Displaying publications 1 - 20 of 117 in total

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  1. The role of regional myocardial topography post-myocardial infarction on infarct extension
    Leong CO, Leong CN, Liew YM, Al Abed A, Aziz YFA, Chee KH, et al.
    Int J Numer Method Biomed Eng, 2021 08;37(8):e3501.
    PMID: 34057819 DOI: 10.1002/cnm.3501
    Infarct extension involves necrosis of healthy myocardium in the border zone (BZ), progressively enlarging the infarct zone (IZ) and recruiting the remote zone (RZ) into the BZ, eventually leading to heart failure. The mechanisms underlying infarct extension remain unclear, but myocyte stretching has been suggested as the most likely cause. Using human patient-specific left-ventricular (LV) numerical simulations established from cardiac magnetic resonance imaging (MRI) of myocardial infarction (MI) patients, the correlation between infarct extension and regional mechanics abnormality was investigated by analysing the fibre stress-strain loops (FSSLs). FSSL abnormality was characterised using the directional regional external work (DREW) index, which measures FSSL area and loop direction. Sensitivity studies were also performed to investigate the effect of infarct stiffness on regional myocardial mechanics and potential for infarct extension. We found that infarct extension was correlated to severely abnormal FSSL in the form of counter-clockwise loop at the RZ close to the infarct, as indicated by negative DREW values. In regions demonstrating negative DREW values, we observed substantial fibre stretching in the isovolumic relaxation (IVR) phase accompanied by a reduced rate of systolic shortening. Such stretching in IVR phase in part of the RZ was due to its inability to withstand the high LV pressure that was still present and possibly caused by regional myocardial stiffness inhomogeneity. Further analysis revealed that the occurrence of severely abnormal FSSL due to IVR fibre stretching near the RZ-BZ boundary was due to a large amount of surrounding infarcted tissue, or an excessively stiff IZ.
    Matched MeSH terms: Myocardium*
  2. Fulltext The Pleiotropic Role of Extracellular ATP in Myocardial Remodelling
    Sudi S, Thomas FM, Daud SK, Ag Daud DM, Sunggip C
    Molecules, 2023 Feb 23;28(5).
    PMID: 36903347 DOI: 10.3390/molecules28052102
    Myocardial remodelling is a molecular, cellular, and interstitial adaptation of the heart in response to altered environmental demands. The heart undergoes reversible physiological remodelling in response to changes in mechanical loading or irreversible pathological remodelling induced by neurohumoral factors and chronic stress, leading to heart failure. Adenosine triphosphate (ATP) is one of the potent mediators in cardiovascular signalling that act on the ligand-gated (P2X) and G-protein-coupled (P2Y) purinoceptors via the autocrine or paracrine manners. These activations mediate numerous intracellular communications by modulating the production of other messengers, including calcium, growth factors, cytokines, and nitric oxide. ATP is known to play a pleiotropic role in cardiovascular pathophysiology, making it a reliable biomarker for cardiac protection. This review outlines the sources of ATP released under physiological and pathological stress and its cell-specific mechanism of action. We further highlight a series of cardiovascular cell-to-cell communications of extracellular ATP signalling cascades in cardiac remodelling, which can be seen in hypertension, ischemia/reperfusion injury, fibrosis, hypertrophy, and atrophy. Finally, we summarize current pharmacological intervention using the ATP network as a target for cardiac protection. A better understanding of ATP communication in myocardial remodelling could be worthwhile for future drug development and repurposing and the management of cardiovascular diseases.
    Matched MeSH terms: Myocardium/metabolism
  3. Fulltext A conducting polymer with enhanced electronic stability applied in cardiac models
    Mawad D, Mansfield C, Lauto A, Perbellini F, Nelson GW, Tonkin J, et al.
    Sci Adv, 2016 Nov;2(11):e1601007.
    PMID: 28138526 DOI: 10.1126/sciadv.1601007
    Electrically active constructs can have a beneficial effect on electroresponsive tissues, such as the brain, heart, and nervous system. Conducting polymers (CPs) are being considered as components of these constructs because of their intrinsic electroactive and flexible nature. However, their clinical application has been largely hampered by their short operational time due to a decrease in their electronic properties. We show that, by immobilizing the dopant in the conductive scaffold, we can prevent its electric deterioration. We grew polyaniline (PANI) doped with phytic acid on the surface of a chitosan film. The strong chelation between phytic acid and chitosan led to a conductive patch with retained electroactivity, low surface resistivity (35.85 ± 9.40 kilohms per square), and oxidized form after 2 weeks of incubation in physiological medium. Ex vivo experiments revealed that the conductive nature of the patch has an immediate effect on the electrophysiology of the heart. Preliminary in vivo experiments showed that the conductive patch does not induce proarrhythmogenic activities in the heart. Our findings set the foundation for the design of electronically stable CP-based scaffolds. This provides a robust conductive system that could be used at the interface with electroresponsive tissue to better understand the interaction and effect of these materials on the electrophysiology of these tissues.
    Matched MeSH terms: Myocardium*
  4. Fulltext Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management
    Yang J, Chen S, Duan F, Wang X, Zhang X, Lian B, et al.
    Cells, 2022 Nov 06;11(21).
    PMID: 36359908 DOI: 10.3390/cells11213511
    Mitochondrial cardiomyopathy (MCM) is characterized by abnormal heart-muscle structure and function, caused by mutations in the nuclear genome or mitochondrial DNA. The heterogeneity of gene mutations and various clinical presentations in patients with cardiomyopathy make its diagnosis, molecular mechanism, and therapeutics great challenges. This review describes the molecular epidemiology of MCM and its clinical features, reviews the promising diagnostic tests applied for mitochondrial diseases and cardiomyopathies, and details the animal and cellular models used for modeling cardiomyopathy and to investigate disease pathogenesis in a controlled in vitro environment. It also discusses the emerging therapeutics tested in pre-clinical and clinical studies of cardiac regeneration.
    Matched MeSH terms: Myocardium/pathology
  5. Fulltext Pirfenidone improves early cardiac function following myocardial infarction by enhancing the elastin/collagen ratio
    Yu Y, Xu Y, Chen J, Yao Y, Liu Y, Chen Y, et al.
    Biomed Pharmacother, 2024 Sep;178:117254.
    PMID: 39142250 DOI: 10.1016/j.biopha.2024.117254
    BACKGROUND: Acute myocardial infarction (AMI) is a leading cause of mortality worldwide, with reduced elastin/collagen ratios exacerbating cardiac dysfunction due to collagen-rich scar tissue replacing necrotic myocardial cells. This study aims to evaluate pirfenidone's therapeutic effect on early cardiac function post-AMI and elucidate its impact on the elastin/collagen ratio.

    METHODS: Sprague-Dawley rats were divided into four groups: Sham, AMI, AMI treated with PBS (AMI-PBS), and AMI treated with pirfenidone (AMI-PFD) (n=12 each). AMI was induced via coronary artery ligation. The AMI-PFD and AMI-PBS groups received pirfenidone and PBS for 14 days, respectively. Cardiac function, fibrosis, serum cytokines, collagen and elastin content, and their ratios were assessed. Cardiac fibroblasts (CFs) from neonatal rats were categorized into control, hypoxia-induced (LO), LO+PBS, and LO+PFD groups. ELISA measured inflammatory factors, and RT-PCR analyzed collagen and elastin gene expression.

    RESULTS: The AMI-PFD group showed improved cardiac function and reduced serum interleukin-1β (IL-1β), IL-6, and transforming growth factor-β (TGF-β). Type I and III collagen decreased by 22.6 % (P=0.0441) and 34.4 % (P=0.0427), respectively, while elastin content increased by 79.4 % (P=0.0126). E/COLI and E/COLIII ratios rose by 81.1 % (P=0.0026) and 88.1 % (P=0.0006). CFs in the LO+PFD group exhibited decreased IL-1β, IL-6, TGF-β, type I and III collagen, with increased elastin mRNA, enhancing the elastin/collagen ratio.

    CONCLUSION: Pirfenidone enhances cardiac function by augmenting the early elastin/collagen ratio post-AMI.

    Matched MeSH terms: Myocardium/metabolism; Myocardium/pathology
  6. Fulltext Mechanoregulation of cardiac myofibroblast differentiation: implications for cardiac fibrosis and therapy
    Yong KW, Li Y, Huang G, Lu TJ, Safwani WK, Pingguan-Murphy B, et al.
    Am J Physiol Heart Circ Physiol, 2015 Aug 15;309(4):H532-42.
    PMID: 26092987 DOI: 10.1152/ajpheart.00299.2015
    Cardiac myofibroblast differentiation, as one of the most important cellular responses to heart injury, plays a critical role in cardiac remodeling and failure. While biochemical cues for this have been extensively investigated, the role of mechanical cues, e.g., extracellular matrix stiffness and mechanical strain, has also been found to mediate cardiac myofibroblast differentiation. Cardiac fibroblasts in vivo are typically subjected to a specific spatiotemporally changed mechanical microenvironment. When exposed to abnormal mechanical conditions (e.g., increased extracellular matrix stiffness or strain), cardiac fibroblasts can undergo myofibroblast differentiation. To date, the impact of mechanical cues on cardiac myofibroblast differentiation has been studied both in vitro and in vivo. Most of the related in vitro research into this has been mainly undertaken in two-dimensional cell culture systems, although a few three-dimensional studies that exist revealed an important role of dimensionality. However, despite remarkable advances, the comprehensive mechanisms for mechanoregulation of cardiac myofibroblast differentiation remain elusive. In this review, we introduce important parameters for evaluating cardiac myofibroblast differentiation and then discuss the development of both in vitro (two and three dimensional) and in vivo studies on mechanoregulation of cardiac myofibroblast differentiation. An understanding of the development of cardiac myofibroblast differentiation in response to changing mechanical microenvironment will underlie potential targets for future therapy of cardiac fibrosis and failure.
    Matched MeSH terms: Myocardium/cytology; Myocardium/metabolism*; Myocardium/pathology
  7. Fulltext Intramyocardial dissecting haematoma mimicking left ventricular clot, a rare complication of myocardial infarction: a case report
    Lee TJ, Roslan A, Teh KC, Ghazi A
    Eur Heart J Case Rep, 2019 Jun 01;3(2).
    PMID: 31449618 DOI: 10.1093/ehjcr/ytz056
    BACKGROUND: Intramyocardial dissecting haematoma is a rare complication of myocardial infarction (MI) associated with high mortality rates. Studies and research of this occurrence are limited largely to isolated case reports or case series.

    CASE SUMMARY: We report a case of late presenting MI, where on initial echocardiogram had what was thought to be an intraventricular clot. However, upon further evaluation, the patient actually had an intramyocardial haematoma, with the supporting echocardiographic features to distinguish it from typical left ventricular (LV) clot. While this prevented the patient from receiving otherwise unnecessary anticoagulation, this diagnosis also put him at a much higher risk of mortality. Despite exhaustive medical and supportive management, death as consequence of pump failure occurred after 2 weeks.

    DISCUSSION: This report highlights the features seen on echocardiography which support the diagnosis of an intramyocardial haematoma rather than an LV clot, notably the various acoustic densities, a well visualized myocardial dissecting tear leading into a neocavity filled with blood, and an independent endocardial layer seen above the haematoma. Based on this report, we wish to highlight the importance of differentiating intramyocardial haematomas from intraventricular clots in patients with recent MI.

    Matched MeSH terms: Myocardium
  8. A novel automated diagnostic system for classification of myocardial infarction ECG signals using an optimal biorthogonal filter bank
    Sharma M, Tan RS, Acharya UR
    Comput Biol Med, 2018 11 01;102:341-356.
    PMID: 30049414 DOI: 10.1016/j.compbiomed.2018.07.005
    Myocardial infarction (MI), also referred to as heart attack, occurs when there is an interruption of blood flow to parts of the heart, due to the acute rupture of atherosclerotic plaque, which leads to damage of heart muscle. The heart muscle damage produces changes in the recorded surface electrocardiogram (ECG). The identification of MI by visual inspection of the ECG requires expert interpretation, and is difficult as the ECG signal changes associated with MI can be short in duration and low in magnitude. Hence, errors in diagnosis can lead to delay the initiation of appropriate medical treatment. To lessen the burden on doctors, an automated ECG based system can be installed in hospitals to help identify MI changes on ECG. In the proposed study, we develop a single-channel single lead ECG based MI diagnostic system validated using noisy and clean datasets. The raw ECG signals are taken from the Physikalisch-Technische Bundesanstalt database. We design a novel two-band optimal biorthogonal filter bank (FB) for analysis of the ECG signals. We present a method to design a novel class of two-band optimal biorthogonal FB in which not only the product filter but the analysis lowpass filter is also a halfband filter. The filter design problem has been composed as a constrained convex optimization problem in which the objective function is a convex combination of multiple quadratic functions and the regularity and perfect reconstruction conditions are imposed in the form linear equalities. ECG signals are decomposed into six subbands (SBs) using the newly designed wavelet FB. Following to this, discriminating features namely, fuzzy entropy (FE), signal-fractal-dimensions (SFD), and renyi entropy (RE) are computed from all the six SBs. The features are fed to the k-nearest neighbor (KNN). The proposed system yields an accuracy of 99.62% for the noisy dataset and an accuracy of 99.74% for the clean dataset, using 10-fold cross validation (CV) technique. Our MI identification system is robust and highly accurate. It can thus be installed in clinics for detecting MI.
    Matched MeSH terms: Myocardium
  9. Fulltext Distinct gut microbiota composition among older adults with myocardial ageing
    Wong JJ, Purbojati RW, Tan RS, Pettersson S, Koh AS
    ESC Heart Fail, 2022 Dec;9(6):4366-4368.
    PMID: 36071622 DOI: 10.1002/ehf2.14139
    Matched MeSH terms: Myocardium
  10. Fulltext Artifacts reduction in strain maps of tagged magnetic resonance imaging using harmonic phase
    Wang D, Fu Y, Ashraf MA
    Open Med (Wars), 2015;10(1):425-433.
    PMID: 28352731 DOI: 10.1515/med-2015-0074
    Tagged Magnetic Resonance Imaging (MRI) is a noninvasive technique for examining myocardial function and deformation. Tagged MRI can also be used in quasi-static MR elastography to acquire strain maps of other biological soft tissues. Harmonic phase (HARP) provides automatic and rapid analysis of tagged MR images for the quantification and visualization of myocardial strain. We propose a new artifact reduction method in strain maps. Image intensity of the DC component is estimated and subtracted from spatial modulation of magnetization (SPAMM) tagged MR images. DC peak interference in harmonic phase extraction is greatly reduced after DC component subtraction. The proposed method is validated using both simulated and MR acquired tagged images. Strain maps are obtained with better accuracy and smoothness after DC component subtraction.
    Matched MeSH terms: Myocardium
  11. Total paralysis regime in severe tetanus
    Alhady SMA, Bowler DP, Reid HA, Scott LT
    Br Med J, 1960;1:540-545.
    Tetanus may be mild, moderate, severe, or inevitably fatal. Our clinical experience suggests it may be classified as severe (or, maybe, inevitably fatal) when a tetanic spasm stops respiration. Ten patients with severe tetanus were treated by the total paralysis regime (T.P.R.), consisting of tracheostomy, curarization, and intermittent positiveor positive/negative-pressure respiration. Two of the patients were saved by T.P.R. and therefore only limited effectiveness can be claimed for the regime. In inevitably fatal cases survival can be prolonged by T.P.R. so that further effects of tetanus toxin emerge. Of these, the most important appears to be direct damage to the myocardium.
    Matched MeSH terms: Myocardium
  12. Fulltext An inverse finite element method for determining the tissue compressibility of human left ventricular wall during the cardiac cycle
    Hassaballah AI, Hassan MA, Mardi AN, Hamdi M
    PLoS One, 2013;8(12):e82703.
    PMID: 24367544 DOI: 10.1371/journal.pone.0082703
    The determination of the myocardium's tissue properties is important in constructing functional finite element (FE) models of the human heart. To obtain accurate properties especially for functional modeling of a heart, tissue properties have to be determined in vivo. At present, there are only few in vivo methods that can be applied to characterize the internal myocardium tissue mechanics. This work introduced and evaluated an FE inverse method to determine the myocardial tissue compressibility. Specifically, it combined an inverse FE method with the experimentally-measured left ventricular (LV) internal cavity pressure and volume versus time curves. Results indicated that the FE inverse method showed good correlation between LV repolarization and the variations in the myocardium tissue bulk modulus K (K = 1/compressibility), as well as provided an ability to describe in vivo human myocardium material behavior. The myocardium bulk modulus can be effectively used as a diagnostic tool of the heart ejection fraction. The model developed is proved to be robust and efficient. It offers a new perspective and means to the study of living-myocardium tissue properties, as it shows the variation of the bulk modulus throughout the cardiac cycle.
    Matched MeSH terms: Myocardium/metabolism
  13. The role of infarct transmural extent in infarct extension: A computational study
    Leong CN, Lim E, Andriyana A, Al Abed A, Lovell NH, Hayward C, et al.
    Int J Numer Method Biomed Eng, 2017 Feb;33(2).
    PMID: 27043925 DOI: 10.1002/cnm.2794
    Infarct extension, a process involving progressive extension of the infarct zone (IZ) into the normally perfused border zone (BZ), leads to continuous degradation of the myocardial function and adverse remodelling. Despite carrying a high risk of mortality, detailed understanding of the mechanisms leading to BZ hypoxia and infarct extension remains unexplored. In the present study, we developed a 3D truncated ellipsoidal left ventricular model incorporating realistic electromechanical properties and fibre orientation to examine the mechanical interaction among the remote, infarct and BZs in the presence of varying infarct transmural extent (TME). Localized highly abnormal systolic fibre stress was observed at the BZ, owing to the simultaneous presence of moderately increased stiffness and fibre strain at this region, caused by the mechanical tethering effect imposed by the overstretched IZ. Our simulations also demonstrated the greatest tethering effect and stress in BZ regions with fibre direction tangential to the BZ-remote zone boundary. This can be explained by the lower stiffness in the cross-fibre direction, which gave rise to a greater stretching of the IZ in this direction. The average fibre strain of the IZ, as well as the maximum stress in the sub-endocardial layer, increased steeply from 10% to 50% infarct TME, and slower thereafter. Based on our stress-strain loop analysis, we found impairment in the myocardial energy efficiency and elevated energy expenditure with increasing infarct TME, which we believe to place the BZ at further risk of hypoxia. Copyright © 2016 John Wiley & Sons, Ltd.
    Matched MeSH terms: Myocardium/pathology
  14. Fulltext Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy
    Arcari L, Hinojar R, Engel J, Freiwald T, Platschek S, Zainal H, et al.
    Int J Cardiol, 2020 05 01;306:102-108.
    PMID: 32169347 DOI: 10.1016/j.ijcard.2020.03.002
    AIMS: Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.

    METHODS: In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).

    RESULTS: Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p 

    Matched MeSH terms: Myocardium/pathology
  15. Fulltext Hypoxia-inducible factor 1 signalling, metabolism and its therapeutic potential in cardiovascular disease
    Sousa Fialho MDL, Abd Jamil AH, Stannard GA, Heather LC
    Biochim Biophys Acta Mol Basis Dis, 2019 04 01;1865(4):831-843.
    PMID: 30266651 DOI: 10.1016/j.bbadis.2018.09.024
    Cardiovascular disease (CVD) accounts for the largest number of deaths worldwide, necessitating the development of novel treatments and prevention strategies. Given the huge energy demands placed on the heart, it is not surprising that changes in energy metabolism play a key role in the development of cardiac dysfunction in CVD. A reduction in oxygen delivery to the heart, hypoxia, is sensed and responded to by the hypoxia-inducible factor (HIF) and its family of proteins, by regulating the oxygen-dependent signalling cascade and subsequent response. Hypoxia is one of the main drivers of metabolic change in ischaemic disease and myocardial infarction, and we therefore suggest that HIF may be an attractive therapeutic target. In this review, we assess cardiac energy metabolism in health and disease, and how these can be regulated by HIF-1α activation. We then present an overview of research in the field of hypoxia-mimetic drugs recently developed in other treatment fields, which provide insight into the potential of systemic HIF-1α activation therapy for treating the heart.
    Matched MeSH terms: Myocardium/metabolism
  16. Problems and usefulness of serum enzyme measurement in the diagnosis of diseases
    Buttery JE
    Med J Malaysia, 1974 Mar;28(3):180-4.
    PMID: 4278233
    Matched MeSH terms: Myocardium/enzymology
  17. Fulltext Non-infarcted myocardium bears the weight in CVD
    Zhou H, Zainal H, Puntmann VO
    Aging (Albany NY), 2019 03 25;11(6):1609-1610.
    PMID: 30908271 DOI: 10.18632/aging.101890
    Matched MeSH terms: Myocardium/pathology*
  18. Fulltext Single-cell profile reveals the landscape of cardiac immunity and identifies a cardio-protective Ym-1hi neutrophil in myocardial ischemia-reperfusion injury
    Dong Y, Kang Z, Zhang Z, Zhang Y, Zhou H, Liu Y, et al.
    Sci Bull (Beijing), 2024 Apr 15;69(7):949-967.
    PMID: 38395651 DOI: 10.1016/j.scib.2024.02.003
    Myocardial ischemia-reperfusion injury (MIRI) is a major hindrance to the success of cardiac reperfusion therapy. Although increased neutrophil infiltration is a hallmark of MIRI, the subtypes and alterations of neutrophils in this process remain unclear. Here, we performed single-cell sequencing of cardiac CD45+ cells isolated from the murine myocardium subjected to MIRI at six-time points. We identified diverse types of infiltrating immune cells and their dynamic changes during MIRI. Cardiac neutrophils showed the most immediate response and largest changes and featured with functionally heterogeneous subpopulations, including Ccl3hi Neu and Ym-1hi Neu, which were increased at 6 h and 1 d after reperfusion, respectively. Ym-1hi Neu selectively expressed genes with protective effects and was, therefore, identified as a novel specific type of cardiac cell in the injured heart. Further analysis indicated that neutrophils and their subtypes orchestrated subsequent immune responses in the cardiac tissues, especially instructing the response of macrophages. The abundance of Ym-1hi Neu was closely correlated with the therapeutic efficacy of MIRI when neutrophils were specifically targeted by anti-Lymphocyte antigen 6 complex locus G6D (Ly6G) or anti-Intercellular cell adhesion molecule-1 (ICAM-1) neutralizing antibodies. In addition, a neutrophil subtype with the same phenotype as Ym-1hi Neu was detected in clinical samples and correlated with prognosis. Ym-1 inhibition exacerbated myocardial injury, whereas Ym-1 supplementation significantly ameliorated injury in MIRI mice, which was attributed to the tilt of Ym-1 on the polarization of macrophages toward the repair phenotype in myocardial tissue. Overall, our findings reveal the anti-inflammatory phenotype of Ym-1hi Neu and highlight its critical role in myocardial protection during the early stages of MIRI.
    Matched MeSH terms: Myocardium
  19. An online open-source tool for automated quantification of liver and myocardial iron concentrations by T2* magnetic resonance imaging
    Git KA, Fioravante LA, Fernandes JL
    Br J Radiol, 2015 Sep;88(1053):20150269.
    PMID: 26118302 DOI: 10.1259/bjr.20150269
    To assess whether an online open-source tool would provide accurate calculations of T2(*) values for iron concentrations in the liver and heart compared with a standard reference software.
    Matched MeSH terms: Myocardium/metabolism; Myocardium/chemistry*
  20. Intrapericardial Administration of Human Pericardial Fluid Cells Improves Cardiac Functions in Rats with Heart Failure
    Xu Y, Zhang X, Fu Z, Dong Y, Yu Y, Liu Y, et al.
    Stem Cells Dev, 2024 Nov;33(21-22):616-629.
    PMID: 39155804 DOI: 10.1089/scd.2024.0072
    Heart failure (HF) is still the main cause of mortality worldwide. This study investigated the characteristics of human pericardial fluid-derived cells (hPFCs) and their effects in treating doxorubicin (DOX)-induced HF rats through intrapericardial injection. hPFCs were isolated from patients who underwent heart transplantation (N = 5). These cells that primarily expressed SCA-1, NANOG, and mesenchymal markers, CD90, CD105, and CD73, were able to form adipocytes, osteoblasts, and cardiomyocytes in vitro. Passage 3 hPFCs (2.5 × 105 cells/heart) were injected into the pericardial cavity of the DOX-injured rat hearts, significantly improving cardiac functions after 4 weeks. The tracked and engrafted red fluorescent protein-tagged hPFCs coexpressed cardiac troponin T and connexin 43 after 4 weeks in the host myocardium. This observation was also coupled with a significant reduction in cardiac fibrosis following hPFC treatment (P < 0.0001 vs. untreated). The elevated inflammatory cytokines interleukin (IL)-6, IL-10, and tumor necrosis factor-α in the DOX-treated hearts were found to be significantly reduced (P < 0.001 vs. untreated), while the regional proangiogenic vascular endothelial growth factor A (VEGFA) level was increased in the hPFC-treated group after 4 weeks (P < 0.05 vs. untreated). hPFCs possess stem cell characteristics and can improve the cardiac functions of DOX-induced HF rats after 4 weeks through pericardial administration. The improvements were attributed to a significant reduction in cardiac fibrosis, inflammation, and elevated regional proangiogenesis factor VEGFA, with evidence of cellular engraftment and differentiation in the host myocardium.
    Matched MeSH terms: Myocardium/metabolism; Myocardium/pathology
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