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The No-Reflow Phenomenon: A Misnomer?
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Lewis C. Becker, Giuseppe Ambrosio, John Manissi, Harlan F. Weisman
Several years ago Reimer and Jennings from Duke demonstrated that the no-reflow phenomenon was associated with microvascular necrosis. Very meticulous histologic evaluation showed that this microvascular damage only occurred in the areas where the myocardium was already necrotic. I wonder whether you have ever seen evidence of no-reflow outside an area of myocardial necrosis and, if not, whether you have demonstrated the no-reflow phenomenon in the absence of microvascular histologic changes, suggesting that maybe two different kinds of no-reflow exist?
Nursing care of the cardiac catheterisation patient
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Julie Parkinson, Jo-Anne M. Vidal, Eva Kline-Rogers
The no-reflow phenomenon describes the abrupt cessation of coronary flow without evidence of mechanical coronary obstruction, typically during primary PCI (PPCI) and complex PCI (particularly vein graft intervention or when rotational atherectomy devices are used).34(p728) No re-flow occurs infrequently (0.6%–3%)132(p168),133 and common to all procedures is the liberation and distal embolisation of significant amounts of plaque coupled with vasoconstriction of the distal arterial bed.132(p168) No re-flow is associated with significant morbidity including reduced myocardial salvage, larger infarct size, reduced left ventricular ejection fraction at 6 months and increased risk of 1-year mortality.133,134
Skin Flap Physiology
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Colin MacIver, Stergios Doumas
Vasospasm in the flap following raising of the flap is a normal physiological response to reduce blood loss. Under normal circumstances, this vasospasm resolves without intra-vascular thrombosis because the spasm empties the lumen of the vessel. In addition, vessel lumen irrigation with heparin can resolve potential clots during anastomosis. In the presence of intact endothelium, the coagulation cascade is not activated. Hence, endothelial cell integrity plays a vital role in the maintenance of blood flow. Where flow to the flap is not established (or is compromised for a prolonged period of time) it has been shown experimentally in rabbits that ‘no flow’ occurs after a period of several hours of ischaemia. This has become known as ‘no reflow phenomenon’ coined by Ames et al. in 1968 and studied first in flap reperfusion in 1978.31-32 In the no reflow phenomenon, reperfusion of the ischaemic tissue results in the formation of oxygen-derived free radicals. Furthermore, it has been shown that the vasodilator effect of acetyl choline is mediated through endothelial production of nitric oxide.33 The net effect of acetyl choline following reperfusion is the presence of damaged endothelial cells in vasoconstriction.
Association between serum SCUBE1 levels and thrombus burden in patients with ST-segment elevation myocardial infarction
Published in Acta Cardiologica, 2021
Arafat Yıldırım, Mehmet Kücükosmanoglu, Nermin Yildiz Koyunsever, Yusuf Cekici, Mustafa Dogdus, Erhan Saracoglu, Salih Kilic
ST-segment elevation myocardial infarction (STEMI) is currently one of the major causes of cardiovascular mortality and morbidity [1]. Coronary thrombosis is unequivocally the most important pathophysiological process underlying STEMI. High thrombus burden in the coronary artery responsible for STEMI (infarct related artery, IRA) was shown to be associated with distal emboli, stent thrombosis, no-reflow phenomenon and long-term mortality and morbidity [2–5]. No-reflow phenomenon is an important problem in STEMI patients undergoing primary percutaneous coronary intervention (PPCI) and is associated with a high coronary thrombus burden [2]. In addition, no-reflow phenomenon is known to be associated with long-term mortality and morbidity in STEMI patients [2]. Platelet and endothelial adhesion molecules play an important pathological role in intracoronary thrombus formation.
Predictors and prognosis of no-reflow during primary percutaneous coronary intervention
Published in Baylor University Medical Center Proceedings, 2019
Govindan Nair Rajesh, Narayanapillai Jayaprasad, Suresh Madhavan, Vasantha Sudha Kumary, Kesavapillai Jayaprakash, Kamarudheenkunju Jameelabeevi Raihanathul Misiriya, Vaikathusseril Lembodaran Jayaprakash, Raju George
Primary percutaneous coronary intervention (PPCI) has been established as the most effective management strategy to restore antegrade blood flow in ST-elevation myocardial infarction (STEMI). The no-reflow phenomenon occurs in a considerable number of patients with acute STEMI (11%–41%) undergoing primary reperfusion therapy.1,2 Experimental and clinical studies have shown that the no-reflow phenomenon is associated with large myocardial necrosis and high mortality.3,4 Suggested mechanisms for no-reflow or slow flow include coronary microcirculation disturbances, such as distal embolization of thrombus and plaque debris, microvascular damage, and reperfusion injury.1,2 A number of clinical, serologic, and angiographic parameters have been shown to be associated with no-reflow.2 In addition, a number of treatment strategies have been tried with variable results in no-reflow.5–8 Knowing the predictors or risk factors of no-reflow can help prevent this dreaded complication of PPCI. The aim of this study was to identify clinical, angiographic, and procedural factors that predict the no-reflow phenomenon in patients with STEMI undergoing PPCI and to determine the impact of no-reflow on in-hospital mortality.
Pharmacological thrombolysis: the last choice for salvaging free flaps
Published in Journal of Plastic Surgery and Hand Surgery, 2018
Sik Namgoong, Jong-Phil Yang, Seong Ho Jeong, Seung Kyu Han, Woo Kyung Kim, Eun Sang Dhong
Finally, intrinsic problems within the flap [9], such as no-reflow phenomenon [10,11], perforasome selection issues [12,13], and intra-flap microthrombosis, should be ruled out. The no-reflow phenomenon refers to the state whereby venous outflow is absent despite re-establishment of arterial inflow owing to microcirculatory collapse [14]. In fasciocutaneous flap elevation, perforasome selection issues such as extremely large flap territory for the area perfused by a single perforator should also be addressed to determine the possible cause of sluggish venous outflow. It is suggested that perforator-based free flaps are more likely to be vulnerable to partial flap failure owing to unpredictable perforasome perfusion characteristics [9,15,16]. Thus, the perforasome anatomy should always be kept in mind during flap elevation.