The rapid restoration of coronary flow to the jeopardized myocardium has become an essential part of therapy after acute myocardial infarction. Despite an open infarct-related artery, breakdown of or obstruction to coronary microvasculature can markedly reduce blood flow to the infarct zone. This effect is known as the no-reflow phenomenon. Advances in imaging modalities have improved visualization of no reflow, showing its frequency to be higher than was estimated by clinical judgment alone. This phenomenon is important because it correlates with infarct size and provides useful prognostic information. No reflow is associated with reduced left ventricular ejection fraction, left ventricular remodeling, and poor clinical outcomes, placing patients with this effect in a high-risk group among reperfused patients. The focus of reperfusion therapy is shifting towards improved myocardial perfusion, which could promote functional recovery of viable muscle, reduce infarct expansion, and increase the delivery of blood-borne components, thereby accelerating the healing process. Various pharmacologic interventions and catheter-based devices to retrieve embolic materials have been proposed. Further studies to improve understanding of the pathophysiology of microvascular dysfunction will, however, help in the further development of preventive and therapeutic strategies. In this article, I discuss in depth the data available on the no-reflow phenomenon.
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http://dx.doi.org/10.1038/ncpcardio0632 | DOI Listing |
Medicine (Baltimore)
January 2025
Zhengzhou Central Hospital Affiliated to Zhengzhou University, Henan, China.
Inflammatory responses and lipid metabolism disorders are key components in the development of coronary artery disease and contribute to no-reflow after coronary intervention. This study aimed to investigate the association between the neutrophil to high-density lipoprotein ratio (NHR) and no-reflow phenomenon in ST-segment elevation myocardial infarction (STEMI) patients after primary percutaneous coronary intervention (PPCI). This study enrolled 288 patients with STEMI from September 1st, 2022 to February 29th, 2024, in the Zhengzhou Central Hospital Affiliated to Zhengzhou University.
View Article and Find Full Text PDFActa Cardiol
January 2025
Cardiology Department, Bakırköy Dr. Sadi Konuk Training and Research Hospital, University of Health Sciences Turkey, Istanbul, Turkey.
Background: The present study aimed to investigate whether newly defined serum uric acid (SUA) to serum creatinine ratio (SUA/SCr) predicts no-reflow phenomenon (NRP) development in patients with non-ST-elevated acute coronary syndrome (NSTE-ACS).
Methods: The study group was divided into two groups: those who developed NRP and those who did not. Complete blood counts, SUA, serum creatinine, C-reactive protein (CRP) and albumin were obtained at admission.
Acta Cardiol
January 2025
Division of Cardiology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Objective: Current guidelines recommend the use of glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors in patients with ST-segment elevation myocardial infarction (STEMI) only as a bail-out therapy. However, drug penetration to the jeopardised area may not be achieved due to impeded blood flow and increased microvascular resistance. Aim of our study is to investigate the impact of distal intracoronary GpIIb/IIIa inhibitor agent infusion in STEMI patients.
View Article and Find Full Text PDFJ Saudi Heart Assoc
November 2024
Cardiology Department, Adana City Training and Research Hospital, Adana, Turkey.
Background: Spontaneous reperfusion (SR) occurring before primary percutaneous coronary intervention (PPCI) can offer additional clinical benefits to patients with ST-segment elevation myocardial infarction (STEMI). The Platelet-to-White Blood Cell Ratio (PWR) has been recognized as a prognostic indicator in various diseases. We aimed to explore the relationship between PWR and SR in patients with STEMI undergoing PPCI.
View Article and Find Full Text PDFStroke
December 2024
Department of Neurology, Institut de Psychiatrie et Neurosciences de Paris, INSERM U1266, GHU Paris Psychiatrie et Neurosciences, Université Paris Cité, France.
Reperfusion injury (RI) refers to an array of detrimental cellular and biochemical processes that are widely believed to be triggered by reperfusion following focal cerebral ischemia and to contribute to infarct extension and poor outcome despite complete recanalization. Accordingly, it is widely recommended that therapies targeting RI be administered after recanalization. The present topical review demonstrates, however, that the vast majority of, and possibly all, processes considered part of RI are not actually provoked by reperfusion but develop during the ischemic phase.
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