Randomized trial of intracoronary adenosine as adjunctive therapy for prevention of the no-reflow phenomenon

Naghshtabrizi, Nima; Sajedi, Manijeh; Naghshtabrizi, Behshad; Mozayanimonfared, Azadeh; Seifrabiei, Mohammad Ali; Kanonisabet, Ali

doi:10.1097/mca.0000000000000863

Cited by 3 publications

(2 citation statements)

References 6 publications

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“…Intracoronary administration of adenosine reduced the incidence of MVO in patients with AMI treated by PCI [ 108 ] , which suggests that adenosine may alleviate MVO.…”

Section: Triggers and Modulators Of Mvo: Analysis Of Clinical Datamentioning

confidence: 99%

“…Can adenosine reduce the incidence of MVO? As Naghshtabrizi et al reported, intracoronary administration of adenosinehave could reduce the incidence of MVO in AMI patients and PCI [ 108 ] . However, Niccoli et al found that intracoronary administration of adenosine had no effect on the incidence of MVO in STEMI patients ( n = 160) underwent PCI [ 117 ] .…”

Section: Treatment For Microvascular Obstructionmentioning

confidence: 99%

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A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena

Maslov¹,

Naryzhnaya²,

Popov³

et al. 2023

J Biomed Res

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The analysis of experimental data demonstrates that platelets and neutrophils are involved in the no-reflow phenomenon, also known as microvascular obstruction (MVO). However, studies performed in the isolated perfused hearts subjected to ischemia/reperfusion (I/R) do not suggest the involvement of microembolization and microthrombi in this phenomenon. The intracoronary administration of alteplase has been found to have no effect on the occurrence of MVO in patients with acute myocardial infarction. Consequently, the major events preceding the appearance of MVO in coronary arteries are independent of microthrombi, platelets, and neutrophils. Endothelial cells appear to be the target where ischemia can disrupt the endothelium-dependent vasodilation of coronary arteries. However, reperfusion triggers more pronounced damage, possibly mediated by pyroptosis. MVO and intra-myocardial hemorrhage contribute to the adverse post-infarction myocardial remodeling. Therefore, pharmacological agents used to treat MVO should prevent endothelial injury and induce relaxation of smooth muscles. Ischemic conditioning protocols have been shown to prevent MVO, with L-type Ca 2+ channel blockers appearing the most effective in treating MVO.

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“…Intracoronary administration of adenosine reduced the incidence of MVO in patients with AMI treated by PCI [ 108 ] , which suggests that adenosine may alleviate MVO.…”

Section: Triggers and Modulators Of Mvo: Analysis Of Clinical Datamentioning

confidence: 99%

Section: Treatment For Microvascular Obstructionmentioning

confidence: 99%

A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena

Maslov¹,

Naryzhnaya²,

Popov³

et al. 2023

J Biomed Res

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Adenosine as adjunctive therapy in acute coronary syndrome: a meta-analysis of randomized controlled trials

Laborante

Bianchini

Restivo

et al. 2022

European Heart Journal - Cardiovascular Pharmacotherapy

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Aim Adenosine has been tested in several randomized controlled trials (RCTs) to minimize the incidence of coronary microvascular obstruction (CMVO). The aim of the present study was to pool all the RCTs comparing intracoronary or intravenous adenosine versus placebo in patients with acute coronary syndrome (ACS) undergoing myocardial revascularization. Methods and results PubMed and Scopus electronic databases were scanned for eligible studies up to June 5th 2022. A total of 26 RCTs with 5843 patients were included. Efficacy endpoints were major adverse cardiac events (MACE), all-cause-death, non-fatal myocardial infarction and heart failure. Atrioventricular blocks and ventricular fibrillation/sustained ventricular tachycardia (VF/SVT) were the safety endpoints. Myocardial blush grade, Thrombolysis In Myocardial Infarction (TIMI) flow grade, left ventricular ejection fraction (LVEF), infarct size, and ST-segment resolution were also assessed. Adenosine administration was not associated with any clinical benefit in terms of MACE, all-cause death, non-fatal myocardial infarction, and heart failure. However, adenosine was associated with an increased rate of advanced atrioventricular blocks and of VF/SVT in studies with total mean ischemic time > 3 hours, compared to placebo. Remarkably, among patients undergoing percutaneous coronary intervention, adenosine was associated with reduced myocardial blush grade 0–1 and TIMI flow grade 0–2, compared to placebo. Furthermore, adenosine did not show favourable effects on LVEF and infarct size. Conclusion Adenosine infusion, as adjunctive therapy in ACS, was associated with an increased risk of advanced atrioventricular blocks and increased rates of adenosine-triggered ventricular arrhythmias in patients with long ischemic time, without providing any clinical benefit compared to placebo.

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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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Randomized trial of intracoronary adenosine as adjunctive therapy for prevention of the no-reflow phenomenon

Cited by 3 publications

References 6 publications

A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena

A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena

Adenosine as adjunctive therapy in acute coronary syndrome: a meta-analysis of randomized controlled trials

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

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