and their percentage decreased slightly), their IA was significantly lower than in the control group (95 %) and in patients of subgroup 2 (92 %, р<0,001). In patients of subgroup 2, the decrease of the percentage of «classic» monocytes was –7.7 % (from 90.4±0.8 to 83.4±1.2 %). Despite the fact that the number and percentage of intermediate monocytes increased in dynamics, their IA decreased almost 2 times, which may indicate a decrease in the pro-inflammatory ability these monocytes. The percentage and number of «patrolling» monocytes increased in dynamics by 37.4 % (р<0.0001) and by 268.3 % (р<0.01), respectively. IA of patrolling monocytes was almost 12 and 7 times higher than in patients of subgroup 1 on the 1st and 7th day of observation, respectively, which may indicate a significant activation of anti-inflammatory activity of patrolling monocytes. Intracardiac thrombosis was 3.3 times more common in patients of subgroup 1, in this subgroup was also more often noted (compared to the subgroup 2): dilatation of the left ventricle (almost 8 times), reduction of left ventricular ejection fraction (4 times), and pathological post-infarction remodeling of the left ventricle (almost 7 times).Conclusions. The results of the study indicate the important role of different subpopulations of blood monocytes in the processes of myocardial damage and recovery (in particular, the pro-inflammatory role of increasing the number of classical monocytes and increasing the activity of intermediate monocytes, as well as the anti-inflammatory role of increasing the number, percentage and activity of patrolling monocytes) in patients with AMI and can be the basis for developing new approaches to the diagnosis and prevention of complications of this disease.

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.

A 42-year-old woman with acute myocardial infarction

Heart ◽  
2018 ◽  
Vol 104 (19) ◽  
pp. 1607-1607 ◽  
Author(s):  
James K Fahey ◽  
Abdul Rahman Ihdayhid ◽  
Anthony John White
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Iliac Artery ◽  
Fibromuscular Dysplasia ◽  
External Iliac Artery ◽  
List Type ◽  
System A ◽  
Invasive Angiography ◽  
St Elevation ◽  
The Right

Clinical introductionA 42-year-old woman presented with anterior ST elevation myocardial infarction. Urgent coronary angiography revealed tapering then occlusion of the distal left anterior descending (LAD) coronary artery with no flow in the distal LAD (figure 1A). Balloon angioplasty with a 2.0×8 mm balloon re-established flow into the distal LAD. An angiogram of the right external iliac artery was also performed (figure 1B).Figure 1Invasive angiography of the left coronary system (A) and the right external iliac artery (B). The coronary angiogram (A) shows tapering and then occlusion (arrow) of the distal left anterior descending coronary artery.QuestionWhich of the following explains the abnormal appearance of the external iliac artery (figure 1B)?Atherosclerosis.Concertina effect.Fibromuscular dysplasia.Perforation.Multiple aneurysms.

scholarly journals A silent myocardial infarction in the diabetes outpatient clinic: case report and review of the literature

2013 ◽  
Vol 2013 ◽  
Author(s):  
M S Draman ◽  
H Thabit ◽  
T J Kiernan ◽  
J O'Neill ◽  
S Sreenan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Annual Review ◽  
List Type ◽  
Silent Myocardial Ischaemia ◽  
Objective Evidence ◽  
Patients With Diabetes ◽  
Artery Disease

Summary Silent myocardial ischaemia (SMI), defined as objective evidence of myocardial ischaemia in the absence of symptoms, has important clinical implications for the patient with coronary artery disease. We present a dramatic case of SMI in a diabetes patient who attended annual review clinic with ST elevation myocardial infarction. His troponin was normal on admission but raised to 10.7 ng/ml (normal <0.5) when repeated the next day. His angiogram showed diffused coronary artery disease. We here discuss the implications of silent ischaemia for the patient and for the physician caring for patients with diabetes. Learning points Silent myocardial ischaemia (SMI) is an important clinical entity. SMI is common and occurs with increased frequency in patients with diabetes. SMI is an independent predictor of mortality. Recognition may lead to early intervention.

Abstract 568: Coronary Artery Plaque Spatial Distribution Matches that of Thrombosis in STEMI, and is Underestimated by Calcified Plaque Segments Alone

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Catherine A Pastorius ◽  
Stacia Merkel-Kraus ◽  
Jonathan G Schwartz ◽  
Robert S Schwartz ◽  
Vicki Pink ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Plaque ◽  
Lesion Length ◽  
List Type ◽  
Plaque Volume ◽  
Coronary Artery Plaque ◽  
Atypical Symptoms ◽  
Calcified Plaque ◽  
Major Vessel

Angiographic studies of ST-elevation myocardial infarction (STEMI) show that occlusive thrombi occur in coronary arteries within the proximal third of each major vessel, within about 35 mm from the ostium. These findings suggest that these high-risk regions are sites of plaque vulnerability. Multidetector CTA (MDCTA) visualizes not only lumen but also calcified and uncalcified coronary plaque. We therefore studied the distribution of coronary plaque in patients to determine plaque distribution to compare result with location of angiographic myocardial infarction thrombus. Methods: 48 outpatients (mean age 57 +− 5) undergoing Dual Source MDCTA (asymptomatic or with atypical symptoms) were studied. Most distal plaque location was measured for ostial-termination distance and composition (calcified/noncalcified) determined by one expert observer using validated, commercial plaque characterization software for lesion location and lesion length. Results: Location of the most distal plaque was as follows, LAD (n=35) 31.8 mm, LCX (n=21) 33.0 mm, and RCA (n=24) 56.0 mm. Mean lesion lengths were LAD 19.4 +− 13.4 mm, LCX 15.1 +− 9.6 and RCA 18.4 +− 9.8 mm. Mean volume (cu mm) for calcified and noncalcified plaque was 130 +− 176 and 204 +− 249 respectively, for a ratio of 0.64. There was no propensity of either calcified or uncalcified plaque to aggregate longitudinally in the arteries. Conclusions: The distribution and location of coronary artery plaque by MDCTA identically matches the known location of coronary artery vulnerability determined by angiographic studies. This finding suggests that STEMI does not occur in distal coronary locations simply because little plaque occurs in these areas. Calcified plaque volume measured in 3-dimensions underestimates total plaque volume by a factor of 2.6. Calcific plaque is thus the ‘tip of the iceberg’.

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.

scholarly journals Microthrombi As A Major Cause of Cardiac Injury in COVID-19: A Pathologic Study

Circulation ◽  
2021 ◽  
Author(s):  
Dario Pellegrini ◽  
Rika Kawakami ◽  
Giulio Guagliumi ◽  
Atsushi Sakamoto ◽  
Kenji Kawai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Coronary Intervention ◽  
Hospitalized Patients ◽  
Cross Sectional ◽  
St Segment Elevation ◽  
Pathologic Analysis ◽  
Underlying Mechanisms

Background: Cardiac injury is common in hospitalized patients with COVID-19 and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with SARS-CoV-2 remain uncertain. Methods: We conducted a systematic pathologic analysis of 40 hearts from hospitalized patients dying of Coronavirus Disease 2019 (COVID-19) in Bergamo, Italy to determine the pathologic mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury. Results: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. As compared to subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and shorter symptom onset to admission. The incidence of severe coronary artery disease (i.e., >75% cross sectional narrowing) was not significantly different between those with and without necrosis. 3/14 (21 .4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction defined as ≥1 cm 2 area of necrosis while 11/14 (78.6%) showed evidence of focal (> 20 necrotic myocytes with an area of ≥ 0.05 mm 2 but <1 cm 2 ) myocyte necrosis. Cardiac thrombi were present in 11/14 (78.6%) cases with necrosis, with 2/14 (14.2%) having epicardial coronary artery thrombi while 9/14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19 positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19 infected patients presenting with ST-segment elevation myocardial infarction (STEMI). Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining as compared to intramyocardial thromboemboli from COVID-19 negative subjects and to aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19 positive and negative STEMI patients. Conclusions: The most common pathologic cause of myocyte necrosis was microthrombi. Microthrombi were different in composition as compared to intramyocardial thromboemboli from COVID-19 negative subjects and to coronary thrombi retrieved from COVID-19 positive and negative STEMI patients. Tailored anti-thrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection.

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