Pharmacological protection of reperfusion injury in ST-segment elevation myocardial infarction. Gone with the wind?

Tonet, Elisabetta; Bernucci, Davide; Morciano, Giampaolo; Campo, Gianluca

doi:10.5114/aic.2018.74349

Cited by 6 publications

(6 citation statements)

References 15 publications

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“…A consequence of AS is ischemic heart disease (IHD), where the full or partial recovery of myocardial function is always difficult to achieve due to severe mitochondrial impairment [75,76]. Events consisting of I/R phases are accompanied by oxidative stress, pH changes, and cytosolic and mitochondrial Ca 2+ overload, which lead to the opening of the mitochondrial permeability transition pore complex (PTPC) and contribute to cardiomyocyte death [12,[77][78][79][80].…”

Section: Ischemic Heart Diseasementioning

confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

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Section: Ischemic Heart Diseasementioning

confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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“…Так, при увеличении времени до реваскуляризации более 3 ч от начала болевого синдрома у пациентов значительно увеличивался риск феномена no-reflow. Также высокий риск феномена no-reflow определялся в случаях, когда время от начала болевого синдрома до реваскуляризации составляло менее 1 ч. Несмотря на то что проведение максимально быстрой реваскуляризации инфаркт-связанной артерии является важнейшей задачей в лечении ОИМпST и позволяет значительно уменьшить зону инфаркта, ранняя реперфузия может увеличивать риск реперфузионного повреждения [13].…”

Section: Discussionunclassified

“…Нейтрофилы являются основным источником оксидантов, образующихся в миокарде после длительной ишемии. Инфильтрация тканей нейтрофилами и провоспалительными цитокинами характеризуется значительным усилением ишемического повреждения [13]. Кроме того, считает-ся, что скопление нейтрофилов и их последующая активация в месте эндотелиального повреждения являются первым звеном в формировании тромба в коронарной артерии.…”

Section: Discussionunclassified

Development of a risk score for no-reflow phenomenon after percutaneous coronary interventions in patients with ST-segment elevation myocardial infarction

Бессонов¹,

Кузнецов²,

Горбатенко³

et al. 2020

PKiK

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Background. No-reflow phenomenon during primary percutaneous coronary intervention (PCI) is a significant clinical problem in patients with ST-elevation myocardial infarction (STEMI), and its predictors remain unclear.Aim. To develop a scoring system to predict the risk of no-reflow in patients undergoing PCI for STEMI.Methods. Data were collected from 1280 consecutive patients with STEMI (59.2±11.4 years, 74.2% men, 5.2% no-reflow) who were admitted to the coronary care unit and underwent PCI. Baseline clinical, angiographic and procedural variables were used to develop the risk score in a training dataset (n=888, 70%) which was then validated in a test dataset (n=392, 30%). A credit risk assessment tool was used to construct a precise screening tool for no-reflow.Results. The model comprised age, pain to revascularisation time, neutrophil count, admission plasma glucose level, initial TIMI flow and direct stenting as the only independent predictors of no-reflow. These factors were weighted and used to develop a risk score ranging from 0 to 7. In the training dataset, the optimal threshold score for predicting no-reflow was ≥35, with 69% sensitivity and 81% specificity (area under the curve (AUC) = 0.84, p < 0.001). When these findings were applied to the test dataset, the AUC was 0.75 (p < 0.001), with 70% sensitivity and 80% specificity.Conclusion. The score developed in this study, based on clinical, angiographic and procedural features, can be used with acceptable accuracy to predict no-reflow in STEMI patients treated by PCI.Received 29 August 2019. Revised 25 March 2020. Accepted 16 April 2020.Funding: The study did not have sponsorship.Conflict of interest: Authors declare no conflict of interest.

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“…Hypoxia is a bio-clinical condition in which either portion or whole tissues are subjected to a significant imbalance between O 2 consumption and blood perfusion [ 149 ]. It is often associated with nutrient deprivation.…”

Section: Mitochondrial Dysfunction and Inflammation In Cvds And Cancermentioning

confidence: 99%

The Interplay of Hypoxia Signaling on Mitochondrial Dysfunction and Inflammation in Cardiovascular Diseases and Cancer: From Molecular Mechanisms to Therapeutic Approaches

Bouhamida

Morciano

Perrone

et al. 2022

Biology

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Cardiovascular diseases (CVDs) and cancer continue to be the primary cause of mortality worldwide and their pathomechanisms are a complex and multifactorial process. Insufficient oxygen availability (hypoxia) plays critical roles in the pathogenesis of both CVDs and cancer diseases, and hypoxia-inducible factor 1 (HIF-1), the main sensor of hypoxia, acts as a central regulator of multiple target genes in the human body. Accumulating evidence demonstrates that mitochondria are the major target of hypoxic injury, the most common source of reactive oxygen species during hypoxia and key elements for inflammation regulation during the development of both CVDs and cancer. Taken together, observations propose that hypoxia, mitochondrial abnormality, oxidative stress, inflammation in CVDs, and cancer are closely linked. Based upon these facts, this review aims to deeply discuss these intimate relationships and to summarize current significant findings corroborating the molecular mechanisms and potential therapies involved in hypoxia and mitochondrial dysfunction in CVDs and cancer.

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Pharmacological protection of reperfusion injury in ST-segment elevation myocardial infarction. Gone with the wind?

Cited by 6 publications

References 15 publications

Mitophagy in Cardiovascular Diseases

Mitophagy in Cardiovascular Diseases

Development of a risk score for no-reflow phenomenon after percutaneous coronary interventions in patients with ST-segment elevation myocardial infarction

The Interplay of Hypoxia Signaling on Mitochondrial Dysfunction and Inflammation in Cardiovascular Diseases and Cancer: From Molecular Mechanisms to Therapeutic Approaches

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