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Journal articles on the topic 'Myocardial'
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1
A. Meenakshi, Martin, and Erik G. Seth. "Protective role of TAT-HSP70 after myocardial I/R injury." American Journal of BioMedicine 5, no. 3 (September 22, 2017): 279–84. http://dx.doi.org/10.18081/2333-5106/015-04/289-294.
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Myocardial ischemia reperfusion injury I/R adversely affects cardiac function. Heat shock proteins (HSPs) are a highly conserved family of proteins with diverse functions expressed by all cells exposed to environmental stress including myocardila injury. We investigated release of small constitutive heat shock proteins (HSPs) from mouse myocardium and the effects of TAT-HSP70 after myocardial I/R via occluding the left coronary artery (LAD). The results support the hypothesis that elevated HSPs in myocardium after ischemia and reperfusion and contributes to the inflammatory mechanism of myocardial functional injury. Further investigation of the significance of HSPs accumulation to the evolution of myocardial injury.
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Micic-Labudovic, Jelena, Tatjana Atanasijevic, Vesna Popovic, Zoran Mihailovic, Slobodan Nikolic, and Dragana Puzovic. "Myocardial bridges: A prospective forensic autopsy study." Srpski arhiv za celokupno lekarstvo 143, no. 3-4 (2015): 153–57. http://dx.doi.org/10.2298/sarh1504153m.
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Introduction. When the coronary artery, located subepicardially, submerges into the myocardium and appears again subepicardially after a short intramural course, it represents an embedded coronary artery, while the part of the myocardium above is a myocardial bridge. Objective. We investigated the frequency of the embedded left coronary artery (LAD) in the autopsy material considering the descending branch of the LAD to be the most important one in the nourishment of the myocardium and myocardial bridges to be the most frequent in its area, as well as clinically important. Methods. A prospective autopsy study of 975 cases was performed, including both, natural (21.33%) and violent (78.67%) deaths. The sample consisted of 74.56% males and 25.44% females. In order to discover myocardyal bridges and their characteristics, the hearts were examined by both transverse cuts and longitudinal openings of the LAD. Results. Myocardial bridge was found in 78 cases (8.00%), more commonly in males (9.35%) than females (4.03%). The average length of the myocardial bridge was 21.85?16.10mm and thickness 3.744?1.48 mm. The common localization of the myocardial bridge was the proximal half of the LAD (89.74%). The upper part of the artery, proximal to the bridge, was a common site of atherosclerotic changes. Myocardial bridge was found in 12.50% of natural deaths, but in 13.38% out of all cases of sudden cardiac deaths. Conclusion. Therefore, the presence of the myocardial bridge by itself is not predominant, but it is certainly a contributing factor to a sudden cardiac death.
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Zhong, Ze, Jia-qing Hu, Xin-dong Wu, Yong Sun, and Jun Jiang. "Anti-apoptotic effects of myocardin-related transcription factor-A on rat cardiomyocytes following hypoxia-induced injury." Canadian Journal of Physiology and Pharmacology 94, no. 4 (April 2016): 379–87. http://dx.doi.org/10.1139/cjpp-2014-0461.
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Myocardin-related transcription factor-A (MRTF-A) can transduce both biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction. However, the molecular mechanism that underlies the contribution that MRTF-A provides to the myocardium is not completely understood. The objective of this study was to investigate the effects of MRTF-A on myocardium apoptosis and its mechanisms. Our experiment results showed that MRTF-A expression increased and Bcl-2 expression reduced during myocardial ischemia–reperfusion in rat. Meanwhile, primary cardiomyocytes were pretreated with wild-type MRTF-A or siRNA of MRTF-A before exposure to hypoxia. We found that overexpression of MRTF-A in myocardial cells inhibited apoptosis and the release of cytochrome c. MRTF-A enhanced Bcl-2, which contributes to MRTF-A interaction with Bcl-2 in the nuclei of cardiomyocytes. MRTF-A upregulation expression of Bcl-2 in cardiomyocytes induced by hypoxia was inhibited by PD98059, an ERK1/2 inhibitor. In conclusions, MRTF-A improved myocardial cell survival in a cardiomyocyte model of hypoxia-induced injury; this effect was correlated with the upregulation of anti-apoptotic gene Bcl-2 through the activation of ERK1/2.
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Bhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth, and Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development." Journal of Cardiovascular Development and Disease 8, no. 3 (March 2, 2021): 26. http://dx.doi.org/10.3390/jcdd8030026.
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Among the three transforming growth factor beta (TGFβ) ligands, TGFβ2 is essential for heart development and is produced by multiple cell types, including myocardium. Heterozygous mutations in TGFB2 in patients of connective tissue disorders result in congenital heart defects and adult valve malformations, including mitral valve prolapse (MVP) with or without regurgitation. Tgfb2 germline knockout fetuses exhibit multiple cardiac defects but the role of myocardial-TGFβ2 in heart development is yet to be elucidated. Here, myocardial Tgfb2 conditional knockout (CKO) embryos were generated by crossing Tgfb2flox mice with Tgfb2+/−; cTntCre mice. Tgfb2flox/− embryos were normal, viable. Cell fate mapping was done using dual-fluorescent mT/mG+/− mice. Cre-mediated Tgfb2 deletion was assessed by genomic PCR. RNAscope in situ hybridization was used to detect the loss of myocardial Tgfb2 expression. Histological, morphometric, immunohistochemical, and in situ hybridization analyses of CKOs and littermate controls at different stages of heart development (E12.5–E18.5) were used to determine the role of myocardium-derived TGFβ2 in atrioventricular (AV) cushion remodeling and myocardial development. CKOs exhibit a thin ventricular myocardium, AV cushion remodeling defects and developed incomplete AV septation defects. The loss of myocardial Tgfb2 resulted in impaired cushion maturation and dysregulated cell death. Phosphorylated SMAD2, a surrogate for TGFβ signaling, was “paradoxically” increased in both AV cushion mesenchyme and ventricular myocardium in the CKOs. Our results indicate that TGFβ2 produced by cardiomyocytes acting as cells autonomously on myocardium and via paracrine signaling on AV cushions are required for heart development.
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Berry, Mark F., Adam J. Engler, Y. Joseph Woo, Timothy J. Pirolli, Lawrence T. Bish, Vasant Jayasankar, Kevin J. Morine, Timothy J. Gardner, Dennis E. Discher, and H. Lee Sweeney. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.
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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSCs) into the acutely ischemic myocardium. Two weeks postinfarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were twofold stiffer than myocardium from noninfarcted animals but softer than myocardium from vehicle-treated infarcted animals. After 8 wk, the following variables were evaluated: MSC engraftment and left ventricular geometry by histological methods, cardiac function with a pressure-volume conductance catheter, myocardial fibrosis by Masson Trichrome staining, vascularity by immunohistochemistry, and apoptosis by TdT-mediated dUTP nick-end labeling assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated postinfarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Khubulava, G. G., A. N. Shishkevich, S. S. Mikhailov, and E. Yu Bessonov. "Myocardial reperfusion syndrome. Pathogenesis, clinic, diagnosis." Bulletin of the Russian Military Medical Academy 22, no. 1 (December 15, 2020): 196–200. http://dx.doi.org/10.17816/brmma25992.
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The basics of pathogenesis, clinic and diagnosis of myocardial reperfusion syndrome are considered. Myocardial reperfusion syndrome is defined. Its relevance as one of the most poorly studied and formidable complications of cardiac reperfusion in myocardial infarction with elevation of the S-T segment has been explained. A brief review of the historical review of this problem and such types of manifestations of myocardial reperfusion syndrome as: diastolic myocardial dysfunction, post-reperfusion disturbances of the heart rhythm, the phenomenon of no-reflow and irreversible damage to the myocardium are briefly reviewed. The modern views on the pathological physiology of diastolic myocardial dysfunction, post-reperfusion damage to the myocardium, and the no-reflow phenomenon are analyzed. A review of current views on the pathological physiology of the development of post-reperfusion disturbances in heart rhythm is carried out. The clinical picture and the effect on the hemodynamics of such a manifestation of myocardial reperfusion syndrome as diastolic myocardial dysfunction are described. A brief description of the clinical picture of irreversible post-reperfusion damage to the myocardium is given. The clinical picture and types of post-reperfusion rhythm disturbances are described. The diagnostics of the no-reflow phenomenon has been analyzed in detail, the coronary angiographic scales for assessing thrombolysis in myocardial infarction and for assessing myocardial perfusion are graphically shown. A description of the basics of diagnosing post-reperfusion disturbances in heart rhythm, diastolic myocardial dysfunction, and post-reperfusion irreversible damage to the myocardium is given. A brief description of the known in the world literature predictors of the development of myocardial reperfusion syndrome is presented.
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Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer, and Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.
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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.
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Brown, TA. "Hibernating myocardium." American Journal of Critical Care 10, no. 2 (March 1, 2001): 84–91. http://dx.doi.org/10.4037/ajcc2001.10.2.84.
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According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.
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Xiao, Ying, Tao Wang, Xin Song, Dan Yang, Qing Chu, and Y. James Kang. "Copper promotion of myocardial regeneration." Experimental Biology and Medicine 245, no. 10 (March 8, 2020): 911–21. http://dx.doi.org/10.1177/1535370220911604.
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Myocardial regeneration is the key to the functional recovery of ischemic heart. Angiogenesis plays a pivotal role in myocardial regeneration by resetting a rejuvenation microenvironment under ischemic conditions. Hypoxia-inducible factor 1 (HIF-1) is the predominant transcription factor in the regulation of angiogenesis. In prolonged myocardial infarction, HIF-1α, the critical subunit of HIF-1, is accumulated in the infarcted myocardium, but fails to activate angiogenesis, suggesting a missing of a critical factor in the HIF-1 regulation of angiogenesis. Copper is involved in multiple steps of HIF-1 regulation of target gene expression. However, copper is deprived during myocardial ischemic injury, leading to deactivation of HIF-1-regulated angiogenesis. Multiple approaches are applied to increasing copper availability in the ischemic heart, effectively reactivating transcription of HIF-1 target angiogenic genes. Copper-induced angiogenesis thus reconstructs the conduit for the transduction of tissue injury signaling, recruitment of tissue repair materials such as stem cells, and the homing of stem cells, leading to the promotion of myocardial regeneration. Thus, copper promotes myocardial regeneration through reactivation of HIF-1-regulated angiogenesis. This would constitute an alternative therapeutic approach to ischemic heart disease. Impact statement Copper promotes angiogenesis, but the mechanistic insights have not been fully elucidated until recently. In addition, the significance of copper promotion of angiogenesis in myocardial regeneration was increasingly revealed. Copper critically participates in the regulation of hypoxia-inducible factor 1 (HIF-1) of angiogenic gene expression. Interestingly, myocardial ischemia causes copper efflux from the heart, leading to suppression of angiogenesis, although HIF-1α, the critical subunit of HIF-1, remains accumulated in the ischemic myocardium. Strategies targeting copper specific delivery to the ischemic myocardium lead to selective activation of HIF-1-regulated angiogenic gene expression. Vascularization of the ischemic myocardium re-establishes the tissue injury microenvironment, and rebuilds the conduit for communication between the tissue injury signals and the remote regenerative responses including stem cells. This process promotes myocardial regeneration. Thus, a simple and effective copper supplementation to the ischemic myocardium would become a novel therapeutic approach to the treatment of patients with ischemic heart diseases.
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Abdrahmanova, A. I., N. B. Amirov, and N. A. Cibulkin. "Application of Perfusion Single Photon Emission Computed Tomography of the Myocardium in Pain-Free Myocardial Ischemia." Russian Archives of Internal Medicine 10, no. 5 (October 9, 2020): 340–47. http://dx.doi.org/10.20514/2226-6704-2020-10-5-340-347.
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This literature review provides data on the use of single-photon emission computed tomography of myocardium in silent myocardial ischemia. The presence of silent myocardial ischemia increases the risk of cardiovascular complications several times and may be the first manifestation of coronary heart disease. Assessing the state of morphofunctional processes in the myocardium is the main goal of diagnostic imaging using singlephoton emission computed tomography of the myocardium. This allows to get three-dimensional image of left ventricle with information about distribution of perfusion volume across myocardium, makes it possible to more accurately differentiate such condition as silent myocardial ischemia. Conducting single-photon emission computed tomography in ECG synchronization mode allows you to visualize the kinetics of the myocardial walls in different phases of the cardiac cycle and thereby simultaneously assess the functional state of the left ventricular myocardium. Indicators of contractile function of the left ventricular myocardium in areas of transient hypoperfusion can be predictors of cardiac events after myocardial infarction and independent predictors of perioperative cardiac events in patients undergoing cardiac surgery. Performing single-photon emission computed tomography in ECG-synchronization mode allows visualizing kinetics of myocardial walls in different phases of cardiac cycle and thereby simultaneously assessing functional state of left ventricle myocardium. In combination with physical exercise and pharmacological tests, it helps to identify coronary stenosis among patients with silent myocardial ischemia. Perfusion single-photon emission computed tomography of myocardium is a necessary tool for stratification and assessment of prognosis of cardiac diseases in asymptomatic patients.
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Leung, Melissa, and Dominic Y. Leung. "Evaluation of Myocardial Viability – Contrast and Stress Echocardiography." Asia Pacific Cardiology 3, no. 1 (2011): 13. http://dx.doi.org/10.15420/apc.2011:3:1:13.
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Viable myocardium are myocardial segments with reduced function that often appear dyssynergic. These dyssynergic myocardial segments are capable of functional recovery, either spontaneously or after the offending insult, usually ischaemia, is removed by revascularisation. Patients with impaired left ventricular function but with viable myocardium are at increased risk of death and adverse cardiovascular outcome. The detection and recognition of viable myocardium is critical for risk stratification, guiding the selection of patients likely to benefit from revascularisation and predicting left ventricular remodelling. Contrast and stress echocardiography are important clinical tools for the assessment of myocardial viability. An end diastolic wall thickness of <0.6cm at the dyssynergic segments generally indicates scarring. The presence of post-systolic thickening at these segments suggests either myocardial viability or ischaemia. Useful in assessing contractile reserve in dyssynergic segments, dobutamine echocardiography is an established tool for detecting myocardial viability with accuracies comparable to other techniques. A biphasic response is diagnostic and specific for hibernating myocardium. The newer techniques of strain and strain rate imaging are the focus of research activities and have been used in conjunction with dobutamine stress to improve overall accuracy. Myocardial contrast echocardiography (MCE) is useful in assessing coronary microvascular integrity, a pre-requisite for myocardial viability. The presence of an intact coronary microvasculature alone is insufficient for myocardial viability, however, explaining the high sensitivity but low specificity of MCE for such purposes. MCE, therefore, with its high negative predictive value, should be used in conjunction with dobutamine stress for the identification of viable myocardium. Due to its availability, safety, relatively low costs and high accuracy, rest and stress echocardiography are indispensable tools in the assessment of myocardial viability.
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Nilsson, S., G. Wikström, A. Ericsson, M. Wikström, A. Øksendal, A. Waldenström, and A. Hemmingsson. "Myocardial Cell Death in Reperfused and Nonreperfused Myocardial Infarctions." Acta Radiologica 37, no. 1P1 (January 1996): 18–26. http://dx.doi.org/10.1177/02841851960371p105.
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Purpose: To investigate whether Dy-DTPA-BMA-enhanced MR imaging would permit identification of myocardial cell death, myocardial infarction was induced in 12 domestic pigs. Material and Methods: In 6 pigs with irreversible cell damage, Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. 70 min after coronary occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Dy-DTPA-BMA after 30 min of reperfusion. In 4 additional pigs, the hearts were reperfused after 2 min of occlusion. All 16 pigs were sacrificed 10 min after the injection of Dy-DTPA-BMA. The hearts were excised and imaged with MR. Results: Reversibly injured myocardium could not be distinguished from adjacent nonischaemic myocardium after the administration of Dy-DTPA-BMA. Reperfused, infarcted myocardium demonstrated a high signal intensity in the proton-density- and T2-weighted sequences, despite a 5-fold higher Dy concentration compared with both nonreperfused infarcted and nonischaemic myocardium. Conclusion: This lack of susceptibility effect in infarcted myocardium, due to a homogeneous distribution of Dy, indicates the usefulness of Dy as a marker of tissue viability.
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Stănescu, Alexandra, Diana Opincariu, Nora Rat, Mirabela Morariu, Sebastian Condrea, Imre Benedek, and Theodora Benedek. "Hybrid Imaging in the Assessment of Myocardial Ischemia and Viability." Journal of Interdisciplinary Medicine 1, no. 3 (December 1, 2016): 242–46. http://dx.doi.org/10.1515/jim-2016-0071.
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Abstract Myocardial ischemia results from a reduction in blood flow as a consequence of a coronary stenosis, which produces ischemia in the myocardial territories irrigated by the stenotic artery. Myocardial viability is a concept that derived from several studies in which it was observed that, even if revascularization occurred, an irreversible left ventricular contractile dysfunction remained. The terms “stunned” and “hibernating” myocardium have been traditionally associated with the viable myocardium, and many controversies still exist on the most appropriate method to assess the presence and extent of viable myocardium. During the last decades, many efforts have been made to identify the best method to determine the viability of the myocardial tissue. Due to the fact that none of the stand-alone imaging methods provide sufficient data about myocardial viability, new methods for the investigation of myocardial viability became necessary. Thus, the concept of hybrid imaging was developed, consisting in the association of different imaging techniques, finally resulting in a single image that offers all the details provided by the two isolated methods of diagnosis, therefore being more precise in regards to the identification of viable myocardium territory. This review aims to appraise the recent studies related to myocardial viability investigated with hybrid imaging.
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Baran, I., B. Ozdemir, S. Gullulu, AA Kaderli, T. Senturk, and A. Aydinlar. "Prognostic Value of Viable Myocardium in Patients with Non-Q-wave and Q-wave Myocardial Infarction." Journal of International Medical Research 33, no. 5 (September 2005): 574–82. http://dx.doi.org/10.1177/147323000503300513.
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This study assessed the amount and prognostic value of myocardial viability in patients with non-Q-wave myocardial infarction (NQMI) and Q-wave myocardial infarction (QMI). A total of 175 patients with MI and an ejection fraction ≤ 45% underwent dobutamine stress echocardiography. On the basis of clinical criteria and myocardial viability, 110 patients were revascularized. The amount of viable myocardium and the clinical outcome were compared in the NQMI and QMI groups. Patients with NQMI exhibited a larger amount of viable myocardium compared with those with QMI. The mortality rate was 6% in patients with NQMI with viable myocardium and subsequent revascularization, 33% in patients with NQMI without viable myocardium or revascularization, 27% in patients with QMI with viable myocardium and subsequent revascularization, and 33% in patients with QMI without viable myocardium or revascularization. In conclusion, our data suggest that patients with NQMI and viable myocardium have the best prognosis after revascularization.
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Jin, Jiyang, Min Chen, Yongjun Li, YaLing Wang, Shijun Zhang, Zhen Wang, Lin Wang, and Shenghong Ju. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (October 1, 2016): 383–91. http://dx.doi.org/10.14503/thij-15-5462.
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We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (<4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.
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Gamperl, A. K., M. M. Vijayan, C. Pereira, and A. P. Farrell. "β-Receptors and stress protein 70 expression in hypoxic myocardium of rainbow trout and chinook salmon." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 2 (February 1, 1998): R428—R436. http://dx.doi.org/10.1152/ajpregu.1998.274.2.r428.
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We examined the in vivo effect of acute hypoxemia on myocardial cell-surface (sarcolemmal) β-adrenoreceptor density (Bmax) and binding affinity ( K D) and on stress protein 70 (sp70) expression by exposing rainbow trout ( Oncorhynchus mykiss; 2.1–2.7 kg) to hypoxic water (3 mg/l O2) at 15°C for 6 h. This degree of hypoxia was the minimum O2 level that these trout could tolerate without losing equilibrium and struggling violently. Hypoxic exposure reduced arterial [Formula: see text]([Formula: see text]) from 98 to 26 mmHg and arterial oxygen content ([Formula: see text]) from 10.8 to 7.4 vol/100 vol, but did not elevate epinephrine and norepinephrine levels above 10 and 30 nM, respectively. Despite the substantial reduction in blood oxygen status, the Bmax and K D of myocardial cell-surface β-adrenoreceptors were unaffected by 6 h of hypoxic exposure. In addition, acute hypoxemia did not increase myocardial sp70 expression. The failure of short-term hypoxia to decrease trout myocardial β-adrenoreceptor density clearly contrasts with the established hypoxia-mediated downregulation shown for mammals. To further investigate the influence of low[Formula: see text] on salmonid myocardial β-adrenoreceptors, binding studies were performed on the spongy (continuously exposed to deoxygenated venous blood) and compact (perfused by oxygenated blood supplied by the coronary artery) myocardia of chinook salmon. The spongy myocardium has adapted to its microenvironment of continuous low[Formula: see text] by having 14% more cell-surface β-adrenoreceptors compared with the compact myocardium. There was no tissue-specific difference in K D and no evidence of sexual dimorphism in Bmax or K D. We conclude from our studies that the salmonid heart is well adapted for sustained performance under hypoxic conditions. We found that wild chinook salmon had 2.8× more cell-surface β-adrenoreceptors compared with hatchery-reared rainbow trout. This difference suggests a significant degree of plasticity exists for fish myocardial β-adrenoreceptors. The signals underlying such differences await further study, but are not likely to include moderate hypoxia and sexual dimorphism.
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Thukkani, Arun K., Bradley D. Martinson, Carolyn J. Albert, George A. Vogler, and David A. Ford. "Neutrophil-mediated accumulation of 2-ClHDA during myocardial infarction: 2-ClHDA-mediated myocardial injury." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H2955—H2964. http://dx.doi.org/10.1152/ajpheart.00834.2004.
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The pathophysiological sequelae of myocardial infarction include neutrophil infiltration into the infarct zone that contributes to additional damage to viable tissue and removal of cellular debris from necrosed tissue. Reactive chlorinating species produced by myeloperoxidase amplify the oxidant capacity of activated neutrophils. Plasmalogens are a major phospholipid subclass of both endothelial cells and cardiac myocytes. Recent studies have shown that plasmalogens are targeted by neutrophil-derived reactive chlorinating species that lead to the production of α-chloro fatty aldehydes. Results herein demonstrate that the α-chloro fatty aldehyde 2-chlorohexadecanal (2-ClHDA) accumulates in rat hearts subjected to left anterior descending coronary artery occlusion. Myocardia from rats subjected to surgical infarction had increased 2-ClHDA and neutrophil infiltration levels compared with myocardia from rats subjected to sham surgery. Additionally, infarcted myocardia from rats rendered neutropenic by treatments with an anti-neutrophil antibody had diminished 2-ClHDA and neutrophil infiltration levels compared with infarcted myocardia from normopenic rats; 2-ClHDA was shown to elicit myocardial damage as determined by lactate dehydrogenase release in isolated perfused rat hearts. Additionally, 2-ClHDA treatment of hearts resulted in decreased heart rate and ventricular performance. Taken together, the present results demonstrate a novel neutrophil-dependent myeloperoxidase-based mechanism that results in 2-ClHDA production in response to regional myocardial infarction that may also contribute to cardiac dysfunction.
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Ushakov, Alexey, Vera Ivanchenko, and Alina Gagarina. "Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling." Current Cardiology Reviews 16, no. 1 (January 28, 2020): 11–24. http://dx.doi.org/10.2174/1573403x15666190509090832.
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The article represents literature review dedicated to molecular and cellular mechanisms underlying clinical manifestations and outcomes of acute myocardial infarction. Extracellular matrix adaptive changes are described in detail as one of the most important factors contributing to healing of damaged myocardium and post-infarction cardiac remodeling. Extracellular matrix is reviewed as dynamic constantly remodeling structure that plays a pivotal role in myocardial repair. The role of matrix metalloproteinases and their tissue inhibitors in fragmentation and degradation of extracellular matrix as well as in myocardium healing is discussed. This review provides current information about fibroblasts activity, the role of growth factors, particularly transforming growth factor β and cardiotrophin-1, colony-stimulating factors, adipokines and gastrointestinal hormones, various matricellular proteins. In conclusion considering the fact that dynamic transformation of extracellular matrix after myocardial ischemic damage plays a pivotal role in myocardial infarction outcomes and prognosis, we suggest a high importance of further investigation of mechanisms underlying extracellular matrix remodeling and cell-matrix interactions in cardiovascular diseases.
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Howard-Quijano, Kimberly, Tatsuo Takamiya, Erica A. Dale, Jasmine Kipke, Yukiko Kubo, Tristan Grogan, Andyshea Afyouni, Kalyanam Shivkumar, and Aman Mahajan. "Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 2 (August 1, 2017): H421—H431. http://dx.doi.org/10.1152/ajpheart.00129.2017.
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Myocardial ischemia creates autonomic nervous system imbalance and can trigger cardiac arrhythmias. We hypothesized that neuromodulation by spinal cord stimulation (SCS) will attenuate local cardiac sympathoexcitation from ischemia-induced increases in afferent signaling, reduce ventricular arrhythmias, and improve myocardial function during acute ischemia. Yorkshire pigs ( n = 20) were randomized to SCS (50 Hz at 200-μs duration, current 90% motor threshold) or sham operation (sham) for 30 min before ischemia. A four-pole SCS lead was placed percutaneously in the epidural space (T1–T4), and a 56-electrode mesh was placed over the heart for high-resolution electrophysiological recordings, including activation recovery intervals (ARIs), activation time, repolarization time, and dispersion of repolarization. Electrophysiological and hemodynamic measures were recorded at baseline, after SCS/sham, during acute ischemia (300-s coronary artery ligation), and throughout reperfusion. SCS 1) reduced sympathoexcitation-induced ARI and repolarization time shortening in the ischemic myocardium; 2) attenuated increases in the dispersion of repolarization; 3) reduced ventricular tachyarrythmias [nonsustained ventricular tachycardias: 24 events (3 sham animals) vs. 1 event (1 SCS animal), P < 0.001]; and 4) improved myocardial function (dP/d t from baseline to ischemia: 1,814 ± 213 to 1,596 ± 282 mmHg/s in sham vs. 1,422 ± 299 to 1,380 ± 299 mmHg/s in SCS, P < 0.01). There was no change in ventricular electrophysiology during baseline conditions without myocardial stress or in the nonischemic myocardium. In conclusion, in a porcine model of acute ventricular ischemia, SCS reduced regional myocardial sympathoexcitation, decreased ventricular arrhythmias, and improved myocardial function. SCS decreased sympathetic nerve activation locally in the ischemic myocardium with no effect observed in the normal myocardium, thus providing mechanistic insights into the antiarrhythmic and myocardial protective effects of SCS. NEW & NOTEWORTHY In a porcine model of ventricular ischemia, spinal cord stimulation decreased sympathetic nerve activation regionally in ischemic myocardium with no effect on normal myocardium, demonstrating that the antiarrhythmic effects of spinal cord stimulation are likely due to attenuation of local sympathoexcitation in the ischemic myocardium and not changes in global myocardial electrophysiology.
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Zhao, Jie, Yi Ouyang, Huanhuan Wang, Huaqing Lai, Shaowei Hu, Liying Tang, Hongjun Yang, and Hongwei Wu. "An Energy Metabolism Study on the Efficacy of Naoxintong Capsules against Myocardial Infarction in a Rat Model." Oxidative Medicine and Cellular Longevity 2022 (July 23, 2022): 1–14. http://dx.doi.org/10.1155/2022/3712500.
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Background. In myocardial ischemia, optimizing the myocardial metabolic phenotype to improve cardiac function is critical. Naoxintong capsules (NXT) are widely prescribed in Chinese medicine for the treatment of cerebrovascular and cardiovascular diseases. Methods. In this study, a rat model of myocardial infarction was established by ligation of the left anterior descending coronary artery. The structure and function of the heart were evaluated using echocardiography. The pathological changes of the rat myocardium and the myocardial volume collagen fraction (CVF) were examined using hematoxylin-eosin (HE) and Masson’s trichrome staining (Masson). The expression of TNF-α and IL-6 were detected by immunohistochemistry. The level of cTnT was also measured to evaluate myocardial injury. In order to study the changes in energy metabolism in myocardial infarction and the effects of NXT, a targeted analysis method for detecting the 29 energy metabolites in cardiac muscle tissue was developed based on UPLC-QQQ-MS. Western blotting was used to detect the expression of proteins related to energy metabolism in myocardia. Results. In the rat model of myocardial infarction, NXT showed obvious effects, such as improving heart function and increasing LVEF and LVFS. HE staining, Masson staining, and immunohistochemical results revealed that NXT decreased inflammatory infiltration, improved myocardial fibrosis, and reduced infarct size. In addition, NXT significantly reduced the level of serum cTnT. The levels of the 29 energy metabolites in cardiac muscle tissue were analyzed using a newly developed targeted analysis method. Compared to the sham group, the levels of 17 metabolites from different energy metabolic pathways, including four compounds in glycolysis metabolism, four compounds in TCA cycle, three compounds in oxidative phosphorylation, four compounds in purine metabolism, and two compounds in glutathione metabolism, displayed obvious changes induced by myocardial ischemia. Expressions of SIRT1, PGC-1α, and ATP5D proteins related to energy metabolism were decreased after myocardial infarction. These perturbations could all be reversed by NXT intervention, suggesting that the therapeutic effects of NXT were partially due to interferences with energy metabolisms. Conclusion. This study provides a useful approach for investigating the mechanism of myocardial infarction and evaluating the efficacy of NXT from energy metabolism.
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Heusch, Gerd, Rainer Schulz, and Shahbudin H. Rahimtoola. "Myocardial hibernation: a delicate balance." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (March 2005): H984—H999. http://dx.doi.org/10.1152/ajpheart.01109.2004.
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The pathophysiology of myocardial hibernation is characterized as a situation of reduced regional contractile function distal to a coronary artery stenosis that recovers after removal of the coronary stenosis. A subacute “downregulation” of contractile function in response to reduced regional myocardial blood flow exists, which normalizes regional energy and substrate metabolism but does not persist for more than 12–24 h. Chronic hibernation develops in response to one or more episodes of myocardial ischemia-reperfusion, possibly progressing from repetitive stunning with normal blood flow to hibernation with reduced blood flow. An upregulation of a protective gene program is seen in hibernating myocardium, putting it into the context of preconditioning. The morphology of hibernating myocardium is characterized by both adaptive and degenerative features.
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Galeone, Antonella, Maria Grano, and Giacomina Brunetti. "Tumor Necrosis Factor Family Members and Myocardial Ischemia-Reperfusion Injury: State of the Art and Therapeutic Implications." International Journal of Molecular Sciences 24, no. 5 (February 27, 2023): 4606. http://dx.doi.org/10.3390/ijms24054606.
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Ischemic heart disease is the principal cause of death worldwide and clinically manifests as myocardial infarction (MI), stable angina, and ischemic cardiomyopathy. Myocardial infarction is defined as an irreversible injury due to severe and prolonged myocardial ischemia inducing myocardial cell death. Revascularization is helpful in reducing loss of contractile myocardium and improving clinical outcome. Reperfusion rescues myocardium from cell death but also induces an additional injury called ischemia-reperfusion injury. Multiple mechanisms are involved in ischemia-reperfusion injury, such as oxidative stress, intracellular calcium overload, apoptosis, necroptosis, pyroptosis, and inflammation. Various members of the tumor necrosis factor family play a key role in myocardial ischemia-reperfusion injury. In this article, the role of TNFα, CD95L/CD95, TRAIL, and the RANK/RANKL/OPG axis in the regulation of myocardial tissue damage is reviewed together with their potential use as a therapeutic target.
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Dean, Andrew Peter, Dom Higgs, Peter Robins, Paul Stobie, Philip Craven, Ciara Daly, and Samantha Carija. "Use of FDG PET scanning to evaluate 5-FU myocardial toxicity as a global metabolic effect rather than vascular spasm." Journal of Clinical Oncology 36, no. 4_suppl (February 1, 2018): 792. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.792.
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792 Background: This is the first ever case series which presents a series of PET images that conclusively demonstrate reversible abnormal myocardial glucose utilisation in 7 patients with normal coronary arteries occurring during 5-FU infusions. Fluoropyrimidine induced myocardial toxicity is estimated to occur in 9% of cases, with some instances proving fatal. Traditionally some hypothesised coronary artery spasm as the mechanism of action behind such events and an animal study suggesting dysfunction of the Krebs cycle, with depletion of high-energy phosphate compounds, was largely ignored. Having observed abnormal myocardial FDG uptake in a patient with chest pain undergoing FDG PET scanning, we prospectively evaluated a further 6 patients presenting with cardiac symptoms whilst receiving infusional 5-FU. Methods: Over an eighteen-month period, 7 patients experienced cardiac like chest pain during 5FU infusion. All were investigated for cardiac ischaemia as per institutional protocol (serial troponin, ECGs and coronary artery imaging), as well as FDG PET scanning to assess FDG uptake in the myocardium. Results: All 7 cases showed reduced FDG uptake throughout the myocardium, with the ventricular blood pool demonstrating a higher affinity for FDG than the myocardium itself. All 7 cases showed normal physiological uptake of FDG in the myocardium on previous and subsequent PET imaging. Imaging of the myocardium and coronary arteries in all cases showed no structural vascular disease. Conclusions: All cases demonstrated a global pattern of reduced FDG myocardial uptake that could not be isolated to a single coronary territory. Angiography or myocardial perfusion scanning demonstrated no significant coronary artery disease, and there were no features consistent with coronary artery spasm found on ECG. This supports the hypothesis that 5FU inhibits physiological myocardial glucose utilisation, thus acting as a direct myocardial toxin. We believe our findings warrant further investigation into the metabolic effects of 5FU on myocardial tissue.
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Rogovskaya, Yuliya, Roman Botalov, Vyacheslav Ryabov, Mariya Rebenkova, Rostislav Karpov, Sergey Popov, and Julia Kzhyshkowska. "Role of Inflammation, Viruses and Tissue Macrophages in the Development of Idiopathic Arrhythmia and Heart Failure." Key Engineering Materials 683 (February 2016): 487–92. http://dx.doi.org/10.4028/www.scientific.net/kem.683.487.
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Endomyocardial biopsy is the gold standard in the diagnosis of myocardial pathology. Intravital study of endomyocardial samples offers the possibility to determine the morphological substrate and etiology of disease, to monitor the effectiveness of treatment. We studied morphological features, viral antigens, macrophages and specifically alternatively activated macrophages in endomyocardial biopsies of 25 patients with idiopathic arrhythmias and heart failure. Immunohistological study was performed to identify type of lymphocytes, macrophages and antigens of cardiotropic viruses. We observed the presence of alternatively activated macrophages in myocardium of patients with myocarditis and without it. We detected the presence of viral antigens in the myocardium of patients with myocardial fibrosis without of histological criteria myocarditis. Small focal infiltration of the myocardial CD68+ macrophages associated with heart failure and ventricular arrhythmias. The presence of virus antigens in myocardium associated with fewer myocardial stabilin-1+ macrophages [negative correlation]. On the other side small focal infiltration of stabilin-1+ macrophages correlated with severity of myocardial interstitial fibrosis [positive correlation]
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Galagudza, M. M., D. L. Sonin, and I. V. Aleksandrov. "Myocardial hibernation: molecular mechanisms, clinical significance and diagnostic methods." Regional blood circulation and microcirculation 18, no. 3 (October 7, 2019): 9–15. http://dx.doi.org/10.24884/1682-6655-2019-18-3-9-15.
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Myocardial hibernation is a persistent inhibition of contractility of the viable myocardium of the left ventricle, resulting from its hypoperfusion. The most important manifestation of hibernation is the preservation of the viability of the myocardial tissue. This phenomenon is based on three main mechanisms: 1) myocardial metabolic adaptation, manifested by enhanced glucose uptake; 2) activation of the cardiomyocyte death gene program; 3) programmed cell death, i. e. autophagy and apoptosis of cardiomyocytes. Methods for diagnosing viable myocardium include dobutamine stress echocardiography, single photon emission computed tomography of the myocardium, positron emission tomography, magnetic resonance imaging and electromechanical mapping. In the clinical aspect, the presence and volume of viable myocardium are taken into account when addressing the issue of revascularization in patients with one- and two-vessel coronary artery disease without involvement of the anterior descending artery, as well as in patients with a significant decrease in the global myocardial contractile function, when surgery can lead to an increase in the left ventricular ejection fraction.
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Evtushenko, A. V., V. V. Evtushenko, A. N. Bykov, V. S. Sergeev, V. I. Syryamkin, Yu V. Kistenev, and Yana Anfinogenova. "Physical Justification of an Increase in the Efficacy of Radiofrequency Systems for Myocardial Ablation." Key Engineering Materials 685 (February 2016): 432–35. http://dx.doi.org/10.4028/www.scientific.net/kem.685.432.
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The article presents data on dependence of the myocardial electrical impedance on the temperature. These data have high clinical relevance because radio frequency energy-induced destruction of the myocardium in the course of surgical treatment of cardiac arrhythmias should be performed transmurally. Insufficient transmural myocardial damage results in recurrence of cardiac arrhythmias. Therefore, achieving transmural treatments of the myocardium is of high significance.Studies were performed by using 20 isolated hearts. To evaluate the effectiveness of radio frequency exposure, we studied two temperature settings: myocardial normothermia (36.6 °C) and myocardial hypothermia (20 °C). The depth of destruction as well as the temperatures of the epicardial, endocardial, and intramural myocardium at the points of impact were estimated. Data showed that lower temperature decreases tissue electrical impedance and results in a greater depth of damage.
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Dean, Andrew Peter, Domenic Higgs, Peter Robins, Paul Stobie, Philip Craven, Ciara Daly, and Samantha Carija. "Fluoropyrimidine-associated myocardial toxicity as a global metabolic effect compared to vascular spasm and visibility on FDG PET scanning." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e14013-e14013. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e14013.
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e14013 Background: Myocardial toxicity from fluoropyrimidines is a rare but potentially serious side effect, estimated by some as occurring in up to 9%. Coronary spasm has been suggested as the underlying mechanism, despite a lack of supporting evidence and other toxicity mechanisms have been proposed. Matsubara described Krebs cycle dysfunction in the presence of 5FU with depletion of high energy phosphate compounds in rodent myocardial tissue with ECG changes. Following a chance discovery of abnormal myocardial FDG uptake on a PET scan shortly after presenting with presumed 5FU cardiac toxicity (angina, ST elevation, troponin rise; normal coronary vessels on imaging), we prospectively evaluated all instances of angina occurring during 5FU infusion with coronary artery imaging and FDG PET scan. Methods: We identified 5 patients who experienced angina during 5FU therapy. They were investigated for coronary ischaemia and also underwent PET scanning to assess myocardial FDG uptake. Data was collected from patient records, and subsequent cardiac investigations. Results: In all 5 cases, PET scan demonstrated markedly abnormal FDG uptake throughout the myocardium, with the ventricular blood pool demonstrating more FDG activity than myocardium. No significant underlying coronary artery disease was identified. All 5 patients had previous PET scans with normal myocardial FDG uptake. Conclusions: We identified a consistent pattern of abnormal FDG uptake throughout the myocardium for all scanned patients with chest pain following administration of 5FU. This was not restricted to a single arterial territory. There were no typical ECG changes of spasm. Obstructive coronary disease was excluded with angiographic imaging or myocardial perfusion scanning. The FDG PET scans suggest global myocardial metabolic change, supporting the notion of 5FU being a direct myocardial toxin inhibiting myocardial glucose utilization. The myocardium may then be dependent on fatty acid metabolism, posing additional risk to patients on low fat diets. Our data provides new insight into the mechanism of 5-FU myocardial toxicity and further prospective assessment using PET is warranted.
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Perko, Mario J., and Henning Bay-Nielsen. "Regional Myocardial Oxygenation during Surgical Revascularisation." Cardiovascular Surgery 10, no. 6 (December 2002): 590–94. http://dx.doi.org/10.1177/096721090201000613.
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The aim of the study was to assess changes in myocardial oxygenation in patients with ischaemic heart disease during surgical revascularisation. In 20 patients, regional oxygen saturation, oxyhaemoglobin and total haemoglobin concentrations were examined by near-infrared spectroscopy in the myocardium and in a non-ischaemic skeletal muscle, which served as a control. Pre-revascularisation values of all spectroscopy parameters were 40–50% lower in the myocardium than in the control. After successful revascularisation 02 saturation, oxy-, and total haemoglobin in the myocardium increased by 20, 29. and 18%, respectively (P<0.01). A negative correlation was found between aorta cross-clamping time and the post-operative increase in the myocardial 02 saturation. In the control muscle and in a patient with incomplete revascularisation the regional 02 saturation decreased. This preliminary report indicates potential value of the near infrared spectroscopy in an immediate assessment of postoperative changes in myocardial perfusion and oxygenation.
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Turler, Mark, and Shel Thoma. "Dopamine signaling attenuated myocardial injury during endotoxemia." American Journal of BioMedicine 6, no. 1 (February 14, 2018): 33–43. http://dx.doi.org/10.18081/2333-5106/018-19-29.
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Myocardial depression is a well-recognized manifestation of organ dysfunction in sepsis, the direct protective effect of Dopamine on myocardial is still not clear. Here, we aimed to study whether Dopamine can directly protect myocardial from endotoxemia. To test that, we used adult C57/BL6 mice were treated with endotoxin (0.5 mg/kg, iv). Clozapine was administered as D2 antagonist, (intraperitoneal administration shortly before the model of sepsis). Electron microscopy, TUNEL staining, caspase-3 expression, and the Bcl-2/Bax ratio were used to measure myocardial apoptosis. Left ventricle (LV) function was assessed using a microcatheter system. Chemokines and cytokines in plasma and myocardium were analyzed by enzyme-linked immunosorbent assay (ELISA). Mononuclear cells in the myocardium were examined using immunofluorescence staining. In conclusion, our results for the first time showed the role of Dopamine to directly protect myocardial from endotoxemia through attenuated proinflammatory cytokines and partly through inhibiting apoptosis.
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JEGATHESE, REGINALD C., EDDIE Y. K. NG, and DHANJOO N. GHISTA. "ANALYSIS OF LEFT VENTRICULAR MYOCARDIAL PROPERTIES." Journal of Mechanics in Medicine and Biology 04, no. 02 (June 2004): 173–85. http://dx.doi.org/10.1142/s0219519404000953.
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This work centers around the analysis and quantification of myocardial perfusion, in which the cardiac parameters have been identified to quantify Myocardial Perfusion Index (MPI). The fundamental poroelastic behaviour has been analysed within the physiological range of cardiac parameters. An in-depth investigation of the myocardium behaviour is essential, and two factors that are desirable but complicate the analysis are: the myocardial structure element (fibrous soft tissue), undergoes cyclic deformation during each cardiac cycle and the myocardial fluid component (blood), undergoes variable rate of perfusion through the myocardial soft tissue.
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Prasad, M. Renuka, Ronald Clement, Hajime Otani, Randall Jones, Dipak K. Das, Richard M. Engelman, Robert H. Breyer, and John A. Rousou. "Improved myocardial performance induced by dofibrate during reperfusion after acute myocardial infarction." Canadian Journal of Physiology and Pharmacology 66, no. 12 (December 1, 1988): 1518–23. http://dx.doi.org/10.1139/y88-248.
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The increase of cellular fatty acids appears to be one of the causes of the myocardial injury during ischemia and reperfusion. This study was designed to examine whether a hypolipidemic drug such as clofibrate can reduce the myocardial injury during ischemia and reperfusion. Clofibrate was fed to experimental pigs for 9 days. Isolated in situ hearts from both experimental and control pigs were subjected to 60 min of regional ischemia induced by occluding the left anterior descending coronary artery, followed by 60 min of global ischemia by hypothermic cardioplegic arrest and 60 min of reperfusion. The clofibrate feeding resulted in the better cardiac performance as judged by increased coronary blood flow, improved left ventricular function, and reduced myocardial injury as judged by creatine kinase release. Although the clofibrate-fed animals contained higher levels of thiobarbituric reactive materials, the free fatty acid levels of plasma and myocardium were much lower compared with control animals. The clofibrate feeding was also associated with increased peroxisomal catalase and (β-oxidation of fatty acids. These results suggest that decreased levels of free fatty acids in the plasma and the myocardium and increased catalase activity induced by antilipolytic therapy appear to provide beneficial effects to the myocardium during ischemia and reperfusion.
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Chen, Harn-Shen, Jia Jia, Hou-Fen Su, Hong-Da Lin, Jaw-Wen Chen, Shing-Jong Lin, Jia-Ying Yang, Hui-Chin Lai, Ruben Mestril, and Ping H. Wang. "Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency." Journal of Endocrinology 190, no. 2 (August 2006): 433–40. http://dx.doi.org/10.1677/joe.1.06692.
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The 70 kDa heat shock protein family plays important cardiac protective roles against myocardial injuries. Reduced myocardial protection is a common feature of diabetic myocardium. This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle. In the diabetic myocardium, the abundance of Hsc70 was significantly reduced. The abundance of Hsp70 was low in cardiac muscle and was not induced in the diabetic myocardium. Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells. In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70. Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70. These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency. Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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Herzog, C. A., X. Z. Dai, and R. J. Bache. "Effect of alpha 1-adrenergic blockade on myocardial blood flow during exercise after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 2 (August 1, 1991): H280—H286. http://dx.doi.org/10.1152/ajpheart.1991.261.2.h280.
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The effect of alpha 1-adrenergic blockade with prazosin on myocardial blood flow at rest and during two levels of treadmill exercise was assessed in 16 chronically instrumented dogs 9-14 days after myocardial infarction had been produced by occlusion of the left circumflex coronary artery. During resting conditions prazosin did not alter mean myocardial blood flow or the subendocardial-to-subepicardial flow ratio in either normally perfused or collateral-dependent myocardium. However, during exercise at comparable external work loads and comparable rate-pressure products, prazosin significantly increased blood flow to normally perfused (27% increase at the second level of exercise, P less than 0.001) and collateral-dependent myocardium (35% increase at the second level of exercise, P less than 0.001) compared with control. In addition, prazosin caused a small but significant decrease in the subendocardial-to-subepicardial flow ratio in both normal (1.27 +/- 0.04 to 1.19 +/- 0.04; P less than 0.01) and collateral-dependent myocardium (0.57 +/- 0.11 to 0.52 +/- 0.11; P less than 0.01) compared with control, reflecting a disproportionally greater increase in subepicardial flow in response to alpha 1-adrenergic blockade. These data demonstrate that alpha 1-adrenergic vasoconstriction inhibits coronary vasodilation during exercise, even in areas of collateral-dependent myocardium relatively early after coronary artery occlusion.
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Dzhyhaliuk, O. V., D. A. Lysenko, D. G. Smolko, I. M. Kyrychenko, and S. V. Prokopenko. "Morphological changes in the conditions of adrenaline myocardial dystrophy against the background of the introduction of the compound PC-66 and amiodarone to rats." Reports of Morphology 26, no. 1 (May 22, 2020): 48–53. http://dx.doi.org/10.31393/morphology-journal-2020-26(1)-07.
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Adrenaline damage to the myocardium is an important element in the pathogenesis of myocardial infarction in humans. Despite the use of modern methods of treatment of myocardial infarction, the issue of cardioprotection of reperfusion myocardial damage remains open. Promising in this direction is the use of quinazolone derivatives, which have already shown cardioprotective properties in other models of myocardial infarction. The aim of the study was to establish morphological changes in the conditions of adrenaline myocardiodystrophy (AMD) against the background of the introduction of the compound PC-66 and amiodarone in rats. The study was performed on 100 nonlinear rats of both sexes weighing 165-220 g, divided into four groups of 25 animals each: 1 – intact rats; 2 – rats with a model of adrenaline myocardial infarction without treatment (control); 3 – rats with AMD treated with amiodarone (10 mg/kg, intraperitoneally); 4 – rats with AMD treated with compound PC-66 (10 mg/kg, intraperitoneally). It was found that control rats under conditions of cardiotoxic dose of adrenaline in the left ventricular myocardium for up to 8 days of the experiment does not fully restore the myocardial structure, dystrophic and necrobiotic changes were found in both cardiomyocytes and walls of vessels of a blood microcirculatory channel of a myocardium. Course intraperitoneal administration to rats of the compound PC-66 in the conditions of adrenaline myocardial infarction as well as amiodarone, contributes to the attenuation of signs of dystrophic and destructive processes. The degree of protective effect on the myocardium under conditions of cardiotoxic dose of adrenaline compound PC-66 was not lower to the reference drug – amiodarone. Thus, it is morphologically confirmed that in adrenaline myocardial infarction the compound PC-66, similar to the action of amiodarone, has a cardioprotective effect.
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Fan, Yi, Yiwei Cheng, Yafei Li, Bingrui Chen, Zimu Wang, Tianwen Wei, Hao Zhang, et al. "Phosphoproteomic Analysis of Neonatal Regenerative Myocardium Revealed Important Roles of Checkpoint Kinase 1 via Activating Mammalian Target of Rapamycin C1/Ribosomal Protein S6 Kinase b-1 Pathway." Circulation 141, no. 19 (May 12, 2020): 1554–69. http://dx.doi.org/10.1161/circulationaha.119.040747.
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Background: In mammals, regenerative therapy after myocardial infarction is hampered by the limited regenerative capacity of adult heart, whereas a transient regenerative capacity is maintained in the neonatal heart. Systemic phosphorylation signaling analysis on ischemic neonatal myocardium might be helpful to identify key pathways involved in heart regeneration. Our aim was to define the kinase-substrate network in ischemic neonatal myocardium and to identify key pathways involved in heart regeneration after ischemic insult. Methods: Quantitative phosphoproteomics profiling was performed on infarct border zone of neonatal myocardium, and kinase-substrate network analysis revealed 11 kinases with enriched substrates and upregulated phosphorylation levels, including checkpoint kinase 1 (CHK1) kinase. The effect of CHK1 on cardiac regeneration was tested on Institute of Cancer Research CD1 neonatal and adult mice that underwent apical resection or myocardial infarction. Results: In vitro, CHK1 overexpression promoted whereas CHK1 knockdown blunted cardiomyocyte proliferation. In vivo, inhibition of CHK1 hindered myocardial regeneration on resection border zone in neonatal mice. In adult myocardial infarction mice, CHK1 overexpression on infarct border zone upregulated mammalian target of rapamycin C1/ribosomal protein S6 kinase b-1 pathway, promoted cardiomyocyte proliferation, and improved cardiac function. Inhibiting mammalian target of rapamycin activity by rapamycin blunted the neonatal cardiomyocyte proliferation induced by CHK1 overexpression in vitro. Conclusions: Our study indicates that phosphoproteome of neonatal regenerative myocardium could help identify important signaling pathways involved in myocardial regeneration. CHK1 is found to be a key signaling responsible for neonatal regeneration. Myocardial overexpression of CHK1 could improve cardiac regeneration in adult hearts by activating the mammalian target of rapamycin C1/ribosomal protein S6 kinase b-1 pathway. Thus, CHK1 might serve as a potential novel target in myocardial repair after myocardial infarction.
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Shames, Brian D., Daniel R. Meldrum, Craig H. Selzman, Edward J. Pulido, Brian S. Cain, Anirban Banerjee, Alden H. Harken, and Xianzhong Meng. "Increased levels of myocardial IκB-α protein promote tolerance to endotoxin." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 3 (September 1, 1998): H1084—H1091. http://dx.doi.org/10.1152/ajpheart.1998.275.3.h1084.
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Endotoxin [lipopolysaccharide (LPS)] causes tumor necrosis factor-α (TNF-α)-mediated myocardial contractile depression. Tolerance to the cardiac toxicity of LPS can be induced by a prior exposure to LPS or by pretreatment with glucocorticoids. The mechanisms by which the myocardium acquires tolerance to LPS remain unknown. LPS causes phosphorylation and degradation of inhibitory κB-α (IκB-α), releasing nuclear factor-κB (NF-κB) to activate TNF-α gene transcription. We hypothesized that LPS induces supranormal synthesis of myocardial IκB-α protein and thus renders the myocardium tolerant to subsequent LPS. Rats were challenged with LPS after pretreatment with LPS, dexamethasone, or saline. In saline-pretreated rats, LPS caused a rapid decrease in myocardial IκB-α protein levels, activation of NF-κB, and increased TNF-α production. These events were followed by myocardial contractile depression. After the initial decrease in myocardial IκB-α, IκB-α protein levels rebounded to a level greater than control levels by 24 h. Dexamethasone pretreatment similarly increased myocardial IκB-α protein levels. In rats pretreated with either LPS or dexamethasone, myocardial IκB-α protein levels remained similar to control levels after LPS challenge. The preserved level of myocardial IκB-α protein was associated with diminished NF-κB activation, attenuated myocardial TNF-α production, and improved cardiac contractility. We conclude that LPS and dexamethasone upregulate myocardial IκB-α protein expression and that an increased level of myocardial IκB-α protein may promote cardiac tolerance to LPS by inhibition of NF-κB intranuclear translocation and myocardial TNF-α production.
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Micic, Jelena, Slobodan Nikolic, and Slobodan Savic. "Myocardial bridge and proximal complicated atherosclerosis of descending branch of left coronary artery as a cause of sudden cardiac death - case report." Srpski arhiv za celokupno lekarstvo 131, no. 3-4 (2003): 173–75. http://dx.doi.org/10.2298/sarh0304173m.
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When coronary artery, which is located subepicardially, submerges into myocardium and then, after a short intramural course, again appears subepicardially, it is called embedded coronary, while a part of myocardium above - a myocardial bridge. Muscular bridges are usually small and have no clinical significance. In the proximal part of coronary artery, preceding a myocardial bridge, there occurs a disturbance of blood course and myocardial perfusion, turbulence, collecting of lipids and mucopolysaccharides, lesion of elastica, which all leads to atheromatous lesions of intima of the arterial proximal part and to the resultant complications of atheroma. Degenerative changes of myocardium and its blood vessels, and in connection with it myocardial vulnerability, could be a consequence of this congenital arterial variation. We report a case of a 40-year-old male, without medical data about previous diseases, who died suddenly and unexpectedly in his apartment. The autopsy and microscopical examination revealed an acute ischemic lesion, myocardial bridge in the middle part of the left coronary artery descending branch and the complicated atherosclerotic plaque proximally of this bridge.
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HASENFUSS, G. "Myocardial energetics in failing human myocardium." Journal of Molecular and Cellular Cardiology 23 (July 1991): S102. http://dx.doi.org/10.1016/0022-2828(91)90819-8.
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Yermola, Yu A., A. A. Galyshevskaya, A. A. Davydova, A. A. Beketov, T. P. Makalish, and M. A. Kriventsov. "Myocardial lesions in patients with COVID-19. Autopsy case series." CLINICAL AND EXPERIMENTAL MORPHOLOGY 11, no. 4 (2022): 59–69. http://dx.doi.org/10.31088/cem2022.11.4.59-69.
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Introduction. Morphological data on SARS-CoV-2-associated heart damage and its mechanisms are rather limited. However, clinical and morphological features of myocardial lesions in COVID-19 patients have been described and include myocardial ischemia, acute coronary syndrome, and acute myocarditis. The prevailing features of myocardial lesions and their consequences are still controversial. The aim of our research was to evaluate the morphological features of myocardial lesions in patients with severe COVID-19, using routine histological examination and immunohistochemistry (CD45) to confirm myocardial inflam-matory infiltration. Materials and methods. We analyzed samples of the left ventricular myocardium obtained during autopsy examination of 48 patients with severe COVID-19 who died from SARS-CoV-2-associated pneumonia. We used histological description and immunohistochemical methods. Results. The results revealed several histopathological features of COVID-19-associated myocardial lesions, including acute ischemia (25% of cases) and mild inflammatory changes termed borderline myocarditis (18.75% of cases). Other significant findings in the myocardium included microcirculatory vessel thrombosis. Conclusion. The study confirms the existing data on damage to myocardium in severe COVID-19. However, further studies are warranted. It may contribute to the development of new management strategies for severe COVID-19 patients. Keywords: SARS-CoV-2, heart, ischemia, myocarditis
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Lao, Qun, Wenping Xia, Jing Jin, Yuzhu Jia, and Jianju Feng. "Modified Look-Locker Inverse-Recovery (MOLLI) Sequence of Quantitative Imaging in Dirty Magnetic Resonance Longitudinal Relaxation Time Diagnostic Value of GE Combined with Longitudinal Relaxation Time Quantitative Imaging for Myocardial Amyloidosis." Journal of Healthcare Engineering 2021 (October 19, 2021): 1–12. http://dx.doi.org/10.1155/2021/2800891.
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The pathological changes of myocarditis include degeneration and necrosis of myocardial cells and infiltration of inflammatory cells in the myocardial interstitium, accompanied by obvious myocardial fibrosis. Myocardial fibrosis is a determinant of ventricular remodeling and an important indicator of the classification of clinical risk factors and has an important value in evaluating the prognosis of heart disease. Cardiac magnetic resonance (CMR) is the “gold standard” for evaluating the shape and function of the heart, and it can show the characteristic pathological changes of myocardial tissue. The traditional gadolinium imaging agent delays the enhanced sequence images to visually show the extent of the affected myocardial fibrosis, but it cannot effectively identify small focal fibrosis or widespread diffuse fibrosis. The CMR longitudinal relaxation time quantitative technique can directly measure the relaxation time (T1) determined by the myocardial tissue and does not depend on the signal strength of the reference tissue and can quantitatively analyze the affected myocardium. In this study, the initial and enhanced quantitative imaging techniques of CMR were used to measure the magnetic value of the myocardium in patients with myocarditis, to explore the diagnostic value of myocardial fibrosis, and to analyze the correlation between cardiac fibrosis and cardiac function.
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Spath, Nick B., Trisha Singh, Giorgos Papanastasiou, Andrew Baker, Rob J. Janiczek, Gerry P. McCann, Marc R. Dweck, Lucy Kershaw, David E. Newby, and Scott Semple. "Assessment of stunned and viable myocardium using manganese-enhanced MRI." Open Heart 8, no. 1 (June 2021): e001646. http://dx.doi.org/10.1136/openhrt-2021-001646.
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ObjectiveIn a proof-of-concept study, to quantify myocardial viability in patients with acute myocardial infarction using manganese-enhanced MRI (MEMRI), a measure of intracellular calcium handling.MethodsHealthy volunteers (n=20) and patients with ST-elevation myocardial infarction (n=20) underwent late gadolinium enhancement (LGE) using gadobutrol and MEMRI using manganese dipyridoxyl diphosphate. Patients were scanned ≤7 days after reperfusion and rescanned after 3 months. Differential manganese uptake was described using a two-compartment model.ResultsAfter manganese administration, healthy control and remote non-infarcted myocardium showed a sustained 25% reduction in T1 values (mean reductions, 288±34 and 281±12 ms). Infarcted myocardium demonstrated less T1 shortening than healthy control or remote myocardium (1157±74 vs 859±36 and 835±28 ms; both p<0.0001) with intermediate T1 values (1007±31 ms) in peri-infarct regions. Compared with LGE, MEMRI was more sensitive in detecting dysfunctional myocardium (dysfunctional fraction 40.5±11.9 vs 34.9%±13.9%; p=0.02) and tracked more closely with abnormal wall motion (r2=0.72 vs 0.55; p<0.0001). Kinetic modelling showed reduced myocardial manganese influx between remote, peri-infarct and infarct regions, enabling absolute discrimination of infarcted myocardium. After 3 months, manganese uptake increased in peri-infarct regions (16.5±3.5 vs 22.8±3.5 mL/100 g/min, p<0.0001), but not the remote (23.3±2.8 vs 23.0±3.2 mL/100 g/min, p=0.8) or infarcted (11.5±3.7 vs 14.0±1.2 mL/100 g/min, p>0.1) myocardium.ConclusionsThrough visualisation of intracellular calcium handling, MEMRI accurately differentiates infarcted, stunned and viable myocardium, and correlates with myocardial dysfunction better than LGE. MEMRI holds major promise in directly assessing myocardial viability, function and calcium handling across a range of cardiac diseases.Trial registration numbersNCT03607669; EudraCT number 2016-003782-25.
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Abel, F. L. "Myocardial function in sepsis and endotoxin shock." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 6 (December 1, 1989): R1265—R1281. http://dx.doi.org/10.1152/ajpregu.1989.257.6.r1265.
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Myocardial function in sepsis and endotoxin shock is reviewed. Clinical, whole animal, and isolated tissue studies are compared to answer the question whether sepsis and/or endotoxin directly damage the myocardium. Myocardial performance is considered relative to control of preload, afterload, and heart rate. Despite the fact that these vary widely in different studies, there is overwhelming evidence that myocardial performance is depressed in both sepsis and endotoxin shock. The depression is dose related, occurs early after large doses of endotoxin but may follow a hyperdynamic phase in sepsis or after low doses of endotoxin. Endotoxin itself does not appear to be the depressant factor; the final depressant substance(s) is unknown. Calcium transport by the sarcoplasmic reticulum is depressed. This defect is more prominent in the endocardium than in the epicardium. Myocardial adenosinetriphosphatase (ATPase) and norepinephrine stores may be depleted. The septic myocardium has an increased dependence on sympathetic nerve stimulation. There is little evidence that the cause of the myocardial depression is an inadequate coronary blood flow.
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Baskurt, O. K., M. Edremitlioglu, and A. Temiz. "Effect of erythrocyte deformability on myocardial hematocrit gradient." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 1 (January 1, 1995): H260—H264. http://dx.doi.org/10.1152/ajpheart.1995.268.1.h260.
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Myocardial hematocrit gradient was determined between epicardium and endocardium of the left ventricular wall in rat heart under the influence of erythrocyte deformability alterations. Hematocrit determinations were performed by measuring two different radionuclides labeling plasma (125I-labeled albumin) and erythrocytes (99mTc) in 100-microns-thick left ventricular myocardium slices. Myocardial hematocrit gradient calculated after exchange transfusions with partially hardened red blood cell suspensions was compared with the results of the control group, in which the exchange transfusions were done using normal, hematocrit-matched blood. In the control group, the hematocrit value in the myocardium adjacent to epicardium was 0.331 +/- 0.076 l/l and decreased to 0.232 +/- 0.054 l/l near the endocardium. Myocardial hematocrit between these two was represented by a linear gradient. In the group with impaired erythrocyte deformability, the hematocrit value was 0.359 +/- 0.074 l/l in the epicardial myocardium and remained at 0.341 +/- 0.082 l/l in the endocardial layer. These results indicate that tissue hematocrit gradient in the left ventricular myocardium may be disturbed if erythrocyte deformability is altered.
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Rustamova, Ya K. "Actual Problems of Diagnostics of Viable Myocardium." Kardiologiia 59, no. 2 (March 8, 2019): 68–78. http://dx.doi.org/10.18087/cardio.2019.2.10243.
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The article presents modern analysis of the studies and reflects the key problems concerning the feasibility of performing cardiac MRI for assessment of myocardial viability in patients with history of myocardial infarction (with postinfarction cardiosclerosis), as well as the effectiveness of the method for predicting restoration of the function of hibernating myocardium after myocardial revascularization.
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Xia, Rui, Bo Zhao, Yang Wu, Jia-Bao Hou, Li Zhang, Jin-Jin Xu, and Zhong-Yuan Xia. "Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats." Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/767930.
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Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P<0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P<0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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Kadokami, Toshiaki, Charles F. McTiernan, Toru Kubota, Carole S. Frye, George S. Bounoutas, Paul D. Robbins, Simon C. Watkins, and Arthur M. Feldman. "Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (May 1, 2001): H2281—H2291. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2281.
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Tumor necrosis factor (TNF)-α plays a key role in the pathogenesis of septic shock syndrome, and myocardial TNF-α expression may contribute to this pathophysiology. We examined the myocardial expression of TNF-α-related cytokines and chemokines in mice exposed to lipopolysaccharide (LPS) and tested the effects of anti-TNF therapy on myocardial cytokine expression. Cytokine mRNA levels were measured by RNase protection assay, and protein levels in the plasma and myocardium were assessed by enzyme-linked immunosorbent assays. LPS (4 μg/g body wt ip) induced marked cytokine expression, including TNF-α, interleukin (IL)-1β, IL-6, and monocyte chemotactic protein (MCP)-1, in both the plasma and myocardium. Pretreatment with adenovirus-mediated TNF receptor fusion protein (AdTNFR1; 109plaque-forming units iv) decreased plasma cytokine levels. In contrast, whereas myocardial IL-1β expression was also suppressed, expression of IL-6 and MCP-1 was not inhibited by AdTNFR1. In summary, anti-TNF treatment differentially altered the cytokine expression in the plasma and myocardium during endotoxemia. Inability to block myocardial expression of IL-6 and MCP-1 suggests a possible mechanism for the failure of anti-TNF therapies in the treatment of endotoxin shock.
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Pulido, María, María Ángeles de Pedro, Verónica Álvarez, Ana María Marchena, Virginia Blanco-Blázquez, Claudia Báez-Díaz, Verónica Crisóstomo, Javier G. Casado, Francisco Miguel Sánchez-Margallo, and Esther López. "Transcriptome Profile Reveals Differences between Remote and Ischemic Myocardium after Acute Myocardial Infarction in a Swine Model." Biology 12, no. 3 (February 21, 2023): 340. http://dx.doi.org/10.3390/biology12030340.
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Acute myocardial infarction (AMI) is the consequence of an acute interruption of myocardial blood flow delimiting an area with ischemic necrosis. The loss of cardiomyocytes initiates cardiac remodeling in the myocardium, leading to molecular changes in an attempt to recover myocardial function. The purpose of this study was to unravel the differences in the molecular profile between ischemic and remote myocardium after AMI in an experimental model. To mimic human myocardial infarction, healthy pigs were subjected to occlusion of the mid-left anterior descending coronary artery, and myocardial tissue was collected from ischemic and remote zones for omics techniques. Comparative transcriptome analysis of both areas was accurately validated by proteomic analysis, resulting in mitochondrion-related biological processes being the most impaired mechanisms in the infarcted area. Moreover, Immune system process-related genes were up-regulated in the remote tissue, mainly due to the increase of neutrophil migration in this area. These results provide valuable information regarding differentially expressed genes and their biological functions between ischemic and remote myocardium after AMI, which could be useful for establishing therapeutic targets for the development of new treatments.
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Chen, Chih-Hung, Shu-Yuan Hsu, Chien-Chih Chiu, and Steve Leu. "MicroRNA-21 Mediates the Protective Effect of Cardiomyocyte-Derived Conditioned Medium on Ameliorating Myocardial Infarction in Rats." Cells 8, no. 8 (August 19, 2019): 935. http://dx.doi.org/10.3390/cells8080935.
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Conditioned medium derived from ischemic myocardium improves rodent cardiac function after myocardial infarction. Exosomal miRNA-mediated intercellular communication is considered to mediate the protective effect of conditioned medium against ischemic injury. Oxygen–glucose-deprivation (OGD)-treated cardiac cells and a rat model with acute myocardial infarction (AMI) were applied. The expression profiles of myocardial-disease-associated miRNAs in cardiomyocytes, cardiac fibroblasts, ventricular myocardium, and conditioned medium derived from cardiomyocytes under ischemic stresses were analyzed. Primary cultured cell model and a rat model with myocardial infarction were applied to examine the role of miRNA in regulating cardiomyocyte apoptosis, fibroblast activation, immune cell infiltration, and myocardial infarction. Results showed that expression levels of miR-21 in cardiomyocytes, cardiac fibroblasts, and conditioned medium (CM) derived from cardiomyocytes were up-regulated with OGD treatment. With the depletion of miR-21, the protective effect of CM on cardiomyocytes against oxidative stress, enhanced fibroblast activation, and promotion of angiogenesis in endothelial cells were reduced. Administration of CM reduced the infarcted size and immune cell infiltration in myocardium of rats with AMI, while depletion of miR-21 reduced the effect of CM. In conclusion, miR-21 plays a role in intercellular communication among ischemic cardiac cells. The expression of miR-21 is important for the protective effect of conditioned medium against myocardial infarction.
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Hiesinger, William, Sergei A. Vinogradov, Pavan Atluri, J. Raymond Fitzpatrick, John R. Frederick, Rebecca D. Levit, Ryan C. McCormick, et al. "Oxygen-dependent quenching of phosphorescence used to characterize improved myocardial oxygenation resulting from vasculogenic cytokine therapy." Journal of Applied Physiology 110, no. 5 (May 2011): 1460–65. http://dx.doi.org/10.1152/japplphysiol.01138.2010.
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This study evaluates a therapy for infarct modulation and acute myocardial rescue and utilizes a novel technique to measure local myocardial oxygenation in vivo. Bone marrow-derived endothelial progenitor cells (EPCs) were targeted to the heart with peri-infarct intramyocardial injection of the potent EPC chemokine stromal cell-derived factor 1α (SDF). Myocardial oxygen pressure was assessed using a noninvasive, real-time optical technique for measuring oxygen pressures within microvasculature based on the oxygen-dependent quenching of the phosphorescence of Oxyphor G3. Myocardial infarction was induced in male Wistar rats ( n = 15) through left anterior descending coronary artery ligation. At the time of infarction, animals were randomized into two groups: saline control ( n = 8) and treatment with SDF ( n = 7). After 48 h, the animals underwent repeat thoracotomy and 20 μl of the phosphor Oxyphor G3 was injected into three areas (peri-infarct myocardium, myocardial scar, and remote left hindlimb muscle). Measurements of the oxygen distribution within the tissue were then made in vivo by applying the end of a light guide to the beating heart. Compared with controls, animals in the SDF group exhibited a significantly decreased percentage of hypoxic (defined as oxygen pressure ≤ 15.0 Torr) peri-infarct myocardium (9.7 ± 6.7% vs. 21.8 ± 11.9%, P = 0.017). The peak oxygen pressures in the peri-infarct region of the animals in the SDF group were significantly higher than the saline controls (39.5 ± 36.7 vs. 9.2 ± 8.6 Torr, P = 0.02). This strategy for targeting EPCs to vulnerable peri-infarct myocardium via the potent chemokine SDF-1α significantly decreased the degree of hypoxia in peri-infarct myocardium as measured in vivo by phosphorescence quenching. This effect could potentially mitigate the vicious cycle of myocyte death, myocardial fibrosis, progressive ventricular dilatation, and eventual heart failure seen after acute myocardial infarction.
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Huelnhagen, Till, Bert Flemming, Erdmann Seeliger, Jeanette Schulz-Menger, and Thoralf Niendorf. "Myocardial T2* mapping at ultrahigh magnetic fields: in vivo myocardial tissue characteri-zation and assessment of cardiac physiology with magnetic resonance imaging." Current Directions in Biomedical Engineering 3, no. 2 (September 7, 2017): 433–36. http://dx.doi.org/10.1515/cdbme-2017-0091.
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AbstractMapping the effective transverse relaxation time T2* represents an emerging MRI tool for non-invasive myocardial tissue characterization and holds the promise to provide means for assessing myocardial (patho)physiology in vivo. This work takes advantage of the linear increase of susceptibility effects with magnetic field strength which renders it appealing to perform T2* mapping at ultrahigh magnetic fields and enables temporally resolved T2* mapping. Recognizing this potential this study examines the applicability of myocardial CINE T2* mapping in healthy volunteers and hypertrophic cardiomyopathy (HCM) patients at 7.0 Tesla and investigates its capability to distinguish between healthy myocardium and myocardium affected by HCM.