In <scp>ST</scp>‐segment elevation myocardial infarction, the echocardiographic parameters of microvascular obstruction are not associated with left ventricular remodeling at five years of follow‐up

Dregoesc, Mihaela Ioana; Iancu, Adrian Corneliu; Ober, Camelia; Homorodean, Călin; Bălănescu, Şerban Mihai; Bolboacă, Sorana D.

doi:10.1111/echo.14371

Cited by 3 publications

(2 citation statements)

References 38 publications

(64 reference statements)

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“…However, Dregoesc et al . [ 89 ] could not find a relationship between post-infarction remodeling of the heart and MVO.…”

Section: The Pathogenesis Of Microvascular Obstruction Analysis Of Cl...mentioning

confidence: 99%

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data

Ryabov,

Vyshlov,

Maslov

et al. 2024

Rev. Cardiovasc. Med.

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Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41–50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn’t been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type channel blockers result in the long-term improvement of coronary blood flow in patients with MVO.

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“…However, Dregoesc et al . [ 89 ] could not find a relationship between post-infarction remodeling of the heart and MVO.…”

Section: The Pathogenesis Of Microvascular Obstruction Analysis Of Cl...mentioning

confidence: 99%

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data

Ryabov,

Vyshlov,

Maslov

et al. 2024

Rev. Cardiovasc. Med.

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“…Dregoesc и соавт. (2019) не смогли найти взаимосвязи между постинфарктным ремоделированием сердца и МВО [29].…”

Section: микроваскулярная обструкция и неблагоприятное постинфарктное...unclassified

Reperfusion cardiac injury. The role of microvascular obstruction

Ryabov

Popov

Вышлов

et al. 2023

SJCEM

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Microvascular obstruction (MVO) of coronary arteries increases the mortality rate and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). According to preliminary data platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. Many questions related to the pathogenesis of MVO remain unanswered. The role of endothelial cell damage in the formation of MVO in patients with AMI and PCI is unknown. It is unclear whether nitric oxide (NO) production reduces or decreases sensitivity of smooth muscle cells of coronary arteries to NO in patients with MVO. It was obtained only indirect evidence on the involvement of inflammation in the development of MVO. The role of ROS in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied.The significance of thromboxane A, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is unknown before. It was not obtained conclusive evidence on the involvement of coronary artery spasm in the development of MVO. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI was not performed. It is not clear whether endogenous adrenaline exacerbates MVO or, conversely, prevents MVO.

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The role of microvascular obstruction and intramyocardial hemorrhage in reperfusion injury to the heart

Zavadovsky,

Mukhomedzyanov,

Maslov

et al. 2024

Sibirskij nauchnyj medicinskij zhurnal

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Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41–50 % of patients with ST-segment elevation myocardial infarction and PCI and is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO, which is associated with infarct size, the duration of ischemia, and myocardial edema. However, there is no conclusive evidence that the latter plays an important role in the development of MVO. There is evidence that platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell dysfunction in MVO formation in patients with AMI and PCI remains under question. It is unclear whether nitric oxide production is decreased in patients with MVO. It was obtained only indirect evidence on the involvement of inflammation in the development of MVO. The role of reactive oxygen species, necroptosis and pyroptosis in the pathogenesis of MVO is also not studied. The participation of thromboxane A2, vasopressin, and prostacyclin in the formation of MVO is unknown. It was not obtained conclusive evidence on the involvement of coronary artery spasm in the development of MVO. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type Ca2+-channel blockers improves coronary blood flow in patients with MVO.

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In ST‐segment elevation myocardial infarction, the echocardiographic parameters of microvascular obstruction are not associated with left ventricular remodeling at five years of follow‐up

Cited by 3 publications

References 38 publications

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data

Reperfusion cardiac injury. The role of microvascular obstruction

The role of microvascular obstruction and intramyocardial hemorrhage in reperfusion injury to the heart

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