Two novel direct SPIO labels and in vivo MRI detection of labeled cells after acute myocardial infarct.
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ABSTRACT:
SUBMITTER: Korpi RM
PROVIDER: S-EPMC5544151 | biostudies-other | 2017 Aug
REPOSITORIES: biostudies-other
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Project description:Acute myocardial infarction complicated by cardiogenic shock (AMICS), is characterized by critically low cardiac output and decreased myocardial contractility. In this situation, a treatment that unloads the myocardium and restores CO without increasing the myocardial oxygen demand is theoretically appealing. Axial flow pumps offer hemodynamic support without increasing myocardial oxygen consumption. Consequently, the use of axial flow pumps, especially the Impella devices, is increasing. It is likely that the SCAI C patient with predominantly left ventricular failure and without prolonged cardiac arrest is the best candidate for these devices. Registry data suggest that pre-PCI Impella may be advantageous to post-PCI placement. However, several gaps in knowledge exist regarding optimal patient selection, futility criteria, timing, weaning and escalation strategy, and until data from adequately sized randomized trials are available, immediate individual evaluation for mechanical circulatory support by a shock team is warranted when a patient is diagnosed with AMICS.
| S-EPMC9101440 | biostudies-literature
Project description:Background Evaluate the predictive value of myocardial stress measured by magnetic resonance imaging (MRI) on the severity of coronary artery stenosis and acute myocardial infarction (AMI). In the early stage of acute myocardial infarction, many imaging findings are negative, and MRI myocardial stress detection is controversial in the diagnosis of this aspect. Therefore, it is necessary to determine whether MRI myocardial stress can diagnose acute myocardial infarction. Methods A total of 120 patients were divided into an AMI group and non-AMI group. The AMI group was further divided into a mild group, moderate group, and severe group. The myocardial stress was measured by MRI, compared in each group, the correlation between myocardial stress and coronary artery stenosis rate was analyzed, and coronary artery disease (CAD) compared between patients with AMI, and the relationship between myocardial stress and AMI was observed. Results Among the 120 patients, there were 77 cases in the AMI group, including 21 cases in the mild group, 40 cases in the moderate group, and 16 cases in the severe group. There were a total of 43 cases in the non-AMI group. Myocardial stress in the AMI group was significantly higher than that in the non-AMI group (P<0.05). The myocardial stress increased gradually in the mild, moderate, and severe AMI groups (P<0.001). Myocardial stress was positively correlated with coronary artery stenosis rate (P<0.001) and CAD (P<0.05). Logistic regression analysis showed that myocardial stress was an independent risk factor for AMI (P<0.05). The sensitivity and specificity of myocardial stress >5.15 mm in the diagnosis of AMI were 83.5%, 68.6% (AUC =0.834), respectively. Acute myocardial infarction is often caused by risk factors such as hyperlipidemia, hypertension and hyperglycemia, as well as vascular stenosis caused by arterial wall malformation, vascular wall inflammation or vasospasm. Conclusions The MRI measurement of myocardial stress is simple, reliable, and practical to evaluate the degree of coronary artery lesions. Myocardial stress is closely related to AMI and can assist in the diagnosis of AMI.
| S-EPMC9562525 | biostudies-literature
Project description:INTRODUCTION:There are still limited data on the occurrence of multiple stenotic lesions within the infarct-related artery (IRA) in acute myocardial infarction (MI), and there is no consensus on the optimal treatment of this patient subgroup, which varies between centers and operators. AIM:To analyse the clinical efficacy of percutaneous coronary intervention (PCI) strategy of culprit lesion only in patients with myocardial infarction. MATERIAL AND METHODS:Patients with acute MI with the presence of at least two significant lesions in the IRA - (1) the target culprit lesion which required immediate stenting (> 50-100% stenosis) and (2) a second distal critical lesion (70-90%) - were included in the registry. Both lesions in the IRA were considered to be independent lesions requiring two separate stent platforms to be covered (no overlap). The decision on the treatment strategy of either complete (CR) or culprit-lesion-only (CLO) revascularization was at the discretion of the operator. RESULTS:There were altogether 95 patients enrolled in the registry, 63 (66%) in the group with CR of the IRA and 32 (34%) with CLO revascularization, which did not differ in terms of baseline demographics. In-hospital and long-term outcomes were similar between the groups. Stent thrombosis at 1 year occurred in 1.6% in CR and in 6.2% in CLO groups respectively (statistically not significant). There were no patients from the CLO group who had a planned percutaneous coronary intervention (PCI) of the 2(nd) lesion in the IRA during 1-year observation. CONCLUSIONS:At 1 year the clinical outcome was similar between those with complete and CLO PCI. Complete coverage of significant lesions did not increase the risk of stent thrombosis or need for repeated revascularization in long-term observation.
| S-EPMC4495122 | biostudies-literature
Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.
2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress
Project description:BACKGROUND: Despite recent advances, myocardial infarction (MI) remains the leading cause of death worldwide. Pre-clinical animal models that closely mimic human MI are pivotal for a quick translation of research and swine have similarities in anatomy and physiology. Here, we compared coronary surgical ligation versus coil embolization MI models in swine. METHODS: Fifteen animals were randomly distributed to undergo surgical ligation (n=7) or coil embolization (n=8). We evaluated infarct size, scar fibrosis, inflammation, myocardial vascularization, and cardiac function by magnetic resonance imaging (MRI). RESULTS: Thirty-five days after MI, there were no differences between the models in infarct size (P=0.53), left ventricular (LV) ejection fraction (P=0.19), LV end systolic volume (P=0.22), LV end diastolic volume (P=0.84), and cardiac output (P=0.89). Histologically, cardiac scars did not differ and the collagen content, collagen type I (I), collagen type III (III), and the I/III ratio were similar in both groups. Inflammation was assessed using specific anti-CD3 and anti-CD25 antibodies. There was similar activation of inflammation throughout the heart after coil embolization (P=0.78); while, there were more activated lymphocytes in the infarcted myocardium in the surgical occlusion model (P=0.02). Less myocardial vascularization in the infarction areas compared with the border and remote zones only in coil embolization animals was observed (P=0.004 and P=0.014, respectively). CONCLUSIONS: Our results support that surgical occlusion and coil embolization MI models generate similar infarct size, cardiac function impairment, and myocardial fibrosis; although, inflammation and myocardial vascularization levels were closer to those found in humans when coil embolization was performed.
| S-EPMC4047266 | biostudies-literature
Project description:BackgroundHyperglycemia has been associated with increased inflammatory indexes and larger infarct sizes in patients with obstructive acute myocardial infarction (obs-AMI). In contrast, no studies have explored these correlations in non-obstructive acute myocardial infarction (MINOCA). We investigated the relationship between hyperglycemia, inflammation and infarct size in a cohort of AMI patients that included MINOCA.MethodsPatients with AMI undergoing coronary angiography between 2016 and 2020 were enrolled. The following inflammatory markers were evaluated: C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-platelet ratio (NPR). Myocardial infarct size was measured by peak high sensitivity troponin I (Hs-TnI) levels, left-ventricular-end-diastolic-volume (LVEDV) and left ventricular ejection fraction (LVEF).ResultsThe final study population consisted of 2450 patients with obs-AMI and 239 with MINOCA. Hyperglycemia was more prevalent among obs-AMI cases. In all hyperglycemic patients-obs-AMI and MINOCA-NLR, NPR, and LPR were markedly altered. Hyperglycemic obs-AMI subjects exhibited a higher Hs-TnI (p < 0.001), a larger LVEDV (p = 0.003) and a lower LVEF (p < 0.001) compared to normoglycemic ones. Conversely, MINOCA patients showed a trivial myocardial damage, irrespective of admission glucose levels.ConclusionsOur data confirm the association of hyperglycemic obs-AMI with elevated inflammatory markers and larger infarct sizes. MINOCA patients exhibited modest myocardial damage, regardless of admission glucose levels.
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Project description:Although fibrous collagens are major structural components of extracellular matrix in mammals, collagen overproduction is associated with many human diseases including cancers and fibrosis. Collagen is typically identified in biomedical research by Western blot and immunohistochemistry; however, anticollagen antibodies employed in these analyses are difficult to prepare and their affinities to collagen can diminish if collagen becomes denatured during analyses. Previously, we discovered that single-stranded collagen mimetic peptides [CMPs, sequence: (GlyProHyp)(9)] can bind to denatured collagen chains by triple helix hybridization. Here, we present collagen-specific staining methods using simple CMPs conjugated to common fluorophores (e.g., carboxyfluorescein), which allow direct detection of collagens and collagen-like proteins in SDS-PAGE and in various mammalian tissue sections. By directly staining SDS-PAGE gels with fluorescently labeled CMPs, both intact (type I, II, and IV) and MMP-1 cleaved collagen (type I) chains as well as complement factor C1q were detected. Collagen bands containing as little as 5 ng were optically visualized, while no staining was observed for fibronectin, laminin, and a collection of proteins from mammalian cell lysate. The CMP was unable to stain collagen-like bacterial protein, which contains numerous charged amino acids that are believed to stabilize triple helix in place of Hyp. We also show that fluorescently labeled CMPs can specifically visualize collagens in fixed tissue sections (e.g., skin, cornea, and bone) more effectively than anticollagen I antibody, and allow facile identification of pathologic conditions in fibrotic liver tissues.
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Project description:There are conflicting data on the relationship between the time of symptom onset during the 24-hour cycle (circadian dependence) and infarct size in ST-elevation myocardial infarction (STEMI). Moreover, the impact of this circadian pattern of infarct size on clinical outcomes is unknown. We sought to study the circadian dependence of infarct size and its impact on clinical outcomes in STEMI.We studied 6,710 consecutive patients hospitalized for STEMI from 2006 to 2009 in a tropical climate with non-varying day-night cycles. We categorized the time of symptom onset into four 6-hour intervals: midnight-6:00 A.M., 6:00 A.M.-noon, noon-6:00 P.M. and 6:00 P.M.-midnight. We used peak creatine kinase as a surrogate marker of infarct size.Midnight-6:00 A.M patients had the highest prevalence of diabetes mellitus (P = 0.03), more commonly presented with anterior MI (P = 0.03) and received percutaneous coronary intervention less frequently, as compared with other time intervals (P = 0.03). Adjusted mean peak creatine kinase was highest among midnight-6:00 A.M. patients and lowest among 6:00 A.M.-noon patients (2,590.8±2,839.1 IU/L and 2,336.3±2,386.6 IU/L, respectively, P = 0.04). Midnight-6:00 A.M patients were at greatest risk of acute heart failure (P<0.001), 30-day mortality (P = 0.03) and 1-year mortality (P = 0.03), while the converse was observed in 6:00 A.M.-noon patients. After adjusting for diabetes, infarct location and performance of percutaneous coronary intervention, circadian variations in acute heart failure incidence remained strongly significant (P = 0.001).We observed a circadian peak and nadir in infarct size during STEMI onset from midnight-6:00A.M and 6:00A.M.-noon respectively. The peak and nadir incidence of acute heart failure paralleled this circadian pattern. Differences in diabetes prevalence, infarct location and mechanical reperfusion may account partly for the observed circadian pattern of infarct size and acute heart failure.
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Project description:A novel electrochemical detection approach using DNA probes labeled with Anthraquinone (AQ) as a reporter moiety has been successfully exploited as a method for the direct detection of DNA targets. This assay uses simple voltammetry techniques (Differential Pulse Voltammetry) to exploit the unique responsiveness of AQ to its chemical environments within oxygenated aqueous buffers, providing a specific detection mechanism as a result of DNA hybridization. This measurement is based on a cathodic shift of the reduction potential of the AQ tag and the concurrent reduction in peak current upon DNA binding. The further utility of this approach for discrimination of closely related DNA targets is demonstrated using DNA strands specific to B. anthracis and closely related bacillus species. DNA targets were designed to the rpoB gene incorporating nucleotide polymorphisms associated with different bacillus species. This assay was used to demonstrate that the shift in reduction potential is directly related to the homology of the target DNA. The discriminatory mechanism is dependent on the presence of oxygen in the measurement buffer and is strongly linked to the position of the nucleotide polymorphisms; with homology at the terminus carrying the AQ functionalised nucleotide critical to achieving accurate discrimination. This understanding of assay design was used to demonstrate an optimized assay capable of discriminating between Yersinia pestis (the causative agent of plague) and closely related species based on the groEL gene. This method is attractive as it can not only detect DNA binding, but can also discriminate between multiple Single Nucleotide Polymorphisms (SNPs) within that DNA without the need for any additional reagents, reporters, or processes such as melting of DNA strands. This indicates that this approach may have great potential to be exploited within novel biosensors for detection and diagnosis of infectious disease in future Point of Care (PoC) devices.
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