scholarly journals Apo AI Nanoparticles Delivered Post Myocardial Infarction Moderate Inflammation

2020 ◽  
Vol 127 (11) ◽  
pp. 1422-1436
Author(s):  
Adele L. Richart ◽  
Medini Reddy ◽  
Mina Khalaji ◽  
Alaina L. Natoli ◽  
Sarah E. Heywood ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Cardiac Tissue ◽  
Troponin I ◽  
Scavenger Receptor ◽  
Cardiac Injury ◽  
Post Myocardial Infarction ◽  
Intravenous Bolus ◽  
Anti Inflammatory ◽  
Apo Ai

Rationale: Decades of research have examined immune-modulatory strategies to protect the heart after an acute myocardial infarction and prevent progression to heart failure but have failed to translate to clinical benefit. Objective: To determine anti-inflammatory actions of n-apo AI (Apo AI nanoparticles) that contribute to cardiac tissue recovery after myocardial infarction. Methods and Results: Using a preclinical mouse model of myocardial infarction, we demonstrate that a single intravenous bolus of n-apo AI (CSL111, 80 mg/kg) delivered immediately after reperfusion reduced the systemic and cardiac inflammatory response. N-apo AI treatment lowered the number of circulating leukocytes by 30±7% and their recruitment into the ischemic heart by 25±10% (all P <5.0×10 −2 ). This was associated with a reduction in plasma levels of the clinical biomarker of cardiac injury, cardiac troponin-I, by 52±17% ( P =1.01×10 −2 ). N-apo AI reduced the cardiac expression of chemokines that attract neutrophils and monocytes by 60% to 80% and lowered surface expression of integrin CD11b on monocytes by 20±5% (all P <5.0×10 −2 ). Fluorescently labeled n-apo AI entered the infarct and peri-infarct regions and colocalized with cardiomyocytes undergoing apoptosis and with leukocytes. We further demonstrate that n-apo AI binds to neutrophils and monocytes, with preferential binding to the proinflammatory monocyte subtype and partially via SR-BI (scavenger receptor BI). In patients with type 2 diabetes, we also observed that intravenous infusion of the same n-apo AI (CSL111, 80 mg/kg) similarly reduced the level of circulating leukocytes by 12±5% (all P <5.0×10 −2 ). Conclusions: A single intravenous bolus of n-apo AI delivered immediately post–myocardial infarction reduced the systemic and cardiac inflammatory response through direct actions on both the ischemic myocardium and leukocytes. These data highlight the anti-inflammatory effects of n-apo AI and provide preclinical support for investigation of its use for management of acute coronary syndromes in the setting of primary percutaneous coronary interventions.

Involvement of monocytes/macrophages as key factors in the development and progression of cardiovascular diseases

2014 ◽  
Vol 458 (2) ◽  
pp. 187-193 ◽  
Author(s):  
María Fernández-Velasco ◽  
Silvia González-Ramos ◽  
Lisardo Boscá
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Initial Period ◽  
Cardiac Injury ◽  
Key Factors ◽  
Cardiac Damage ◽  
Inflammatory Profile

Emerging evidence points to the involvement of specialized cells of the immune system as key drivers in the pathophysiology of cardiovascular diseases. Monocytes are an essential cell component of the innate immune system that rapidly mobilize from the bone marrow to wounded tissues where they differentiate into macrophages or dendritic cells and trigger an immune response. In the healthy heart a limited, but near-constant, number of resident macrophages have been detected; however, this number significantly increases during cardiac damage. Shortly after initial cardiac injury, e.g. myocardial infarction, a large number of macrophages harbouring a pro-inflammatory profile (M1) are rapidly recruited to the cardiac tissue, where they contribute to cardiac remodelling. After this initial period, resolution takes place in the wound, and the infiltrated macrophages display a predominant deactivation/pro-resolution profile (M2), promoting cardiac repair by mediating pro-fibrotic responses. In the present review we focus on the role of the immune cells, particularly in the monocyte/macrophage population, in the progression of the major cardiac pathologies myocardial infarction and atherosclerosis.

scholarly journals Focal intra-colon cooling reduces organ injury and systemic inflammation after REBOA management of lethal hemorrhage in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Awadhesh K. Arya ◽  
Kurt Hu ◽  
Lalita Subedi ◽  
Tieluo Li ◽  
Bingren Hu
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Balloon Catheter ◽  
Organ Injury ◽  
Upper Body ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

AbstractResuscitative endovascular balloon occlusion of the aorta (REBOA) is a lifesaving maneuver for the management of lethal torso hemorrhage. However, its prolonged use leads to distal organ ischemia–reperfusion injury (IRI) and systemic inflammatory response syndrome (SIRS). The objective of this study is to investigate the blood-based biomarkers of IRI and SIRS and the efficacy of direct intestinal cooling in the prevention of IRI and SIRS. A rat lethal hemorrhage model was produced by bleeding 50% of the total blood volume. A balloon catheter was inserted into the aorta for the implementation of REBOA. A novel TransRectal Intra-Colon (TRIC) device was placed in the descending colon and activated from 10 min after the bleeding to maintain the intra-colon temperature at 37 °C (TRIC37°C group) or 12 °C (TRIC12°C group) for 270 min. The upper body temperature was maintained at as close to 37 °C as possible in both groups. Blood samples were collected before hemorrhage and after REBOA. The organ injury biomarkers and inflammatory cytokines were evaluated by ELISA method. Blood based organ injury biomarkers (endotoxin, creatinine, AST, FABP1/L-FABP, cardiac troponin I, and FABP2/I-FABP) were all drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated these increased organ injury biomarkers. Plasma levels of pro-inflammatory cytokines TNF-α, IL-1b, and IL-17F were also drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated the pro-inflammatory cytokines. In contrast, TRIC12°C significantly upregulated the levels of anti-inflammatory cytokines IL-4 and IL-10 after REBOA. Amazingly, the mortality rate was 100% in TRIC37°C group whereas 0% in TRIC12°C group after REBOA. Directly cooling the intestine offered exceptional protection of the abdominal organs from IRI and SIRS, switched from a harmful pro-inflammatory to a reparative anti-inflammatory response, and mitigated mortality in the rat model of REBOA management of lethal hemorrhage.

scholarly journals Pattern of serum cardiac troponin-I in symptomatic acute myocardial infarction patients in national institute of cardiovascular disease in Bangladesh

2014 ◽  
Vol 42 (1) ◽  
pp. 3-6
Author(s):  
SS Shahina ◽  
JU Ahmed ◽  
S Ahmed ◽  
E Shahriar ◽  
MN Uddin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Clinical Symptoms ◽  
Cardiac Injury ◽  
Circadian Variation ◽  
Assay Method ◽  
Ctni Level

Troponin I (cTnI) isoform is cardiac muscle specific protein and shown to have several features as a preferred marker of myocardial injury. It rises early in acute myocardial infarction (AMI) and attains levels that are clearly separated from baseline values. It remains elevated for several days providing a long window for detection of cardiac injury. The objective of the study was to evaluate for the profile of cTnI level among symptomatic AMI patients. The study was conducted at National Institute of Cardiovascular Disease, Dhaka, Bangladesh from July 2007 to June 2008 and total 9552 patients with type 1 or type 2 MI were included. Blood Sample was taken within 3 days of symptoms and cTnI was measured by chemiluminescent immunometric assay method. cTnI was considered positive when the value was >1ng/ml and study population was divided as per age, sex and cTnI level. The mean (+ SD) age of all patients was 55(+ 12.8) years and majority was males (82.20%). Seasonal variation showed highest positive cases in winter. In case of circadian variation positive cTnI results were suggestive of morning peak of AMI. Positive results were obtained in 32.3% of Cases. cTnI is now considered as a better indicator of myocardial injury. Further study in depth is necessary to correlate with clinical symptoms and other diagnostic tests to make a complete profile of AMI according to the latest subtypes. DOI: http://dx.doi.org/10.3329/bmj.v42i1.18969 Bangladesh Med J. 2013 Jan; 42 (1): 3-6

scholarly journals Aborted myocardial infarction in patients undergoing primary percutaneous coronary intervention

2015 ◽  
Vol 84 (1) ◽  
pp. 27-33
Author(s):  
Małgorzata Pyda ◽  
Stefan Grajek ◽  
Weronika Oleśkowska-Florek ◽  
Maciej Lesiak ◽  
Andrzej Siniawski ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Inflammatory Response ◽  
Primary Percutaneous Coronary Intervention ◽  
Troponin I ◽  
Coronary Intervention ◽  
Lower Serum ◽  
Maximal Increase ◽  
Timi Frame Count ◽  
Percutaneous Coronary

Introduction. The outcome of patients with ST-elevation myocardial infarction (STEMI) strongly depends on a successful reperfusion. In some patients receiving an effective treatment myocardial infarction can be aborted.Aim. The aim of the study was to estimate the incidence, clinical outcome, prognosis and inflammatory response in patients with aborted MI.Material and methods. 119 consecutive patients with STEMI treated with a primary percutaneous coronary intervention (pPCI) were enrolled in the study. Aborted MI was diagnosed when the maximal increase in cardiac enzymes (CK-MB) was up to twice the upper limit of normal (CK-MB ? 50 U/I) and at least 50% reduction of ST-segment deviation was observed within 90 min of pPCI.Results. Aborted MI was diagnosed in 16 subjects (13.4%). Patients with the aborted MI had lower serum troponin I levels (p < 0.0001). The time to treatment was significantly shorter in the aborted MI group (101 min vs. 220 min, p < 0.00001). Patients with aborted MI had a lower corrected TIMI frame count (p < 0.05) and a lower wall motion score index (p < 0.005), less pronounced inflammatory response (lower serum levels of IL-6, p < 0.01, and MCP-1, p < 0.05), higher ejection fraction six months after MI (72% vs. 64%, p < 0.05). None of the aborted MI patients died during the 3-year follow-up, while there were 13 deaths among patients with non-aborted MI.Conclusions. The abortion of myocardial infarction results in a better outcome and more favorable prognosis. An inflammatory response is less pronounced in the aborted MI.

scholarly journals Troponin: the biomarker of choice for the detection of cardiac injury

2005 ◽  
pp. 1191-1202
Author(s):  
Luciano Babuin ◽  
Allan S. Jaffe
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Cardiac Injury ◽  
Transaminase Activity ◽  
Elevated Troponin ◽  
Critical Issues ◽  
European Society Of Cardiology

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease. Troponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated.

Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

1994 ◽  
Vol 40 (7) ◽  
pp. 1291-1295 ◽  
Author(s):  
J E Adams ◽  
K B Schechtman ◽  
Y Landt ◽  
J H Ladenson ◽  
A S Jaffe
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Characteristic Curve ◽  
Cardiac Injury ◽  
Cardiac Troponin I ◽  
Creatine Kinase Mb ◽  
Coronary Care

Abstract Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.

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