Acute Myocardial Injury: A Perspective on Lethal Reperfusion Injury

Jg, Kingma

doi:10.4172/2329-6607.1000216

Cited by 2 publications

(3 citation statements)

References 135 publications

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“…Myocardial ischemia initiates multiple changes in cardiomyocyte structure including marked swelling, development of contraction bands, mitochondrial calcification and membrane disruption; the pathobiology of cellular changes produced by ischemia have been characterized in earlier studies [6][7][8]. Different modes (apoptosis, autophagy, oncosis, and necrosis) of cellular injury have been described [9] and are discussed elsewhere [10]. The cardiomyocyte cytoskeleton (i.e.…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Acute Myocardial Infarction: Perspectives on Physiopathology of Myocardial Injury and Protective Interventions

Kingma¹

2021

Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions

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Diffuse coronary artery injury produces a host of physiopathological, structural and metabolic changes in cardiocytes that, if not rectified, result in significant loss of functional myocardium to cause cardiac contractile dysfunction. Restoration of blood perfusion to the infarct-related artery helps to limit the acute effects of myocardial infarction; however, cardiocyte injury may be exacerbated because of the restoration of blood perfusion to the ischemic zone (i.e. reperfusion injury). Various manifestations of reperfusion injury include no-reflow, myocardial stunning or hibernation and ventricular arrhythmias. Consequently, reperfusion of an infarct related artery is often viewed in the context of being a "double-edged sword." Pharmacologic and non-pharmacologic interventions have been investigated in pre-clinical and clinical studies in the hunt to develop strategies to protect cardiomyocytes against the long-term effects of ischemia, or delay development of necrosis (resulting from ischemia or reperfusion). This book chapter will update current thinking on cardioprotective strategies to improve clinical outcomes in patients with coronary artery disease.

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Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Acute Myocardial Infarction: Perspectives on Physiopathology of Myocardial Injury and Protective Interventions

Kingma¹

2021

Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions

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“…Уже давно в экспериментальных условиях [16] ОРИГИНАЛЬНЫЕ СТАТЬИ § ся в результате реперфузионного повреждения миокарда. С учетом значительного влияния реперфузии на размер инфаркта, появилась концепция смертельного реперфузионного повреждения (the concept of lethal reperfusion injury) [17]. Реперфузия приводит к активации многих сигнальных путей, которые независимо друг от друга способствуют как апоптотическому, так и некротическому повреждению ткани и, таким образом, уменьшают массу жизнеспособного миокарда [17].…”

Section: результаты и обсуждениеunclassified

“…и в не давних исследованиях[17] было показано, что около половины зоны некроза при ИМ развивает-Таблица 4. Частота развития острой СН по классификации Killip у пациентов с ОИМ…”

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Clinical and laboratory features of primary acute myocardial infarction in patients with obstructive and non-obstructive coronary atherosclerosis

et al. 2019

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According to the literature, 40-60% of patients with acute myocardial infarction (AMI) have obstructive multivessel coronary artery disease (CA) and 8.8% of patients have non-obstructive CA lesions. And it is around these two groups of patients that there are active discussions and disputes regarding the choice of optimal treatment tactics and further prognosis. The aim of the study was to study clinical and laboratory features of development and course of primary AMI in patients with multi-and single-vessel obstructive lesion of the CA compared with patients with non-obstructive CA lesions. Methods. The study has included patients hospitalized "through the ambulance channel" in the Department of cardiac intensive care of municipal clinical hospital named after S. S. Yudin Moscow with a diagnosis “primary acute myocardial infarction”, ACS with and without ST segment elevation, unstable angina in 2015-2016. The diagnosis of acute myocardial infarction (AMI) was established at the hospital stage according to the criteria of the "Third universal definition of myocardial infarction" in 2012. The study included 1240 patients who underwent coronary angiography (CAG) no later than 12 hours from the time of admission. The first group (comparison group) consisted of patients with AMI and the first detected multivessel obstructive atherosclerotic lesion of CA (664 patients), the second (interest group) consisted of patients with AMI and non-obstructive atherosclerotic lesion of CA (96 patients) meeting the MINOCA criteria. The third group consisted of patients with single-vessel obstructive lesion and complete acute occlusion of the CA (272 patients). Patients with hemodynamically significant lesions of the left CA trunk were not included in the study. The clinical and laboratory features of the course of acute primary myocardial infarction in patients with obstructive and non-obstructive coronary atherosclerosis were studied. The generally accepted statistical processing methods were used. A year after discharge from the hospital, 727 patients (468 patients from the 1st group, 78 from the 2nd group, 181 from the 3rd group) were interviewed by means of a structured telephone survey about the course of the disease (collection of medical history). The median follow-up was 12 months. (interquartile range 11-13 months). The endpoints were: re-hospitalization for any reason, re-coronary event, death. The received answers are entered into questionnaires and statistically processed. Results and conclusions. In patients with AMI and non-obstructive atherosclerotic CA lesion, pain behind the sternum is observed one and a half times less often (54.2%) than in patients with obstructive CA lesion (MOAPCA 86.1%, OAPCA 89.7%) and the cardiac co duction system is almost three times more likely to be affected ( 30% versus 8.4% and 12%). Only 12.5% of patients in this group had an abnormal Q wave (Q – myocardial infarction) on the ECG, therefore, a smaller volume of myocardial damage and a lower level of troponin than in patients of groups 1 and 3. During the first year after the development of AMI, patients with obstructive coronary atherosclerosis did not experience repeated coronary events, there were no indications for conducting CAG, PCI or CABG, in contrast to patients with obstructive lesion of CA. For multivascular obstruction (group 1), PCI was performed in 9.6% of patients and 3.8% of CABG. PCI was performed in group 3 with obstructive single-vessel lesion of CA in 7.7% of patients. In patients with AMI and obstructive single-vessel atherosclerotic lesion of CA (group 3), two and a half times less often (9.1%) myocardial reperfusion injury is observed, while in patients with multivascular obstructive CA defeat, this syndrome was observed in 21.3%.

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Acute Myocardial Injury: A Perspective on Lethal Reperfusion Injury

Cited by 2 publications

References 135 publications

Acute Myocardial Infarction: Perspectives on Physiopathology of Myocardial Injury and Protective Interventions

Acute Myocardial Infarction: Perspectives on Physiopathology of Myocardial Injury and Protective Interventions

Clinical and laboratory features of primary acute myocardial infarction in patients with obstructive and non-obstructive coronary atherosclerosis

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