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Journal articles on the topic 'Myocardium'
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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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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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Lee, C. Y., Amar Singh, Kevin J. Lee, Roy D. Goldfarb, and Min-Fu Tsan. "Correlation between myocardial glutathione content and extent of ischemia-reperfusion injury." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 1068–69. http://dx.doi.org/10.1017/s0424820100157322.
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Considerable evidence suggests that myocardial injury may occur during reperfusion of the ischemic myocardium. Reactive oxygen species are generated during reperfusion which may play an important role in the genesis of myocardial reperfusion injury. Glutathione (GSH) is an important antioxidant in the heart. A decrease in myocardial GSH content has been observed during ischemia and reperfusion of the ischemic myocardiijm. We hypothesized that this depletion of GSH may be detrimental to the ability of the ischemic myocardium to protect itself against reactive oxygen species during reperfusion.In this study, anesthetized open chest pigs were subjected to coronary occlusion for 45 minutes and 2 hours reperfusion. Myocardial GSH was experimentally depleted by pretreatment with buthionine sulfoximine (BSO), a potent inhibitor of cellular GSH synthesis, and was augmented by intravenous administration of GSH. For ultrastructural study multiple subepicardial biopsies 3 mm deep were taken from myocardium supplied by the occluded artery. The biopsies were processed by routine procedures. Thin sections were stained with uranyl acetate and lead citrate and examined with a Philip EM 300 electron microscope.
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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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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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Ristic, Andjelka, Milorad Damjanovic, Branislav Baskot, and Radomir Matunovic. "Stunned myocardium." Vojnosanitetski pregled 62, no. 2 (2005): 165–69. http://dx.doi.org/10.2298/vsp0502165r.
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Background. Stunned myocardium is a state of delayed recovery of regional contractility after a transient period of ischemia followed by reperfusion. Case report. A 67-year-old patient was admitted to our hospital with acute anterior myocardial infarction, and treated using percutaneous transluminal coronary angioplasty (PTCA) within acute disease stage. Reversible myocardial dysfunction persisted after ischemia following the return of normal perfusion. Abnormal resting wall motion with augmentation of contractility at low and high doses of dobutamine characterizes the stunned myocardium and reflects the normal blood flow reserve, characteristic for these postischemic, reperfused segments. SPECT (Single Photon Emission Computerized Tomography) with Tc 99 and dipyradamole showed normalization of perfusion defects in the apical region. Theree months after the infarction and PTCA, contractility was almost completely recovered. Conclusion. Stunned myocardium recovery lasted from few weeks to few months. Control ultrasonography as well as SPECT showed normalization of systolic function of the left ventricle in the viable segments registered at previous examinations.
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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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Cha, Jehyun, Joonghyun Ryu, Jin-Ho Choi, and Deok-Soo Kim. "Medial-ABC: an algorithm for the correspondence between myocardium and coronary artery mesh models based on the medial axis of coronary artery." Journal of Computational Design and Engineering 7, no. 6 (August 6, 2020): 736–60. http://dx.doi.org/10.1093/jcde/qwaa054.
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Abstract The role of coronary arteries is to supply sufficient blood to myocardium. Obstruction of coronary arteries limits blood supply and causes myocardial ischemia or acute myocardial infarction, a major cause of human death. Hence, the quantification of the regional amount of heart muscle subtended by obstructed coronary arteries is of critical value in clinical medicine. However, conventional methods are inaccurate and frequently disagree with clinical practice. This study proposes a novel medial-axis-based correspondence (Medial-ABC) algorithm to find the correspondence between myocardium and coronary artery in order to segment regional myocardium at risk subtended by any potentially obstructed coronary artery. Given the triangular mesh models of coronary artery and myocardium, the proposed algorithm (i) computes the medial axis of coronary artery, (ii) finds the correspondence using the medial axis of coronary artery, and (iii) segments the coronary artery and myocardium. The proposed algorithm provides a robust mathematical linkage between myocardium at risk and supplying coronary arteries so that ischemic myocardial regions can be accurately identified. Hence, both the extent and severity of myocardial ischemia can be quantified effectively, efficiently, and accurately. Furthermore, the constructed mesh model of segmented coronary artery and myocardium can be post-processed for applications such as building optimization models of cardiac systems. The CardiacVis program, which implements the Medial-ABC algorithm, is freely available at Voronoi Diagram Research Center (http://voronoi.hanyang.ac.kr/software/cardiacvis) and will be an invaluable tool for quantitative patient-specific risk stratification in clinical practice.
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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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Zdebik, Natalia, Rafał Poręba, and Paweł Gać. "Importance of T1-Mapping Sequence in Patients with Hypertrophic Cardiomyopathy without Foci of Non-Ischemic Myocardial Injury in Late Gadolinium Enhancement Sequence." Biomedicines 12, no. 6 (June 14, 2024): 1330. http://dx.doi.org/10.3390/biomedicines12061330.
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Background: The aim of this study was to assess the importance of T1-mapping sequences in the diagnosis of hypertrophic cardiomyopathy (HCM) in patients without foci of non-ischemic myocardial injury in classic cardiac magnetic resonance (CMR) sequences. Methods: Two groups were compared: 28 patients with HCM, without any foci of myocardial injury in the late gadolinium enhancement (LGE) sequence (HCM group), and 28 patients without cardiomyopathy (CON group). Classic CMR sequences and T1-mapping sequences were performed. The following parameters were assessed: T1 time of the whole left ventricular myocardium, T1 time of myocardium in the basal, middle and apical layers of the left ventricle, and T1 time in individual segments of the left ventricular myocardium. Myocardial extracellular volume (ECV) was assessed similarly. Results: ECV was significantly higher in the HCM group than in the CON group, for the whole left ventricular myocardium, for the basal and apical layers of the left ventricle, and for segments 1–3, 8, and 13–16 of the left ventricle. Regression analysis showed that a higher left-ventricular mass index (LVMI), a higher body mass index and older age are factors independently associated with a higher ECV of the whole myocardium but only in the group with LVMI ≥ 131.84 g/m2. Conclusion: In patients with HCM without foci of non-ischemic myocardial injury, higher ECV values of the left ventricular myocardium are observed.
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Ryabykina, G. V. "Changes in the electrocardiogram with focal myocardial damage." Medical alphabet 1, no. 14 (September 9, 2020): 19–31. http://dx.doi.org/10.33667/2078-5631-2020-14-19-31.
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The present report introduces the electrophysiological conception of charging current in myocardium, alteration of ECG in different intensity of necrosis of myocardium, introduces parameter of topical diagnostics of focal changing of myocardium. Numerous clinical-ECG examples show specific ECG patterns in diagnostics of different types of myocardial infarction.
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Arutyunov, G. P., D. O. Dragunov, G. P. Arutyunov, A. V. Sokolova, I. P. Papyshev, E. M. Kildyushov, V. V. Negrebetsky, and V. N. Fedorova. "The effect of the level of total sodium deposited in the myocardium on its stiffness." Terapevticheskii arkhiv 89, no. 1 (January 15, 2017): 32–37. http://dx.doi.org/10.17116/terarkh201789132-37.
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Aim. To determine a relationship between the level of total sodium in the myocardium to its stiffness. Subjects and methods. The investigation enrolled 18 hypertensive patients who had suddenly died; their mean age was 40±10 years; mean waist circumference, 102±12.5 cm; height, 170±7.7 cm; myocardial mass, 319±53 g. Results. The variation in the myocardial level of total sodium averaged 211.7±37.5 (min, 71.5; max, 226.17) mmol/l. The sodium level was ascertained to be affected to the greatest extent by myocardial mass (SS=3615.56; p=0.00029) and age at death (SS=1965.568; p=0.0029), whereas gender and smoking had a considerably lower impact (SS=778.584; p=0.03). A univariate regression analysis showed that there was a relationship between myocardial sodium levels and the thickness of the anterior wall of the left ventricle (β=0.94; p=0.000001; r2=0.88), that of the anterior wall of the right ventricle (β=0.82; p=0.000021; r2=0.66), and that of the interventricular septum (β=0.94; p=0.000001; r2=0.89). The wall thickness of the myocardium was established to depend on its sodium level (SS=21813.89; p=0.000001; r2=0.88): the higher sodium amount in the myocardium, the thicker its walls. The average velocity of acoustic wave propagation was 6.24±0.51 m/sec. A significant correlation was observed between sodium concentrations in the myocardium and its stiffness (β=0.72; p=0.00062; r2=0.49). Conclusion. The level of sodium deposited in the myocardium, which is directly related to dietary sodium intake, is significantly correlated with myocardial stiffness. It can be assumed that the elevated level of sodium deposited in the myocardium is an independent factor that changes the stiffness of the myocardium and appears to influence the development of its diastolic dysfunction.
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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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Jeremy, R. W., L. Stahl, M. Gillinov, M. Litt, T. R. Aversano, and L. C. Becker. "Preservation of coronary flow reserve in stunned myocardium." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (May 1, 1989): H1303—H1310. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1303.
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Microvascular obstruction and persistent focal ischemia have been suggested as a possible cause of myocardial dysfunction (stunning) after brief coronary occlusion. Microvascular occlusion should result in a reduction in maximal coronary flow reserve, although resting transmural coronary flow may be maintained by release of local vasodilators, such as adenosine. To test the microvascular occlusion hypothesis, coronary flow reserve was measured in 14 anesthetized dogs, before and after myocardial stunning produced by 10 min of ischemia. Intracoronary adenosine infusion (5,900 microM/min) increased coronary flow to the same degree in normal [195 +/- 20 (SE) ml/min] and stunned (212 +/- 23 ml/min) myocardium. Peak hyperemic flow after 100 s of coronary occlusion was also similar in normal (205 +/- 25 ml/min) and stunned (218 +/- 23 ml/min) myocardium. The adenosine antagonist 8-phenyltheophylline (5 mg/kg) reduced the flow response to exogenous adenosine, but neither resting coronary flow nor peak hyperemic flow in stunned myocardium was altered. In stunned myocardium, myocardial shortening at rest (0.2 +/- 2.0%) increased during reactive hyperemia (to 13.8 +/- 2.5%, P less than 0.01), but shortening promptly returned to basal levels after each hyperemia. These findings indicate that fixed microvascular occlusion is unlikely to be an important factor in the pathogenesis of stunned myocardium and that local adenosine release does not appear to have a compensatory role in coronary vasoregulation in stunned myocardium.
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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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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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Lindstedt, Sandra, Malin Malmsjö, and Richard Ingemansson. "The Effect of Different Topical Negative Pressures on Microvascular Blood Flow in Reperfused Myocardium during Hypothermia." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 2, no. 5 (September 2007): 231–36. http://dx.doi.org/10.1097/imi.0b013e31816207b3.
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Objective Hypothermia is known to limit the extent of myocardial infarction. The earlier hypothermia is applied to an ischemic myocardium, the more tissue can be salvaged. Topical negative pressure (TNP) is known to increase blood flow and stimulate angiogenesis in subcutaneous tissue and skeletal muscle. We have previously shown that a myocardial TNP of −50 mm Hg significantly increases microvascular blood flow in the underlying myocardium in ischemic and reperfused porcine myocardium. The present study was designed to elucidate the effect of different TNP levels on microvascular blood flow in reperfused myocardium during hypothermia. Methods Seven pigs underwent median sternotomy. The microvascular blood flow in the myocardium was recorded before and after the application of −50, −75, −100, −125, and −150 mm Hg using laser Doppler velocimetry. Analysis was performed in the epicardium and at a depth of 6 to 8 mm in the myocardium after 40 minutes of occlusion of the left anterior descending artery followed by cooling to 31°C, and reperfusion for another 20 minutes. Results A TNP of −50 mm Hg significantly increased blood the flow in the epicardium, from 116.7 ± 10.0 PU to 244.5 ± 52.6 PU (*P < 0.05) at 31°C. A TNP of −50 mm Hg significantly increased microvascular blood flow in the myocardium, from 155.0 ± 8.4 PU to 236.7 ± 61.5 PU (*P < 0.05). Conclusions Only a TNP of −50 mm Hg, applied over the left anterior descending artery region in reperfused hypothermic myocardium significantly increased the microvascular blood flow in the epicardium and in the myocardium.
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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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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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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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Baranov, S. A., V. M. Nechaev, and M. V. Fadeeva. "The clinical case of non-compact left ventricular myocardium in combination with restrictive cardiomyopathy." Meditsinskiy sovet = Medical Council, no. 17 (October 16, 2022): 130–35. http://dx.doi.org/10.21518/2079-701x-2022-16-17-130-135.
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In this paper the information about a comparatively rare form of cardiomyopathy – noncompaction of the left ventricular myocardium is showed. As a result of genetical changes on the early stages of embryogenesis a disability of myocardial fibres develops, and two-layer myocardial structure is formed: thin compact layer and remaining more voluminous non-compact layer with significant trabeculation and deep intratrabecular cavities communicated with ventricular cavity. Mutations in genes which encode sarcomeric, structural and regulatory proteins and proteins, which are responsible for ion channels functioning, are considered to be one of the main reasons of non-compact myocardium. There is a theory that considers a non-compact myocardium as a result of an exposure of various factors during lifetime – so-called non-embryonal (acquired) noncompaction myocardium. “Non-embryonal” hypothesis views non-compact myocardium as a sign of functional maladaptation, possible stage in cardiomyopathy development. By way of illustration the clinical case of 32-year-old female patient is presented in the article. The noncompaction of the left ventricular myocardium in conjunction with restrictive cardiomyopathy was first diagnosed in her. The diagnosis was confirmed by main diagnostic methods for this pathology such as echocardiography and MRI of a heart. This clinical observation is interesting due to formation of disease patterns by two rare combined pathological conditions: noncompaction of the myocardium syndrome and restrictive cardiomyopathy. Changes of heart hemodynamics occurs in interaction between these pathologies. Diastolic filling of left ventricular decreases as a result of restrictive cardiomyopathy, which leads to decreasing of its myocardium load. Therefore, systolic disfunction, which is specific to non-compact myocardium, doesn’t occur. Generally, prognosis for this patient is poor due to presence of two serious pathologies.
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Liu, C. R., L. Y. Li, F. Shi, X. Y. Zang, Y. M. Liu, Y. Sun, and B. H. Kan. "Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium." Journal of Endocrinology 195, no. 3 (September 19, 2007): 429–38. http://dx.doi.org/10.1677/joe-07-0253.
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Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNA was extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRα1 mRNA expression was upregulated by 51% (P<0.01), TRα2 mRNA expression was downregulated by 58% (P<0.01), and TRβ1 mRNA expression remained unchanged in hyperthyroid rat myocardium (P>0.05). TRα1, TRα2, and TRβ1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRα1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRα2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRβ1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.
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Segers, Vincent F. M., Andreas B. Gevaert, Jente R. A. Boen, Emeline M. Van Craenenbroeck, and Gilles W. De Keulenaer. "Epigenetic regulation of intercellular communication in the heart." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 6 (June 1, 2019): H1417—H1425. http://dx.doi.org/10.1152/ajpheart.00038.2019.
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The myocardium is a highly structured tissue consisting of different cell types including cardiomyocytes, endothelial cells, fibroblasts, smooth muscle cells, inflammatory cells, and stem cells. Microvascular endothelial cells are the most abundant cell type in the myocardium and play crucial roles during cardiac development, in normal adult myocardium, and during myocardial diseases such as heart failure. In the last decade, epigenetic changes have been described regulating cellular function in almost every cell type in the organism. Here, we review recent evidence on different epigenetic changes that regulate intercellular communication in normal myocardium and during myocardial diseases, including cardiac remodeling. Epigenetic changes influence many intercellular communication signaling systems, including the nitric oxide, angiotensin, and endothelin signaling systems. In this review, we go beyond discussing classic endothelial function (for instance nitric oxide secretion) and will discuss epigenetic regulation of intercellular communication.
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Patel, Jitandrakumar R., Daniel P. Fitzsimons, Scott H. Buck, Mariappan Muthuchamy, David F. Wieczorek, and Richard L. Moss. "PKA accelerates rate of force development in murine skinned myocardium expressing α- or β-tropomyosin." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (June 1, 2001): H2732—H2739. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2732.
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In myocardium, protein kinase A (PKA) is known to phosphorylate troponin I (TnI) and myosin-binding protein-C (MyBP-C). Here, we used skinned myocardial preparations from nontransgenic (NTG) mouse hearts expressing 100% α-tropomyosin (α-Tm) to examine the effects of phosphorylated TnI and MyBP-C on Ca2+ sensitivity of force and the rate constant of force redevelopment ( k tr). Experiments were also done using transgenic (TG) myocardium expressing ∼60% β-Tm to test the idea that the α-Tm isoform is required to observe the mechanical effects of PKA phosphorylation. Compared with NTG myocardium, TG myocardium exhibited greater Ca2+sensitivity of force and developed submaximal forces at faster rates. Treatment with PKA reduced Ca2+ sensitivity of force in NTG and TG myocardium, had no effect on maximum k trin either NTG or TG myocardium, and increased the rates of submaximal force development in both kinds of myocardium. These results show that PKA-mediated phosphorylation of myofibrillar proteins significantly alters the static and dynamic mechanical properties of myocardium, and these effects occur regardless of the type of Tm expressed.
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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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Bogunetsky, A. A., V. Yu Ussov, and V. Yu Babokin. "CARDIOVASCULAR MAGNETIC RESONANCE WITH CONTRAST AGENT: PROGNOSTIC ROLE IN DETERMINING ARRHYTMOGENIC FOCUS." Bulletin of Siberian Medicine 13, no. 1 (February 28, 2014): 98–102. http://dx.doi.org/10.20538/1682-0363-2014-1-98-102.
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In order to evaluate the possibilities of MRI in detection of proarrhytmogenic areas of myocardium we did compare directly and quantitatively the local myocardial uptake of paramagnetics to the results of electrophysiologic study of myocardium in twenty-two patients with recent transmural myocardial infarction and frequent ventricular extrasystoles verified by ECG studies.Topic quantitative study of myocardial electric potential has been carried out using Carto XP system (by Biosense Webster).By analysis of the images the measurement of Index of transmurality (IT) for the contrast uptake was calculated as ratio of thickness of paramagnetic uptake to overall thickness of myocardium in a specific segment.The the electrophysiologic and MRI data were analyzed topically as segment vs segment and the significant tendency was revealed with simultaneous grow of pro-arrhythmogenic activity and value of IT. In other words, as bigger the IT increases, as arrhythmogenic the lectrical activity becomes. The best border value of IT that provided separation of electrically normal segments from proarrhythmogenic ones was the IT = 0.3.Therefore we conclude the contrast-enhanced MRI of myocardium deliver additional information on risk of arrhythmias, not only the detection of myocardial damage itself.
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Ryabov, Vyacheslav, Aleksandra Gombozhapova, Nikolai Litviakov, Marina Ibragimova, Matvey Tsyganov, Yulia Rogovskaya, and Julia Kzhyshkowska. "Microarray Analysis for Transcriptomic Profiling of Myocardium in Patients with Fatal Myocardial Infarction." Biomedicines 11, no. 12 (December 13, 2023): 3294. http://dx.doi.org/10.3390/biomedicines11123294.
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Transcriptomic evidence from human myocardium in myocardial infarction (MI) is still not sufficient. Thus, there is a need for studies on human cardiac samples in relation to the clinical data of patients. The purpose of our pilot study was to investigate the transcriptomic profile of myocardium in the infarct zone, in comparison to the remote myocardium, in patients with fatal MI, via microarray analysis. This study included four patients with fatal MI type 1. We selected histologically verified samples from within the infarct area (n = 4) and remote myocardium (n = 4). The whole transcriptome was evaluated using microarray analysis. Differentially expressed genes (DEGs) clustered in the infarct area and in the remote myocardium allowed their differentiation. We identified a total of 1785 DEGs (8.32%) in the infarct area, including 1692 up-regulated (94.79%) and 93 down-regulated (5.21%) genes. The top 10 up-regulated genes were TRAIL, SUCLA2, NAE1, PDCL3, OSBPL5, FCGR2C, SELE, CEP63, ST3GAL3 and C4orf3. In the infarct area, we found up-regulation of seventeen apoptosis-related genes, eleven necroptosis-related, and six necrosis-related genes. Transcriptome profiling of the myocardium in patients with MI remains a relevant area of research for the formation of new scientific hypotheses and a potential way to increase the translational significance of studies into myocardial infarction.
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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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Zhang, Shikun, Xiaoyan Du, Kun Zhang, and Haiyan Wang. "Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats." BioMed Research International 2021 (December 31, 2021): 1–6. http://dx.doi.org/10.1155/2021/3347949.
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Background. Cardiomyocyte apoptosis functions essentially in ischemia/reperfusion- (I/R-) induced myocardial injury. It is suggested that autophagy is widely implicated in the regulation of cell survival and death. Sevoflurane, as a largely used inhalational general anesthetic, has been shown to have a protective effect on cardiomyocytes. However, it was yet elusive on the underlying mechanisms. Aim. The objective of this study is to investigate the association of sevoflurane-mediated cardioprotective effects with autophagy regulation. Methods. An in vitro hypoxia model was established in primary cardiomyocytes from fresh myocardial tissue of the rats. The apoptosis rate of myocardial cells treated with hypoxia and treated with sevoflurane was measured. Western blot and immunocytochemical assay were used to measure the protein expression. The cell proliferation rate and cell apoptosis were measured using the MTT assay and flow cytometry, respectively. Results. The expression of apoptotic proteins including B cell lymphoma-2 (Bcl-2), CCAAT/enhancer-binding protein homologous protein (CHOP), glucose-regulated protein 78 (GRP78), and Bcl-2-associated X protein (BAX) in myocardium treated with sevoflurane was significantly lower than that in myocardium treated with hypoxia. The expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in myocardium treated with sevoflurane was higher than that in myocardium treated with hypoxia, suggesting better connectivity of the myocardium. Conclusion. Sevoflurane treatment reduced the apoptosis of myocardial cells after hypoxia treatment.
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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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Chen, Qi, Yu Liu, Xueyan Ding, Qinfeng Li, Fuyu Qiu, Meihui Wang, Zhida Shen, Hao Zheng, and Guosheng Fu. "Bone marrow mesenchymal stem cell-secreted exosomes carrying microRNA-125b protect against myocardial ischemia reperfusion injury via targeting SIRT7." Molecular and Cellular Biochemistry 465, no. 1-2 (December 19, 2019): 103–14. http://dx.doi.org/10.1007/s11010-019-03671-z.
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AbstractMicroRNA-125b (miR-125b) reduces myocardial infarct area and restrains myocardial ischemia reperfusion injury (I/R). In this study, we aimed to investigate the effect of bone marrow mesenchymal stem cell (BMSC)-derived exosomes carrying miR-125b on I/R rats. The myocardial I/R model in rats was constructed by ligation of the left anterior descending coronary artery (LAD). Rats were randomly divided into I/R and Sham group. Lv-cel-miR-67 (control) or Lv-miR-125b was transfected into BMSCs. Exosomes were extracted from transfected BMSCs, and separately named BMSC-Exo-67, BMSC-Exo-125b, and BMSC-Exo. MTT assay and flow cytometry were used to detect the viability and apoptosis of I/R myocardium cells, respectively. The expression of cell apoptosis proteins and the levels of inflammatory factors were examined by Western blot and ELISA assay, respectively. The target relationship between miR-125b and SIRT7 was predicted by using StarBase3.0, and was confirmed by using dual-luciferase reporter gene assay. qRT-PCR, immunohistochemistry staining, and Western blot were used to evaluate the expression of SIRT7 in myocardium tissues in I/R rats. BMSC-derived exosomes were successfully isolated and identified by TEM and positive expression of CD9 and CD63. The expression of miR-125b was down-regulated in I/R myocardium tissues and cells. BMSC-Exo-125b significantly up-regulated miR-125b in I/R myocardium cells. The intervention of BMSC-Exo-125b significantly increased the cell viability, decreased the apoptotic ratio, down-regulated Bax and caspase-3, up-regulated Bcl-2, and decreased the levels of IL-1β, IL-6, and TNF-α in I/R myocardium cells. SIRT7 was a target of miR-125b, and BMSC-Exo-125b significantly down-regulated SIRT7 in myocardium cells. In addition, the injection of BMSC-Exo-125b alleviated the pathological damages and down-regulated SIRT7 in myocardium tissues of I/R rats. BMSC-derived exosomes carrying miR-125b protected against myocardial I/R by targeting SIRT7.
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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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Gazaryan, Georgi G. "Delayed reperfusion for saving vital myocardium in the acute period of myocardial infarction with elevation of ST segment." Clinical Medicine (Russian Journal) 94, no. 4 (June 1, 2016): 307–12. http://dx.doi.org/10.18821/0023-2149-2016-94-4-307-312.
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Reperfusion therapy in case of acute myocardial infarction is especially desirable within 12 hr afterfirst clinical manifestations as shown in studies with the use of thrombolytic therapy (TLT). Its efficiency for saving ischemic myocardium decreases as the time from the onset of pain syndrome increases. Nevertheless, patients admitted to the clinic in the period deemed unfavourable for TLT still preserve large part of vital myocardium even if in the risk zone. Delayed saving myocardium impossible by TLT can be ensured by transdermal coronary interventions. The dependence of myocardial necrosis on the duration of occlusion of the coronary artery is as well recognized as the necessity of early interventions. Transdermal coronary interventions can be performed within days 2 or 3 after onset of acute myocardial infarction if it was impracticable in an earlier period.
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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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Popov, M. A., D. V. Shumakov, L. E. Gurevich, D. N. Fedorov, D. I. Zybin, V. E. Ashevskaya, P. A. Korosteleva, and V. M. Tyurina. "The evaluation of hibernating myocardium function." CLINICAL AND EXPERIMENTAL MORPHOLOGY 12, no. 1 (2023): 59–67. http://dx.doi.org/10.31088/cem2023.12.1.59-67.
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Introduction.Currently, there are different approaches to assessing changes that occur in ischemic myocardium in patients with chronic coronary artery disease (CAD). Researchers argue about the timing and completeness of the restoration of myocardial dysfunction areas. We aimed to assess hibernating myocardium in the zones of hypokinesia in patients with CAD. Materials and methods. We performed a morphological and immunohistochemical study of left ventricular myocardial biopsies of 25 patients who underwent surgical reconstruction of the left ventricle with surgical revascularization. Results. Morphological and immunohistochemical studies revealed violated morphological structure of cardiomyocytes. It correlates with the accumulation of MMP9 in the cytoplasm of cardiomyocytes in the areas of affected myocardium in ischemia against the background of partial or complete destruction of CM basement membranes formed by type IV collagen. It also correlates with long-term consequences of treatment. Conclusion. As a result of the destructed structure of sarcomeres and cardiac basement membrane hibernating myocardium is unable to provide a contractile function in the future. Morphological examination showed that viable cells were likely to function only as a protective mechanism in early scar formation. Keywords: left ventricular remodeling, hibernating myocardium, basement membrane, cardiomyocytes, matrix metalloproteinase 9, type IV collagen
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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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Walton, J., and P. Westrope. "Stunned myocardium: theoretical mechanisms of injury." Critical Care Nurse 16, no. 2 (April 1, 1996): 23–28. http://dx.doi.org/10.4037/ccn1996.16.2.23.
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Stunned myocardium may occur after an episode of prolonged or transient ischemia. This phenomenon can occur in a variety of patient groups including medical, surgical, neurologic, and cardiac patients. In the stunned myocardium, myocardial contractility is temporarily depressed, causing symptoms similar to those of cardiogenic shock. When critical care nurses are familiar with the clinical characteristics and risk factors of stunned myocardium, they can start the appropriate interventions and left ventricular function returns to normal within days with no residual hypokinesis. Critical care nurses play a key role in assisting surgeons and other noncardiac physicians in the diagnosis and care of the patient with stunned myocardium.
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Farias, Fernando, Patricio Morgan, Gladys Chiappe de Cingolani, and María C. Camilión de Hurtado. "Involvement of the Na+-independent Cl–/HCO3– exchange (AE) isoform in the compensation of myocardial Na+/H+ isoform 1 hyperactivity in spontaneously hypertensive rats." Canadian Journal of Physiology and Pharmacology 83, no. 5 (May 1, 2005): 397–404. http://dx.doi.org/10.1139/y05-025.
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Enhanced activity of Na+/H+ isoform 1 (NHE-1) and the Na+-independent Cl–/HCO3– exchange (AE) is a feature of the hypertrophied myocardium in spontaneously hypertensive rats (SHR). The present study explored the possibility that sustained intracellular acidosis due to increased myocardial acid loading through AE causes NHE-1 enhancement. To this aim, SHR were treated for 2 weeks with a rabbit polyclonal antibody against an AE3 isoform that was recently developed and proven to have inhibitory effects on myocardial AE activity. We then compared the AE activity in the left ventricle papillary muscles isolated from untreated SHR with antiAE3-treated SHR; AE activity was measured in terms of the rate of intracellular pH recovery after an intracellular alkali load was introduced. AE activity was diminished by ~ 70% in SHR treated with the antiAE3 antibody, suggesting that the AE3 isoform is a major carrier of acid-equivalent influx in the hypertrophied myocardium. However, the antibody treatment failed to normalize NHE-1 activity that remained elevated in the myocardium of normotensive rats. The data therefore rule out the possibility that NHE-1 hyperactivity in hypertensive myocardium was due to sustained intracellular acidosis induced by increased AE activity that characterizes SHR myocardial tissue.Key words: NHE-1, AE3, cardiac hypertrophy, myocardial AE activity.
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Babes, Elena Emilia, Delia Mirela Tit, Alexa Florina Bungau, Cristiana Bustea, Marius Rus, Simona Gabriela Bungau, and Victor Vlad Babes. "Myocardial Viability Testing in the Management of Ischemic Heart Failure." Life 12, no. 11 (November 1, 2022): 1760. http://dx.doi.org/10.3390/life12111760.
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Although major advances have occurred lately in medical therapy, ischemic heart failure remains an important cause of death and disability. Viable myocardium represents a cause of reversible ischemic left ventricular dysfunction. Coronary revascularization may improve left ventricular function and prognosis in patients with viable myocardium. Although patients with impaired left ventricular function and multi-vessel coronary artery disease benefit the most from revascularization, they are at high risk of complications related to revascularization procedure. An important element in selecting the patients for myocardial revascularization is the presence of the viable myocardium. Multiple imaging modalities can assess myocardial viability and predict functional improvement after revascularization, with dobutamine stress echocardiography, nuclear imaging tests and magnetic resonance imaging being the most frequently used. However, the role of myocardial viability testing in the management of patients with ischemic heart failure is still controversial due to the failure of randomized controlled trials of revascularization to reveal clear benefits of viability testing. This review summarizes the current knowledge regarding the concept of viable myocardium, depicts the role and tools for viability testing, discusses the research involving this topic and the controversies related to the utility of myocardial viability testing and provides a patient-centered approach for clinical practice.
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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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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 (November 30, 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 myocardial blush grade (MBG) of 2 or lower. Similarly, 10 patients with viability and 1 with non-viable myocardium had thrombolysis in myocardial infarction (TIMI) flow of 2 or lower in the infarct related artery (IRA). However, none of these were statistically significant. The TIMI flow in the IRA at the end of the procedure correlated with the MBG. Conclusion: There were no clear angiographic features during primary angioplasty that could predict myocardial viability.
Keywords: Myocardial infarction; Coronary Angiography; Viability; Oman.
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Jenkins, Crystal P., Diana M. Cardona, Jennifer N. Bowers, Bahram R. Oliai, Robert W. Allan, and Sigurd J. Normann. "The Utility of C4d, C9, and Troponin T Immunohistochemistry in Acute Myocardial Infarction." Archives of Pathology & Laboratory Medicine 134, no. 2 (February 1, 2010): 256–63. http://dx.doi.org/10.5858/134.2.256.
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Abstract Context.—Full activation and involvement of the complement pathway follows acute myocardial infarction. Complement fragment C4d is a stable, covalently bound marker of complement activation. Troponin T is specific for cardiomyocytes. Objectives.—To determine the specificity of C4d, C9, and troponin T immunoreactivity in necrotic myocytes and to establish whether they can be used to delineate acute myocardial infarction. Design.—Twenty-six autopsy cases with a total of 54 myocardium areas of infarction were reviewed retrospectively. Immunohistochemistry for C4d, C9, and troponin T was used on paraffin sections of formalin-fixed tissue. Controls consisted of 5 cases without evidence of infarction, and histologically normal myocardium functioned as an internal control. Results.—C4d and C9 antibodies reacted strongly and diffusely with necrotic myocytes in all samples of infarctions for up to 2 days (19 of 19; 100%). Adjacent histologically normal myocytes were nonreactive, resulting in a clear delineation between damaged and viable myocardium. Reactivity declined with increased duration and was absent in scars. Troponin T showed loss of staining in preinflammatory lesions (8 of 13; 62%); however, nonspecific patchy loss of staining was present in negative controls and in viable myocardium. Immunostains provided new diagnoses in 2 cases, including evidence of reinfarction and a newly diagnosed acute myocardial infarction. Conclusions.—C4d and C9 have comparable reactivity and specificity for necrotic myocytes. C4d and C9 staining of necrotic myocytes is apparent before the influx of inflammatory cells, demonstrating utility in early myocardial infarction. Patchy loss of Troponin T in some cases of histologically normal myocardium limited its usefulness as a sole marker of infarction.
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Hsu, Edward W., Rong Xue, Alex Holmes, and John R. Forder. "Delayed reduction of tissue water diffusion after myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H697—H702. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h697.
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The apparent diffusion coefficient (ADC) of water after regional myocardial ischemia was measured in isolated, perfused rabbit hearts by using magnetic resonance imaging (MRI) techniques. After ligation of the left anterior descending coronary artery, the ADC of the nonperfused region showed a gradual but significant decreasing trend over time, whereas that of the normally perfused myocardium remained constant. Morphological analysis revealed that the ADC decrease reflected the expansion of a subregion of reduced ADC within the nonperfused myocardium. The dynamics of the diffusion change and the morphological progression of the affected tissue suggest that the ADC decrease may be linked to the onset of myocardial infarction, which is known to involve myocyte swelling. The ADC reduction provides a potentially valuable MRI tissue-contrast mechanism for noninvasively determining the viability of the ischemic myocardium and assessing the dynamics of acute myocardial infarction.
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Ussov, V. Yu, and A. A. Bogunetsky. "DETECTION OF MYOCARDIAL VIABILITY IN ISСHAEMIC DAMAGE USING MAGNETIC RESONANCE AND EMISSION TOMOGRAPHY." Bulletin of Siberian Medicine 12, no. 6 (December 28, 2013): 154–66. http://dx.doi.org/10.20538/1682-0363-2013-6-154-166.
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A review of modern methods of magnetic resonance imaging (MRI) and emission tomography (singlephoton emission and positron emission computer tomography – SPECT and PET) as toos for diagnosis and prognosis of myocardial ischaemic damage, in particular in coronary revascularization. The definition of term “myocardial viability” is discussed. It has been shown that the integrity of blood-tissue barrier between myocardium and microcirculatory vessels is the most sensitive marker of tissue viability and of functional integrity of myocardium. It’s evaluation by means of contrast-enhanced MRI of myocardium is the most available and most precise technique of diagnosis and prognosis both in patients with postinfarction myocardiosclerosis and in patients with coronary disease without myocardial infarction. It is proposed that in the nearest future the combination of MR-coronarography and contrast-enhanced MRI of myocardium will provide a possibility to obtain the full set of data necessary for planning of endovascular and surgical treatment of various forms of coronary heart disease. PET and SPECT techniques currently are of some essential interest for pathophysiologic research of coronary ishaemia in clinical and experimental studies as well as for qualitative visual studies of pharmacokinetics.
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Sun, Chuhao. "Application of High Molecular Hydrogel in The Treatment of Myocardial Infarction." Highlights in Science, Engineering and Technology 74 (December 29, 2023): 1779–85. http://dx.doi.org/10.54097/z9y86646.
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Myocardial infarction (MI) is the world's leading disabling and fatal disease. Currently, clinical treatment methods mainly include drug therapy, angioplasty, and coronary artery bypass grafting. These traditional treatment methods are difficult to repair damaged myocardial tissue and cannot restore normal necrotic and fibrotic myocardium. Therefore, it is imperative to improve the efficacy of traditional treatment methods and find new treatment strategies. More and more studies have found that stem cell transplantation can repair damaged myocardium, but stem cells transplanted to the affected site undergo oxidative damage, compression loss, and low cell survival and retention rates. At present, there is an urgent need to seek new methods that can effectively repair damaged myocardium and restore cardiac function. In recent years, with the development of regenerative medicine engineering and the continuous optimization of polymer technology and the development of new biomaterials, it has become a reality to create lost or functionally damaged tissues and organs through theoretical methods of biology and engineering, enabling them to have the structure and function of normal tissues and organs. This article will focus on the latest progress in methods for repairing damaged myocardium in myocardial infarction through polymer hydrogel materials.
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Zhang, Wen, Qi Zhang, Yali Liu, Jianming Pei, and Na Feng. "Novel roles of κ-opioid receptor in myocardial ischemia-reperfusion injury." PeerJ 12 (June 25, 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, excessive Ca2+ accumulation, activation of mitochondrial permeable transition pores, swelling of mitochondria, ultimately the death of cardiomyocyte are the consequences of ischemia-reperfusion injury. κ-opioid receptors can alleviate mitochondrial dysfunction, regulate mitochondrial dynamics, mitigate myocardial ischemia-reperfusion injury, exert protective effects on myocardium. The mechanism of κ-OR activation during myocardial ischemia-reperfusion to regulate mitochondrial dynamics and reduce myocardial ischemia-reperfusion injury will be discussed, so as to provide theoretical basis for the protection of ischemic myocardium.
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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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Ivanova, V. V., О. N. Serebryakova, I. V. Sukhodolo, and I. V. Milto. "Type I/III collagen ratio in the left ventricular myocardium of prematurely born rats." CLINICAL AND EXPERIMENTAL MORPHOLOGY 13, no. 2 (2024): 44–52. http://dx.doi.org/10.31088/cem2024.13.2.44-52.
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Introduction. Type I/III collagen ratio in the myocardium plays a key role in determining the biomechanical properties of the heart. The aim was to study type I/III collagen ratio of the myocardial stroma of the left ventricle in prematurely born rats. Materials and methods. The experiment included 120 Wistar rats of both sexes, which were divided into three groups. The control group included full-term animals (22 days of gestation), and groups 1 and 2 involved preterm animals (21.5 and 21 days of gestation, respectively). We used histological (Masson staining) and immunohistochemical (detection of type I and III collagens) methods to analyze the left ventricular myocardium in term and preterm rats on months 1, 1.5, 2, and 6 of the postnatal period. Results. Preterm birth leads to the development of myocardial fibrosis, whose severity correlates with the degree of prematurity. Due to preterm birth, the accumulation rate of type I collagen in the left ventricular myocardium accelerates. From month 2 of the postnatal period, the specific volume of type I collagen in term and preterm rats does not differ. An increase in the specific volume of type III collagen in the left ventricular myocardium in preterm rats is observed up to month 6 of the postnatal period. Preterm birth of rats results in decreased type I/III collagen ratio in the left ventricular myocardium in months 2 and 6 of the postnatal period. Conclusion. Preterm birth of rats leads to adaptive remodeling of the connective tissue of the left ventricular myocardium, which consists in the initial (1–1.5 months of the postnatal period) growth in the specific vol-ume of type I collagen and further (up to month 6 of the postnatal period) increase in the specific volume of type III collagen, compared to the same parameters of the myocardium of full-term animals. The decrease in type I/III collagen ratio on months 2 and 6 of the postnatal period indicates a change in biomechanical properties of the left ventricular myocardium in prematurely born rats. Keywords: preterm birth, prematurity, cardiac remodeling, myocardial fibrosis, type I collagen, type III collagen
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Nasiraei-Moghaddam, Abbas, and Morteza Gharib. "Evidence for the existence of a functional helical myocardial band." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 1 (January 2009): H127—H131. http://dx.doi.org/10.1152/ajpheart.00581.2008.
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Characterization of local and global contractile activities in the myocardium is essential for a better understanding of cardiac form and function. The spatial distribution of regions that contribute the most to cardiac function plays an important role in defining the pumping parameters of the myocardium like ejection fraction and dynamic aspects such as twisting and untwisting. In general, myocardium shortening, tangent to the wall, and ventricular wall thickening are important parameters that characterize the regional contribution within the myocardium to the global function of the heart. We have calculated these parameters using myocardium displacement fields, which were captured through the displacement-encoding with stimulated echoes (DENSE) MRI technique in three volunteers. High spatial resolution of the acquired data revealed transmural changes of thickening and tangential shortening with high fidelity in beating hearts. By filtering myocardium regions that showed a tangential shortening index of <0.23, we were able to identify the complete or a portion of a macrostructure composed of connected regions in the form of a helical bundle within the left ventricle mass. In this study, we present a representative case that shows the complete morphology of a helical myocardial band as well as two other cases that present ascending and descending portions of the helical myocardial band. Our observation of a helical functional band based on dynamics is in agreement with diffusion tensor MRI observations and gross dissection studies in the arrested heart.