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Journal articles on the topic 'Myocardial infarction - Pathophysiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Skyschally, Andreas, Rainer Schulz, and Gerd Heusch. "Pathophysiology of Myocardial Infarction." Herz Kardiovaskuläre Erkrankungen 33, no. 2 (2008): 88–100. http://dx.doi.org/10.1007/s00059-008-3101-9.

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2

Burke, Allen P., and Renu Virmani. "Pathophysiology of Acute Myocardial Infarction." Medical Clinics of North America 91, no. 4 (2007): 553–72. http://dx.doi.org/10.1016/j.mcna.2007.03.005.

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3

Peate, Ian, and Noleen Jones. "Pathophysiology series 2: acute myocardial infarction." British Journal of Healthcare Assistants 8, no. 5 (2014): 214–19. http://dx.doi.org/10.12968/bjha.2014.8.5.214.

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4

Alpert, Joseph S. "The Pathophysiology of Acute Myocardial Infarction." Cardiology 76, no. 2 (1989): 85–95. http://dx.doi.org/10.1159/000174479.

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5

Smit, Marli, A. R. Coetzee, and A. Lochner. "The Pathophysiology of Myocardial Ischemia and Perioperative Myocardial Infarction." Journal of Cardiothoracic and Vascular Anesthesia 34, no. 9 (2020): 2501–12. http://dx.doi.org/10.1053/j.jvca.2019.10.005.

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6

Hasta, Felicia. "A Patient Developing Both Myocardial Infarction and Stroke after COVID-19 Pneumonia." Clinical Cardiology and Cardiovascular Interventions 4, no. 11 (2021): 01–04. http://dx.doi.org/10.31579/2641-0419/181.

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We herein report an unusual case of a patient developing both cardiovascular and cerebrovascular sequelae to COVID-19 pneumonia. While COVID patients have been reported to experience one or the other, there has been little discussion of the presentation and pathophysiology of a patient presenting with injury to both organ systems. This article will consider the pathophysiology common to cardiovascular and cerebrovascular injury in the setting of COVID as well mechanisms that affect each system separately. It also discusses useful investigations which may assist in diagnosis and treatment of pa

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7

Gill, John. "The Pathophysiology and Epidemiology of Myocardial Infarction." Drugs 42, Supplement 2 (1991): 1–7. http://dx.doi.org/10.2165/00003495-199100422-00003.

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8

Biccard, B. M., and R. N. Rodseth. "The pathophysiology of peri-operative myocardial infarction." Anaesthesia 65, no. 7 (2010): 733–41. http://dx.doi.org/10.1111/j.1365-2044.2010.06338.x.

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9

Struthers, A. D. "Pathophysiology of heart failure following myocardial infarction." Heart 91, suppl_2 (2005): ii14—ii16. http://dx.doi.org/10.1136/hrt.2005.062034.

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10

Cabin, Henry S. "The Pathophysiology of Right Ventricular Myocardial Infarction." Journal of Intensive Care Medicine 1, no. 5 (1986): 241–42. http://dx.doi.org/10.1177/088506668600100501.

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11

Alekseeva, Ya V., E. V. Vyshlov, V. Yu Ussov, and V. A. Markov. "MICROVASCULAR INJURY PHENOMENA IN MYOCARDIAL INFARCTION." Siberian Medical Journal 33, no. 4 (2019): 19–26. http://dx.doi.org/10.29001/2073-8552-2018-33-4-19-26.

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At a time of a wide use of coronary reperfusion for treatment of acute myocardial infarction, the microvascular phenomena significantly affecting the postinfarction state of the myocardium have been discovered. These phenomena include microvascular obstruction with a clinical presentation in the form of the no-reflow phenomenon and intramyocardial hemorrhage that strongly aggravate cardiac damage. The aim of this review was to analyze accumulated data on the prevalence, pathophysiology, diagnostic modalities, and approaches for prevention and treatment of microvascular injury.

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12

Lechner, Ivan, Martin Reindl, Bernhard Metzler, and Sebastian J. Reinstadler. "Predictors of Long-Term Outcome in STEMI and NSTEMI—Insights from J-MINUET." Journal of Clinical Medicine 9, no. 10 (2020): 3166. http://dx.doi.org/10.3390/jcm9103166.

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13

Yoshimura, Chikashi, Akiomi Nagasaka, Hitoshi Kurose, and Michio Nakaya. "Efferocytosis during myocardial infarction." Journal of Biochemistry 168, no. 1 (2020): 1–6. http://dx.doi.org/10.1093/jb/mvaa051.

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Abstract Myocardial infarction is one of the major causes of death worldwide. Many heart cells die during myocardial infarction through various processes such as necrosis, apoptosis, necroptosis, autophagy-related cell death, pyroptosis and ferroptosis. These dead cells in infarcted hearts expose the so-called ‘eat-me’ signals, such as phosphatidylserine, on their surfaces, enhancing their removal by professional and non-professional phagocytes. Clearance of dead cells by phagocytes in the diseased hearts plays a crucial role in the pathology of myocardial infarction by inhibiting the inflamma

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14

Kaier, Thomas E., Bashir Alaour, and Michael Marber. "Cardiac troponin and defining myocardial infarction." Cardiovascular Research 117, no. 10 (2021): 2203–15. http://dx.doi.org/10.1093/cvr/cvaa331.

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Abstract The 4th Universal Definition of Myocardial Infarction has stimulated considerable debate since its publication in 2018. The intention was to define the types of myocardial injury through the lens of their underpinning pathophysiology. In this review, we discuss how the 4th Universal Definition of Myocardial Infarction defines infarction and injury and the necessary pragmatic adjustments that appear in clinical guidelines to maximize triage of real-world patients.

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15

Tibaut, Miha, Dusan Mekis, and Daniel Petrovic. "Pathophysiology of Myocardial Infarction and Acute Management Strategies." Cardiovascular & Hematological Agents in Medicinal Chemistry 14, no. 3 (2017): 150–59. http://dx.doi.org/10.2174/1871525714666161216100553.

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16

Aymong, Eve D., Krishnan Ramanathan, and Christopher E. Buller. "Pathophysiology of Cardiogenic Shock Complicating Acute Myocardial Infarction." Medical Clinics of North America 91, no. 4 (2007): 701–12. http://dx.doi.org/10.1016/j.mcna.2007.03.006.

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17

Gabriel-Costa, Daniele. "The pathophysiology of myocardial infarction-induced heart failure." Pathophysiology 25, no. 4 (2018): 277–84. http://dx.doi.org/10.1016/j.pathophys.2018.04.003.

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18

Kakouros, N., and D. V. Cokkinos. "Right ventricular myocardial infarction: pathophysiology, diagnosis, and management." Postgraduate Medical Journal 86, no. 1022 (2010): 719–28. http://dx.doi.org/10.1136/pgmj.2010.103887.

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19

Cheng, Judy W. M. "Recognition, pathophysiology, and management of acute myocardial infarction." American Journal of Health-System Pharmacy 58, no. 18 (2001): 1709–18. http://dx.doi.org/10.1093/ajhp/58.18.1709.

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20

Gualandro, Danielle Menosi, Daniela Calderaro, and Bruno Caramelli. "Controversies regarding the pathophysiology of perioperative myocardial infarction." Catheterization and Cardiovascular Interventions 81, no. 4 (2013): 744. http://dx.doi.org/10.1002/ccd.24631.

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21

de Laat, Bas, Philip G. de Groot, Ronald H. W. M. Derksen, et al. "Association between beta2-glycoprotein I plasma levels and the risk of myocardial infarction in older men." Blood 114, no. 17 (2009): 3656–61. http://dx.doi.org/10.1182/blood-2009-03-212910.

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Abstract von Willebrand factor (VWF) serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2-glycoprotein I is able to inhibit platelet binding to VWF, indicating a role in the pathophysiology of arterial thrombosis. In the present study, we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. We have measured beta2-glycoprotein I and VWF antigen levels in 539 men with a first myocardial infarction and in 611 control subjects. Although we did not find a profound effect of beta2-glyco

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22

Scalone, Giancarla, Giampaolo Niccoli, and Filippo Crea. "Editor’s Choice- Pathophysiology, diagnosis and management of MINOCA: an update." European Heart Journal: Acute Cardiovascular Care 8, no. 1 (2018): 54–62. http://dx.doi.org/10.1177/2048872618782414.

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Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a syndrome with different causes, characterised by clinical evidence of myocardial infarction with normal or near-normal coronary arteries on angiography. Its prevalence ranges between 5% and 25% of all myocardial infarction. The prognosis is extremely variable, depending on the cause of MINOCA. The key principle in the management of this syndrome is to clarify the underlying individual mechanisms to achieve patient-specific treatments. Clinical history, electrocardiogram, cardiac enzymes, echocardiography, coronary angio

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23

Habib, Mohammed. "Cardio-Cerebral Infarction Syndrome: An Overview." International Journal of Clinical Case Reports and Reviews 8, no. 1 (2021): 01–10. http://dx.doi.org/10.31579/2690-4861/140.

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Acute ischemic stroke and coronary artery disease are the major causes of death in Palestine and in the world. The prevalence of coronary artery disease has been reported in one fifth of stroke patients. Although high incidence rate of acute myocardial infarction after recent ischemic stroke and the high risk of acute ischemic stroke after recent myocardial infarction has been reported in several clinical or observational studies. So that acute or recent problem in the heart or brain that could result in an acute infarction of the other. In this review we describe the definition and new classi

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24

Pepine, Carl J. "New concepts in the pathophysiology of acute myocardial infarction." American Journal of Cardiology 64, no. 4 (1989): 2B—8B. http://dx.doi.org/10.1016/s0002-9149(89)80002-5.

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25

Landesberg, Giora. "The pathophysiology of perioperative myocardial infarction: Facts and perspectives." Journal of Cardiothoracic and Vascular Anesthesia 17, no. 1 (2003): 90–100. http://dx.doi.org/10.1053/jcan.2003.18.

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26

Duvall, W. Lane, Brett Sealove, Chetan Pungoti, Daniel Katz, Pedro Moreno, and Michael Kim. "Angiographic investigation of the pathophysiology of perioperative myocardial infarction." Catheterization and Cardiovascular Interventions 80, no. 5 (2012): 768–76. http://dx.doi.org/10.1002/ccd.23446.

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27

Brener, Sorin J. "Insights into the pathophysiology of ST-elevation myocardial infarction." American Heart Journal 151, no. 6 (2006): S4—S10. http://dx.doi.org/10.1016/j.ahj.2006.04.007.

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28

Werf, Y. D. Van Der, M. J. L. De Jongste, and G. J. Ter Horst. "The immune system mediates blood-brain barrier damage; possible implications for pathophysiology of neuropsychiatric illnesses." Acta Neuropsychiatrica 7, no. 4 (1995): 114–21. http://dx.doi.org/10.1017/s0924270800037315.

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SummaryIn this investigation the effects of immune activation on the brain are characterized. In order to study this, we used a model for chronic immune activation, the myocardial infarction, and intravenous injections with the pro-inflammatory cytokine Tumour Necrosis Factor alpha (TNF-α). The incentive for this study is the observation that myocardial infarction is accompanied by behavioural and neuronal abnormalities. The effects of myocardial infarction on the brain and its functioning are widespread. In order to examine the mechanism through which this interaction occurs, a group of rats

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29

Bhindi, Ravinay, Paul Witting, Aisling McMahon, Levon Khachigian, and Harry Lowe. "Rat models of myocardial infarction." Thrombosis and Haemostasis 96, no. 11 (2006): 602–10. http://dx.doi.org/10.1160/th05-07-0514.

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SummaryAnimal models of cardiovascular pathology contribute towards understanding and treatment of a broad range of conditions. Specifically in the context of acute myocardial infarction (AMI), rat models have been commonly used in studies of pathogenesis, investigation and novel therapies, although there has often been difficulty in translating experimental findings to clinical benefit. However, recent years have seen two important changes to our clinical approaches to AMI. First, there is increasing recognition that the pathophysiology of human AMI is a process occurring at many levels, not

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30

Carrick, David, Caroline Haig, Sam Rauhalammi, et al. "PATHOPHYSIOLOGY OF MYOCARDIAL REMODELING IN SURVIVORS OF ST-ELEVATION MYOCARDIAL INFARCTION: INFLAMMATION, REMOTE MYOCARDIUM AND PROGNOSIS." Journal of the American College of Cardiology 65, no. 10 (2015): A172. http://dx.doi.org/10.1016/s0735-1097(15)60172-3.

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31

Fuentes, Eduardo, Rodrigo Moore-Carrasco, Antonio Marcus de Andrade Paes, and Andres Trostchansky. "Role of Platelet Activation and Oxidative Stress in the Evolution of Myocardial Infarction." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 6 (2019): 509–20. http://dx.doi.org/10.1177/1074248419861437.

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Myocardial infarction, commonly known as heart attack, evolves from the rupture of unstable atherosclerotic plaques to coronary thrombosis and myocardial ischemia–reperfusion injury. A body of evidence supports a close relationship between the alterations following an ischemia–reperfusion injury-induced oxidative stress and platelet activity. Through their critical role in thrombogenesis and inflammatory responses, platelets are fully (totally) implicated from atherothrombotic plaque formation to myocardial infarction onset and expansion. However, mere platelet aggregation prevention does not

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32

Mada, Razvan O., Horia Rosianu, Cristina Mada, and Adrian C. Iancu. "Heart rhythm disorders and myocardial remodeling in patients with ST-segment elevation acute myocardial infarction." Romanian Journal of Cardiology 30, no. 2 (2020): 167–72. http://dx.doi.org/10.47803/rjc.2020.30.2.167.

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Acute myocardial infarction is a potential life threatening disease spread all over the world. The continuing progress of medical and interventional therapies requires a comprehensive understanding of the underlying pathophysiology. Moreover, the potential development of heart failure or/and arrhythmias in either acute or chronic setting, demand a deep knowledge of their molecular mechanisms in order to provide adequate treatments. This review aims to summarize the current data regarding the etiopathogenesis of acute myocardial infarction and the heart rhythm disorders associated with this cli

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33

Goldbergova, M. Pavkova, J. ipkova, J. Fedorko, et al. "MicroRNAs in pathophysiology of acute myocardial infarction and cardiogenic shock." Bratislava Medical Journal 119, no. 06 (2018): 341–47. http://dx.doi.org/10.4149/bll_2018_064.

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34

Doering, Lynn V. "Pathophysiology of Acute Coronary Syndromes Leading to Acute Myocardial Infarction." Journal of Cardiovascular Nursing 13, no. 3 (1999): 1–20. http://dx.doi.org/10.1097/00005082-199904000-00002.

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35

Pitts, William R., Richard A. Lange, Joaquin E. Cigarroa, and L. David Hillis. "Cocaine-induced myocardial ischemia and infarction: Pathophysiology, recognition, and management." Progress in Cardiovascular Diseases 40, no. 1 (1997): 65–76. http://dx.doi.org/10.1016/s0033-0620(97)80023-0.

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36

Lucreziotti, Stefano, Francesca Carletti, Giulia Santaguida, and Cesare Fiorentini. "Myocardial Infarction in Major Noncardiac Surgery: Epidemiology, Pathophysiology and Prevention." Heart International 2, no. 2 (2006): 182618680600200. http://dx.doi.org/10.1177/182618680600200203.

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37

Gibson, R. S. "Non-Q-Wave Myocardial Infarction: Pathophysiology, Prognosis, and Therapeutic Strategy." Annual Review of Medicine 40, no. 1 (1989): 395–410. http://dx.doi.org/10.1146/annurev.me.40.020189.002143.

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38

Cohn, Jay N., and Wilson Colucci. "Cardiovascular Effects of Aldosterone and Post–Acute Myocardial Infarction Pathophysiology." American Journal of Cardiology 97, no. 10 (2006): 4–12. http://dx.doi.org/10.1016/j.amjcard.2006.03.004.

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39

Ge, Feixiang, Zetian Wang, and Jianzhong Jeff Xi. "Engineered Maturation Approaches of Human Pluripotent Stem Cell-Derived Ventricular Cardiomyocytes." Cells 9, no. 1 (2019): 9. http://dx.doi.org/10.3390/cells9010009.

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Heart diseases such as myocardial infarction and myocardial ischemia are paroxysmal and fatal in clinical practice. Cardiomyocytes (CMs) differentiated from human pluripotent stem cells provide a promising approach to myocardium regeneration therapy. Identifying the maturity level of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) is currently the main challenge for pathophysiology and therapeutics. In this review, we describe current maturity indicators for cardiac microtissue and microdevice cultivation technologies that accelerate cardiac maturation. It may provide insights in

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40

Nagoor Meeran, M. F., Sheikh Azimullah, Farah Laham та ін. "α-Bisabolol protects against β-adrenergic agonist-induced myocardial infarction in rats by attenuating inflammation, lysosomal dysfunction, NLRP3 inflammasome activation and modulating autophagic flux". Food & Function 11, № 1 (2020): 965–76. http://dx.doi.org/10.1039/c9fo00530g.

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41

Zekios, Konstantinos C., Eleni-Taxiarchia Mouchtouri, Panagiotis Lekkas, Dimitrios N. Nikas, and Theofilos M. Kolettis. "Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?" Journal of Cardiovascular Development and Disease 8, no. 5 (2021): 57. http://dx.doi.org/10.3390/jcdd8050057.

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Myocardial infarction often leads to progressive structural and electrophysiologic remodeling of the left ventricle. Despite the widespread use of β-adrenergic blockade and implantable defibrillators, morbidity and mortality from chronic-phase ventricular tachyarrhythmias remains high, calling for further investigation on the underlying pathophysiology. Histological and functional studies have demonstrated extensive alterations of sympathetic nerve endings at the peri-infarct area and flow-innervation mismatches that create a highly arrhythmogenic milieu. Such accumulated evidence, along with

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42

Serdechnaya, A. Yu, and I. A. Sukmanova. "Modern approaches to the diagnosis and treatment of cardiogenic shock complicating acute myocardial infarction." Cardiovascular Therapy and Prevention 19, no. 5 (2020): 2661. http://dx.doi.org/10.15829/1728-8800-2020-2661.

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Cardiogenic shock (CS) is the most severe complication of myocardial infarction, manifested by an acute tissue hypoperfusion as a result of impaired contractile function of the heart. CS occupies a leading place in the patterns of mortality in patients with myocardial infarction, despite all the advances in medicine. This review presents a modern classification of CS and a risk assessment score, considers the main aspects of epidemiology and pathophysiology of CS, discusses issues of its diagnosis and treatment.

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43

Le Manach, Yannick, Azriel Perel, Pierre Coriat, Gilles Godet, Michèle Bertrand, and Bruno Riou. "Early and Delayed Myocardial Infarction after Abdominal Aortic Surgery." Anesthesiology 102, no. 5 (2005): 885–91. http://dx.doi.org/10.1097/00000542-200505000-00004.

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Background Although postoperative myocardial infarction (PMI) after vascular surgery has been described to be associated with prolonged ischemia, its exact pathophysiology remains unclear. Methods The authors used intense cardiac troponin I (cTnI) surveillance after abdominal aortic surgery in 1,136 consecutive patients to better evaluate the incidence and timing of PMI (cTnI &gt; or = 1.5 ng/ml) or myocardial damage (abnormal cTnI &lt; 1.5 ng/ml). Results Abnormal cTnI concentrations was noted in 163 patients (14%), of which 106 (9%) had myocardial damage and 57 (5%) had PMI. In 34 pa

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44

Al-Hussaini, Abtehale, Ahmed M. S. E. K. Abdelaty, Gaurav S. Gulsin, et al. "Chronic infarct size after spontaneous coronary artery dissection: implications for pathophysiology and clinical management." European Heart Journal 41, no. 23 (2020): 2197–205. http://dx.doi.org/10.1093/eurheartj/ehz895.

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Abstract Aims To report the extent and distribution of myocardial injury and its impact on left ventricular systolic function with cardiac magnetic resonance imaging (CMR) following spontaneous coronary artery dissection (SCAD) and to investigate predictors of myocardial injury. Methods and results One hundred and fifty-eight angiographically confirmed SCAD-survivors (98% female) were phenotyped by CMR and compared in a case–control study with 59 (97% female) healthy controls (44.5 ± 8.4 vs. 45.0 ± 9.1 years). Spontaneous coronary artery dissection presentation was with non-ST-elevation myocar

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45

Zhao, Zhuo, Wei Sun, Ziyuan Guo, Bin Liu, Hongyu Yu, and Jichang Zhang. "Long Noncoding RNAs in Myocardial Ischemia-Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2021 (April 5, 2021): 1–15. http://dx.doi.org/10.1155/2021/8889123.

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Following an acute myocardial infarction, reperfusion therapy is currently the most effective way to save the ischemic myocardium; however, restoring blood flow may lead to a myocardial ischemia-reperfusion injury (MIRI). Recent studies have confirmed that long-chain noncoding RNAs (LncRNAs) play important roles in the pathophysiology of MIRIs. These LncRNA-mediated roles include cardiomyocyte apoptosis, autophagy, necrosis, oxidative stress, inflammation, mitochondrial dysfunction, and calcium overload, which are regulated through the expression of target genes. Thus, LncRNAs may be used as c

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46

Ogawa, Satoshi. "Pathophysiology of Ventricular Fibrillation in the Canine Model of Myocardial Infarction." Japanese Journal of Electrocardiology 37, no. 4 (2017): 295–306. http://dx.doi.org/10.5105/jse.37.295.

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47

Dawood, Moniz M., Dinesh K. Gutpa, James Southern, Ann Walia, James B. Atkinson, and Kim A. Eagle. "Pathology of fatal perioperative myocardial infarction: implications regarding pathophysiology and prevention." International Journal of Cardiology 57, no. 1 (1996): 37–44. http://dx.doi.org/10.1016/s0167-5273(96)02769-6.

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48

Montecucco, Fabrizio, Federico Carbone, and Thomas H. Schindler. "Pathophysiology of ST-segment elevation myocardial infarction: novel mechanisms and treatments." European Heart Journal 37, no. 16 (2015): 1268–83. http://dx.doi.org/10.1093/eurheartj/ehv592.

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49

Uretsky, Barry F. "Pathophysiology and prognosis: The curious case of the periprocedural myocardial infarction." Catheterization and Cardiovascular Interventions 81, no. 6 (2013): 968–69. http://dx.doi.org/10.1002/ccd.24933.

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50

Modesti, Pietro Amedeo, Ignazio Simonetti, and Giuseppe Olivo. "Perioperative myocardial infarction in non-cardiac surgery. Pathophysiology and clinical implications." Internal and Emergency Medicine 1, no. 3 (2006): 177–86. http://dx.doi.org/10.1007/bf02934735.

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