Circadian dependence of microvascular obstruction during ST-segment elevation myocardial infarction

Bonfig, Nicole L; Soukup, Chase R; Shah, Ananya A; Davidson, Sarah J; Stanberry, Larissa; Okeson, Brynn; Traverse, Jay H.

doi:10.1016/j.ijcard.2022.07.012

Cited by 5 publications

(8 citation statements)

References 19 publications

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“…Обнаружено, что у пациентов с ОИМ и ЧКВ продолжительность ишемии миокарда и размер инфаркта являются основными детерминантами тяжелой степени МВО [12][13][14][15]. МВО обнаружена у 59 % пациентов с ИМпST и ЧКВ и трехчасовой ишемией [14].…”

Section: Introductionunclassified

“…При длительности ишемии 4-6 ч МВО выявлялась у 72 % пациентов с ИМпST и ЧКВ [14]. Размер инфаркта у пациентов с ИМпST и МВО был в 2 раза больше, чем у пациентов без МВО [12]. Следовательно, размер инфаркта и продолжительность ишемии являются предикторами развития МВО.…”

Section: Introductionunclassified

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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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Section: Introductionunclassified

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

Zavadovsky,

Mukhomedzyanov,

Maslov

et al. 2024

Sibirskij nauchnyj medicinskij zhurnal

View full text Add to dashboard Cite

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“…There is a correlation between TIMI evaluated angiographically and the MVO size measured by magnetic resonance imaging (MRI) [ 10 , 11 ]. In a study of patients with AMI and PCI it was found that the duration of cardiac ischemia and infarct size are major determinant of severe MVO [ 12 , 13 , 14 , 15 ]. MVO was found in 59% of patients with STEMI + PCI and a 3-h duration of ischemia [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

“…If the duration of ischemia was 4–6 h, MVO was found in 72% of patients with STEMI + PCI [ 13 ]. The MVO area was measured by MRI [ 12 , 14 ]. Infarct size in patients with STEMI and MVO was 2-fold larger than in patients without MVO [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

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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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Microvascular obstruction identifies a subgroup of patients who benefit from stem cell therapy following ST-elevation myocardial infarction

Davidson

Roncalli

Sürder

et al. 2023

American Heart Journal

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Circadian dependence of microvascular obstruction during ST-segment elevation myocardial infarction

Cited by 5 publications

References 19 publications

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

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

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

Microvascular obstruction identifies a subgroup of patients who benefit from stem cell therapy following ST-elevation myocardial infarction

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