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Journal articles on the topic 'Myocardial'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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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 (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 myocar

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2

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 prospecti

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3

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 (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 cardio

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4

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 (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 myoca

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Bhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth та Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development". Journal of Cardiovascular Development and Disease 8, № 3 (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 cro

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6

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 (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). Afte

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7

Brown, TA. "Hibernating myocardium." American Journal of Critical Care 10, no. 2 (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 presenc

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Li, Hongyu, Jimiao Qiu, Chang Liu, et al. "MicroRNA-221 protects myocardial contractility in myocardial ischemia/reperfusion injury through phospholamban." PLOS ONE 20, no. 1 (2025): e0316887. https://doi.org/10.1371/journal.pone.0316887.

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Objective To investigate the effects and mechanisms of miRNA 221 on myocardial ischemia/reperfusion injury (MIRI) in mice through the regulation of phospholamban (PLB) expression. Methods The MIRI mouse model was created and mice were divided into sham, MIRI, MIRI+ 221, and MIRI+ scr groups, with miRNA 221 overexpression induced in the myocardium of MIRI mice by targeted myocardial injection. Quantitative RT-PCR analysis was performed to observe the variation in miRNA 221, PLB, SERCA2, RYR2, NCX1, Cyt C and caspase 3 mRNA levels in myocardium, while Western blot assessed the levels of PLB, p-P

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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 (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

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10

Berry, Mark F., Adam J. Engler, Y. Joseph Woo, et al. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (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

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11

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 v

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12

Stănescu, Alexandra, Diana Opincariu, Nora Rat, et al. "Hybrid Imaging in the Assessment of Myocardial Ischemia and Viability." Journal of Interdisciplinary Medicine 1, no. 3 (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

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13

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 (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

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Gamperl, A. K., M. M. Vijayan, C. Pereira та 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, № 2 (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/1

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15

Tshngryan, Gayane, Iryna Shatynska-Mytsyk, Oksana Makar, and Myroslava Harbar. "Value of the regional myocardial contractility and viability assessment in patients with non-ST-segment elevation myocardial infarction." World Journal of Medical Innovations 3, no. 1 (2023): 12–16. https://doi.org/10.5281/zenodo.13764780.

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In order to study the dynamics of the standard echocardiographic values and parameters of left ventricular regional myocardial contractility in patients with non-ST segment elevation myocardial infarction we had examined 114 patients, of whom 79 presented with hibernated myocardium and 35 patients with non-hibernated myocardium. Along with the assessment of the basic echocardiographic values and left ventricle ejection fraction which do not provide comprehensive information regarding the dynamics of regional myocardial contractility in order to detect viable myocardium in patients with non-ST

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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 (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 o

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Al-Maashari, Suhaib, Yasir Al-Malki, Hatim Al Lawati, Adil Al-Riyami, and Sunil K. Nadar. "Angiographic Predictors of Viability During Intervention for a ST Elevation Myocardial Infarction." Sultan Qaboos University Medical Journal 23, no. 5 (2023): 38–43. http://dx.doi.org/10.18295/squmj.12.2023.078.

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Objectives: This study aimed to identify angiographic features that would predict myocardial viability after coronary intervention for ST elevation myocardial infarction (STEMI). Methods: This retrospective study included patients who attended Sultan Qaboos University Hospital, Muscat, Oman, between January and December 2019 with a STEMI. Results: A total of 72 patients (61 male; mean age = 54.9 ± 12.7 years) were included in the study; 11 patients had evidence of non-viability on echocardiography. There were 13 patients with viable myocardium and 3 with non-viable myocardium who had a myocard

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Howard-Quijano, Kimberly, Tatsuo Takamiya, Erica A. Dale, et al. "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 (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

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Elsaka, O. "PATHOPHYSIOLOGY, INVESTIGATIONS, AND MANAGEMENT IN CASES OF MYOCARDIAL INFARCTION." Asian Journal of Advances in Medical Science 4, no. 1 (2022): 1–14. https://doi.org/10.5281/zenodo.7633499.

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Background: Reduced or full suspension of blood flow to a region of the myocardium causes myocardial infarction (MI), sometimes known as "heart attack." Myocardial infarction can be "silent," causing hemodynamic deterioration and abrupt death, or it can be a catastrophic event that causes hemodynamic deterioration and death. The most common cause of myocardial infarction is coronary artery disease, which is the leading cause of death in the United States. The myocardium is deprived of oxygen when a coronary artery is blocked. Myocardial cell loss and necrosis can occur

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Zhao, Jie, Yi Ouyang, Huanhuan Wang, et al. "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 hematoxyl

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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 (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 a

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Dean, Andrew Peter, Dom Higgs, Peter Robins, et al. "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 (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.

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Rogovskaya, Yuliya, Roman Botalov, Vyacheslav Ryabov, et al. "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 t

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Nilsson, S., G. Wikström, A. Ericsson, et al. "Myocardial Cell Death in Reperfused and Nonreperfused Myocardial Infarctions." Acta Radiologica 37, no. 1P1 (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

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Koutela, Antonella, George Loudos, Maritina Rouchota, et al. "Mesenchymal Stem Cell Transplantation Has a Regenerative Effect in Ischemic Myocardium: An Experimental Rat Model Evaluated by SPECT-CT Assessment." Diagnostics 14, no. 4 (2024): 401. http://dx.doi.org/10.3390/diagnostics14040401.

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Translational perspective: Ischemic heart disease remains a major medical problem with high mortality rates. Beside the great efforts devoted to research worldwide and the use of numerous experimental models, an absolute understanding of myocardial infarction and tissue loss has not yet been achieved. Furthermore, the regeneration of myocardial tissue and the improvement of myocardial activity after ischemia is one of the major areas of interest in the medical (and especially cardiovascular) community. In a novel experimental rat model, the beneficial effect of mesenchymal stem cell transplant

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Açar, Burak, Akin Torun, Umut Celikyurt, Zeki Talas, and Sadan Yavuz. "Acute Myocardial Infarction Due to Myocardial Bridge Treated With Surgery: a Case Report." Kardiologiia 63, no. 11 (2023): 96–100. http://dx.doi.org/10.18087/cardio.2023.11.n2063.

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Myocardial bridging is congenital anomaly characterized by segment of epicardial coronary arteries passing through the myocardium. Various ischemic conditions are related with this pathology. We report a case of myocardial bridging that was complicated with acute anterior myocardial infarction and a review of the literature. The patient was treated successfully with coronary bypass graft surgery after unsuccessful percutaneous intervention.

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Dean, Andrew Peter, Domenic Higgs, Peter Robins, et al. "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 (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 toxic

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Evtushenko, A. V., V. V. Evtushenko, A. N. Bykov, et al. "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

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Chernykh, N. Yu, A. A. Tarasova, and O. S. Groznova. "Left ventricular myocardial hypertrophy and strain changes in children with hypertrophic cardiomyopathy." Meditsinskiy sovet = Medical Council, no. 16 (October 22, 2023): 154–61. http://dx.doi.org/10.21518/ms2023-348.

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Introduction. An assessment of the relationship between the severity of hypertrophy and changes in the myocardial strain at which systolic disfunction is detected in children with hypertrophic cardiomyopathy (HCM) is clearly essential.Aim. To assess the relationship between hypertrophy and the myocardial strain in children with hypertrophic cardiomyopathy (HCM).Materials and methods. 61 patients aged between 7 and 17 years with a primary form of HCM underwent an ultrasound examination of the heart using standard techniques. An assessment of the left ventricular systolic function performed usin

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Jin, Jiyang, Min Chen, Yongjun Li, et al. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (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 myo

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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 (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

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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 (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,

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Shames, Brian D., Daniel R. Meldrum, Craig H. Selzman та ін. "Increased levels of myocardial IκB-α protein promote tolerance to endotoxin". American Journal of Physiology-Heart and Circulatory Physiology 275, № 3 (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 sub

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Chen, Harn-Shen, Jia Jia, Hou-Fen Su, et al. "Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency." Journal of Endocrinology 190, no. 2 (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 m

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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 (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 compo

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Fan, Yi, Yiwei Cheng, Yafei Li, 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 (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

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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 p

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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 (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

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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 my

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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 tis

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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 (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 h

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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 (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

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Spath, Nick B., Trisha Singh, Giorgos Papanastasiou, et al. "Assessment of stunned and viable myocardium using manganese-enhanced MRI." Open Heart 8, no. 1 (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, health

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Turler, Mark, and Shel Thoma. "Dopamine signaling attenuated myocardial injury during endotoxemia." American Journal of BioMedicine 6, no. 1 (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)

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Rustamova, Ya K. "Actual Problems of Diagnostics of Viable Myocardium." Kardiologiia 59, no. 2 (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, et al. "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

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Kadokami, Toshiaki, Charles F. McTiernan, Toru Kubota, et al. "Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (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

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Pulido, María, María Ángeles de Pedro, Verónica Álvarez, et al. "Transcriptome Profile Reveals Differences between Remote and Ischemic Myocardium after Acute Myocardial Infarction in a Swine Model." Biology 12, no. 3 (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

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Martin, Claus, Rainer Schulz, Heiner Post, Petra Gres, and Gerd Heusch. "Effect of NO synthase inhibition on myocardial metabolism during moderate ischemia." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H2320—H2324. http://dx.doi.org/10.1152/ajpheart.01122.2002.

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Nitric oxide (NO) is involved in the control of myocardial metabolism. In normoperfused myocardium, NO synthase inhibition shifts myocardial metabolism from free fatty acid (FFA) toward carbohydrate utilization. Ischemic myocardium is characterized by a similar shift toward preferential carbohydrate utilization, although NO synthesis is increased. The importance of NO for myocardial metabolism during ischemia has not been analyzed in detail. We therefore assessed the influence of NO synthase inhibition with N G-nitro-l-arginine (l-NNA) on myocardial metabolism during moderate ischemia in anest

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Zhang, Wen, Qi Zhang, Yali Liu, Jianming Pei та Na Feng. "Novel roles of κ-opioid receptor in myocardial ischemia-reperfusion injury". PeerJ 12 (25 червня 2024): e17333. http://dx.doi.org/10.7717/peerj.17333.

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Acute heart attack is the primary cause of cardiovascular-related death worldwide. A common treatment is reperfusion of ischemic tissue, which can cause irreversible damage to the myocardium. The number of mitochondria in cardiomyocytes is large, which generate adenosine triphosphate (ATP) to sustain proper cardiac contractile function, and mitochondrial dysfunction plays a crucial role in cell death during myocardial ischemia-reperfusion, leading to an increasing number of studies investigating the impact of mitochondria on ischemia-reperfusion injury. The disarray of mitochondrial dynamics,

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