In Vivo Analysis & Characterization of Myocardial Ischemia & Infarction by Steven Dymarkowski Download PDF EPUB FB2
OBJECTIVE: In this study we present in vivo, whole-animal techniques and experimental protocols for detailed electrophysiological characterization in a mouse model of myocardial ischemia and infarction. METHODS: FVB mice underwent open-chest surgery for ligation of the left anterior descending coronary artery or :// 1.
Introduction. Myocardial infarction (MI) is the most severe type of ischemic myocardial injury. It is caused by the blockage of one or more than one coronary artery, and is the most prevalent form of coronary artery disease (CAD), with approximately 8 million Americans having experienced at least one MI.
1 Chronic MI can trigger a complicated tissue-remodeling process in the left ventricle Animal preparation. Myocardial infarction was created in eleven Yucatan minipigs with the same preparation protocol as the control subjects of a previous study that validated LGE for in vivo infarct characterization .Surgical cut-down to the left carotid artery and left jugular vein was :// In vivo chronic myocardial infarction characterization by spin locked cardiovascular magnetic resonance.
Huber S, Muthupillai R, Lambert B, Pereyra M, Napoli A, Flamm SD. Tissue characterization of myocardial infarction using T1rho: influence of contrast dose and time of Introduction.
Ischemia-reperfusion (IR) injury occurs due to blood restoration after a critical period of coronary artery obstruction. It is associated with clinical problems, such as thrombolysis, angioplasty, and coronary bypass surgery. However, reperfusion may lead to accelerated and additional myocardial injury, resulting in a spectrum of reperfusion-associated pathologies. Restoration of perfusion after acute myocardial infarction is the most frequent and effective medical treatment, but the process may inflict massive ischemia/reperfusion (I/R) injury 1.A hallmark In cross-sectional studies, this LOX-1 gene variation was observed to be associated with an increased incidence of myocardial infarction, as well as with increased carotid intima-media thickn A meta-analysis of 7 case-control studies indicated that the CC allele is significantly associated with ischemic :// Cell death resulting from myocardial infarction contributes to cardiac dysfunction and pathological remodeling.
Wang et al. found that blocking tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), a ligand of death receptor 5 (DR5), reduced inflammation and improved cardiac function after myocardial infarction in multiple animal models. Treating rodents, pigs, and monkeys with a Introduction.
C-reactive protein (CRP) is an acute reactant protein that is rapidly released from the liver when induced by interleukin-6 in the presence of inflammation, cell injury, or infection [1, 2].Serum CRP level increases during acute myocardial infarction and is considered a valuable prognostic marker of ischemic heart disease [3–6].CRP is present in the blood as a pentamer, and Characterization of myocardial insulin resistance after surgically-induced MI.
Elevated basal Akt phosphorylation (without insulin stimulation) was induced by myocardial ischemia. This is well demonstrated both in our laboratory and oth Insulin stimulation of either sham or post-MI rats 1 d after operation caused robust increases in The extent of myocardial infarction per area-at-risk was evaluated at 24 hrs using Evans Blue dye and 2,3,5 triphenyltetrazolium chloride (TTC) staining.
Left ventricular (LV) function was evaluated at one week post ischemia using high-resolution, 2- D echocardiography (VisualSonics Vevo ). In vivo characterization of myocardial infarction using fluorescence and diffuse reflectance spectroscopy Article in Journal of Biomedical Optics 15(3) May with 25 Reads G.
Vilahur, M. Gutierrez, L. Casani, et al.P2Y12 antagonists and cardiac repair post-myocardial infarction: global and regional heart function analysis and molecular assessments in pigs Cardiovasc Res, (), pp.
myocardial ischemia/reperfusion injury and to an attenuation of the cardioprotective eﬀect of preconditioning (Ferdinandy et al.,; Andreadou et al., ). Numerous studies from different labs around the world report human cardiac progenitor cells (hCPCs) as having a role in myocardial repair upon ischemia/reperfusion (I/R) injury, mainly through auto/paracrine signaling.
Even though these cell populations are already being investigated in cell transplantation-based clinical trials, the mechanisms underlying their response are still poorly In vivo contrast free chronic myocardial infarction characterization using diffusion-weighted cardiovascular magnetic resonance.
Nguyen C, Fan Z, Xie Y, Dawkins J, Tseliou E, Bi X, Sharif B, Dharmakumar R, Marbán E, Li :// The development of myocardial stunning, reperfusion arrhythmias, endothelial dysfunction and irreversible cell death leading to infarction are all relevant as clinical consequences of myocardial ischemia–reperfusion injury and also represent important experimental correlates and endpoints ().Here we define and discuss the mechanisms leading to myocardial stunning, reperfusion arrhythmias Exosomes secreted by mesenchymal stem cells have shown great therapeutic potential in regenerative medicine.
In this study, we performed meta-analysis to assess the clinical effectiveness of using exosomes in ischemia/reperfusion injury based on the reports published between January and September and indexed in the PUBMED and Web of Science :// Myocardial infarction and apoptosis after myocardial ischemia and reperfusion: role of the terminal complement components and inhibition by anti-C5 therapy.
Circulation. ;– PubMed CrossRef Google Scholar 2 days ago Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications.
This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in :// The Tt and TZ values were consis- tently increased (p Myocardial ischemia and infarction by NMR um.
We conclude that NMR imgaging can detect acute myocardial ischemia and infarction, but overestimates infarct size and corresponds better to the area of Leukocyte-Associated Immunoglobulin-like Receptor-1 is regulated in human myocardial infarction but its absence does not affect infarct size in mice Guilielmus H.
Ellenbroek 1 na1, Frequency‐domain analysis via power spectral density (PSD) and parameters derived from PSDs can enable one to view the signal from a different perspective than the time domain.
Certain signals such as the PCG and electroencephalogram may not lend themselves to easy interpretation in the time domain and, therefore, may benefit from a move to Herein we investigated the cardioprotective effects of a novel long-term and slow-releasing H2S donor, DATS-MSN, using in vivo myocardial ischemia/reperfusion (I/R) models and in vitro hypoxia Myocardial infarction was produced by placing a silk suture slipknot around the left anterior descending coronary artery.
After 30 min of ischemia, the slipknot was released to allow Ischemia/reperfusion- (I/R-) induced organ damage represents one of the main causes of death worldwide, and new strategies to reduce I/R injury are urgently needed. We have shown that programmable cells of monocytic origin (PCMO) respond to I/R with the release of angiogenic mediators and that transplantation of PCMO results in increased :// Cardiovascular disease remains the leading cause of death and disability in advanced countries.
Stem cell transplantation has emerged as a promising therapeutic strategy Interleukin 18 (IL) is a proinflammatory cytokine in the IL-1 family that has been implicated in a number of disease states. In animal models of acute myocardial infarction (AMI), pressure overload, and LPS-induced dysfunction, IL regulates cardiomyocyte hypertrophy and induces cardiac contractile dysfunction and extracellular matrix :// Despite the established role of late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) in characterizing chronic myocardial infarction (MI), a significant portion of chronic MI patients are contraindicative for the use of contrast agents.
One promising alternative contrast free technique is diffusion weighted CMR (dwCMR), which has been shown ex vivo to be sensitive to The characterization of myocardial edema and hemorrhage by T2 and T2* quantification is feasible post acute myocardial infarction. The evolution of these myocardial injury parameters post STEMI is complex, with hemorrhage resolving faster than ://.
Carrick et al. observed that elevated native T1 values in the remote zone, assessed 2 days after infarction, are associated with the occurrence of post-infarction remodeling and, in a secondary analysis, adverse outcome (cardiac death, nonfatal myocardial infarction or re-hospitalization for heart failure).
The prognostic significance of early An increase in plasma ET-1 has been demonstrated in association with myocardial infarction both in patients 9 and in experimental studies. 10 11 12 A few studies exist that might indicate the production of ET-1 by the ischemic heart.
10 11 12 One study reported that reperfusion of the ischemic heart was necessary to increase venous plasma ET-1 Zamilpa R, Lopez EF, Chiao YA, et al.
Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction. Proteomics. ; – [PMC free article] [Google Scholar]