Background: We investigated an impact of the presence of chronic total coronary occlusion (CTO) in a non-infarct related coronary artery on microvascular reperfusion in patients with a first anterior ST-segment elevation myocardial infarction (STEMI) who underwent percutaneous coronary intervention (PCI).
Methods: In accordance with the presence or absence of CTO in a non-infarct related coronary artery, we analyzed Thrombolysis in Myocardial Infarction myocardial perfusion (TMP) grade on a scale of 0 to 3, with higher scores indicating better perfusion, and ST-segment resolution in sum of lead I, aVL, and V1 through V6 to evaluate microvascular reperfusion in a total of 140 consecutive patients with a first anterior STEMI.
Results: We identified CTO in 15 patients (11% of total). The incidence of impaired microvascular reperfusion was greater in patients with CTO vs without CTO, defined as TMP grades 0 or 1 together with <30% ST-segment resolution (33% vs 6%, respectively; P=.0006) and the enzymatic infarct was larger (10304 ± 8060 IU/L vs 6804 ± 4959 IU/L; P=.009). Logistic regression analysis revealed that CTO is closely associated with incidental impaired microvascular reperfusion (odds ratio, 6.801; 95% confidence interval, 1.284-36.209; P=.024).
Conclusion: The presence of CTO in a non-infarct related coronary artery might confer a considerable disadvantage upon microvascular reperfusion and result in adverse clinical outcomes of PCI for a first anterior STEMI.
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Front Biosci (Landmark Ed)
January 2025
Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, 401336 Chongqing, China.
Background: Myocardial ischemia-reperfusion (I/R) injury and coronary microcirculation dysfunction (CMD) are observed in patients with myocardial infarction after vascular recanalization. The antianginal drug trimetazidine has been demonstrated to exert a protective effect in myocardial ischemia-reperfusion injury.
Objectives: This study aimed to investigate the role of trimetazidine in endothelial cell dysfunction caused by myocardial I/R injury and thus improve coronary microcirculation.
J Clin Med
January 2025
Montefiore-Einstein Center for Heart and Vascular Care, Montefiore Medical Center, Albert Einstein College of Medicine, 111 East 210th Street, Bronx, New York, NY 10467, USA.
Primary percutaneous coronary intervention (PCI) has revolutionized the management of ST-elevation myocardial infarction (STEMI), markedly improving patient outcomes. Despite technological advancements, pharmacological innovations, and refined interventional techniques, STEMI prognosis remains burdened by a persistent incidence of cardiac death and heart failure (HF), with mortality rates plateauing over the last decade. This review examines current practices in primary PCI, focusing on critical factors influencing patient outcomes.
View Article and Find Full Text PDFJ Mol Neurosci
January 2025
Department of Special Examination, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, No. 305 Tianmushan Road, Hangzhou City, 310013, Zhejiang, China.
Cerebral ischemia-reperfusion injury (CIRI), which stays unresolved in the clinic, occurs after recanalization of blood vessels serving brain tissues in acute ischemic stroke patients and can result in massive brain cell death, and cell ferroptosis contributes greatly to this process. Our research firstly found that TNFSF9 expression harbored diagnostic value on CIRI patients and intended to further investigate its regulatory mechanism in CIRI, which might facilitate its diagnostic and therapeutic application in the clinic. The level of TNSF9 mRNA was augmented in the plasma of CIR patients, and its silence impeded ferroptosis, apoptosis, and release of inflammatory mediators of BMECs with OGD/R treatment.
View Article and Find Full Text PDFCell Biochem Biophys
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Department of Pain, Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
This study aimed to observe the mechanism of hydrogen (H) in a lung transplantation model simulated by pulmonary microvascular endothelial cells (PMVECs), which were divided into 5 groups. The blank group was the normal PMVECs. During cold ischemia period, PMVECs in the control, O, or H groups were aerated with no gas, O, or 3% H, and 3% H after transfected with a small interfering RNA targeting Nrf2 in the H+si-Nrf2 group.
View Article and Find Full Text PDFCurr Issues Mol Biol
January 2025
Institute of Experimental Medicine, Almazov National Medical Research Centre, 15B Parkhomenko Street, 194021 Saint Petersburg, Russia.
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase (MLCK)-dependent endothelial hyperpermeability, which is considered a preventable cause of reperfusion injury. In the present study, a single intravenous injection of MLCK peptide inhibitor PIK7 (2.
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