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No-reflow Phenomenon in Patients with Acute Myocardial Infarction:Its Pathophysiology and Clinical Implications
Ito,Hiroshi
Acta Medica Okayama , 2009,
Abstract: For patients with acute myocardial infarction (MI), the immediate therapeutic goal is to establish the patency of the infarct-related artery. Prolonged myocardial ischemia, however, often breaks down the coronary microvasculature, and the flow to the infarct myocardium may be markedly reduced. This is called the no-reflow phenomenon. This phenomenon is important not solely because it correlates with infarct size but because it provides additional prognostic information. With recent advances in imaging modalities, the no-reflow phenomenon is observed more frequently than when clinical judgment alone is used. Patients with this phenomenon are associated with poor functional and clinical outcomes. Now, the no-reflow phenomenon can be a parameter with which to predict high-risk patients. The focus of reperfusion therapy has shifted toward the improvement of myocardial perfusion. The improvement of myocardial perfusion could promote the functional recovery of viable muscle and reduce infarct expansion, which is associated with favorable clinical outcomes. For this purpose, pharmacological interventions and catheter-based devices to retrieve embolic materials have been proposed. Advances in our understanding of the pathophysiology of microvascular dysfunction would aid the development of therapeutic strategies for its prevention and treatment.
Effects of tirofiban on the reperfusion-related no-reflow in rats with acute myocardial infarction
Effects of tirofiban on the no-reflow of reperfused rats with acute myocardial infarction

Xiao Liu,Gui-Zhou Tao,
Xiao Liu
,Gui-Zhou Tao

老年心脏病学杂志(英文版) , 2013,
Abstract: Objective To investigate the effects of tirofiban on the no-reflow phenomenon of acute myocardial infarction (AMI) rats received reperfusion, as well as the underlying mechanisms. Methods Fifty-six male Sprague-Dawley rats were randomly divided into four groups: Sham operation group (Sham), AMI/reperfusion group (AMI/R), Tirofiban group (Tiro) and Tiro+N-nitro-L-arginine group (L-NNA; an endothelial nitric oxide synthase inhibitor). To generate the animal model mimicking the no-reflow phenomenon, the rats first received occlusion of the left anterior descending coronary artery for 60 min and then followed by reperfusion for 120 min. Area of no-reflow, area at risk and area of necrosis were measured by thioflavine S, Evans blue and triphenyl tetrazolium chloride staining, respectively. Haemodynamic function was measured at the end. In the meantime, nitric oxide synthase (NOS) activity was determined by a NOS assay kit. The expression of myocardial endothelial nitric oxide synthase (eNOS) was determined by an enzyme-linked immunosorbent assay (ELISA). The expression of phosphorylated eNOS at ser sup>1177 (p-eNOS ser1177) and vascular endothelial-cadherin (VE-cadherin) were determined by western blot. Results Compared with AMI/R group, tirofiban significantly reduced the no-reflow area and infarct size (all P < 0.05). Tirofiban elevated eNOS activity, lessen inducible nitric oxide synthase (iNOS) activity and increased the expression of Ser1177 phosphorylated eNOS and VE-cadherin in the ischemic myocardium (all P < 0.05). No statistical differences were found in the expression of eNOS among the four groups. Also, tirofiban improved cardiac function with significantly higher levels of left ventricular end systolic pressure, maximum change rate of left ventricular pressure rise and fall, heart rate, and lower level of left ventricular end diastolic pressure than those of the AMI/R group (all P < 0.05). Whereas, these effects of tirofiban were partially abolished by L-NNA. Conclusions Tirofiban could reduce the size of no-reflow and infarct. A possible mechanism underlying this effect is that tirofiban could protect the structural and functional integrity of microvascular endothelium which is partially regulated by eNOS activity.
Effects of tirofiban on the reperfusion-related no-reflow in rats with acute myocardial infarction
Xiao Liu,Gui-Zhou Tao
老年心脏病学杂志(英文版) , 2013,
Abstract: Objective To investigate the effects of tirofiban on the no-reflow phenomenon of acute myocardial infarction (AMI) rats received reperfusion, as well as the underlying mechanisms. Methods Fifty-six male Sprague-Dawley rats were randomly divided into four groups: Sham operation group (Sham), AMI/reperfusion group (AMI/R), Tirofiban group (Tiro) and Tiro+N-nitro-L-arginine group (L-NNA; an endothelial nitric oxide synthase inhibitor). To generate the animal model mimicking the no-reflow phenomenon, the rats first received occlusion of the left anterior descending coronary artery for 60 min and then followed by reperfusion for 120 min. Area of no-reflow, area at risk and area of necrosis were measured by thioflavine S, Evans blue and triphenyl tetrazolium chloride staining, respectively. Haemodynamic function was measured at the end. In the meantime, nitric oxide synthase (NOS) activity was determined by a NOS assay kit. The expression of myocardial endothelial nitric oxide synthase (eNOS) was determined by an enzyme-linked immunosorbent assay (ELISA). The expression of phosphorylated eNOS at Ser1177 (p-eNOS Ser1177) and vascular endothelial-cadherin (VE-cadherin) were determined by western blot. Results Compared with AMI/R group, tirofiban significantly reduced the no-reflow area and infarct size (all P < 0.05). Tirofiban elevated eNOS activity, lessen inducible nitric oxide synthase (iNOS) activity and increased the expression of Ser1177 phosphorylated eNOS and VE-cadherin in the ischemic myocardium (all P < 0.05). No statistical differences were found in the expression of eNOS among the four groups. Also, tirofiban improved cardiac function with significantly higher levels of left ventricular end systolic pressure, maximum change rate of left ventricular pressure rise and fall, heart rate, and lower level of left ventricular end diastolic pressure than those of the AMI/R group (all P < 0.05). Whereas, these effects of tirofiban were partially abolished by L-NNA. Conclusions Tirofiban could reduce the size of no-reflow and infarct. A possible mechanism underlying this effect is that tirofiban could protect the structural and functional integrity of microvascular endothelium which is partially regulated by eNOS activity.
The Relationship Between The Level Of Serum Uric Acid And No-Reflow Phenomenon After Primary Percutaneous Coronary Intervention n Patients With St Segment Elevated Myocardial Infarction  [PDF]
?smail ERDEN, Emine ?akcak ERDEN, Serhat Bahad?r S?ZEN, Osman Kayap?nar, Sabri Onur ?A?LAR, Cengiz BA?AR
Duzce Universitesi Tip Fakültesi Dergisi , 2010,
Abstract: No-reflow phenomenon is the absence of myocardial perfusion despite adequate dilatation ofthe infarct related coronary artery during percutaneous coronary intervention. Uric acid (UA)release during ischemia and washout from the ischemic zone during reperfusion is adeninenucleotide breakdown product. Therefore uric acid may play reperfusion injury and no-reflow. n this study, we aimed to compare serum uric acid value of ST segment elevated M patientsgroups whith no-reflow phenomenon and normal miyocardial perfusion after primary coronaryintervention.47 patients was enrolled consecutively to this study. During hospital admission, patients bloodsamples were taken for serum uric acid value. Patients was grouped as no reflow and normalperfusion groups according to myocardial blush grades (MBG). Patient with myocardial blushgrades 0-1 were accepted as no-reflow group, patients with MBG 2-3 normal perfusion group.When the serum uric acid value of no-reflow and normal perfusion groups was compared, therewas statistificaly significant difference (respectively 6,680±1,11 mg/dl versus 5,066±0,68 mg/dl.p<0,05). A significant correlation was found between the serum uric acid level and the presenceof no-reflow phenomenon (r=0.598; p<0.025). Multivariate logistic regression analysis showedan independent relationship between no-reflow phenomenon and serum uric acid level (OR1.815; 95% CI 1.098-1.493; p<0.031).In ST segment elevated M patients with higher serum uric acid value before primary coronaryintervention, no-reflow phenomenon is developed more frequently. Uric acid may play importantrole in mechanism of no-reflow phenomenon.
Relationship between no-reflow phenomenon and serotonin levels in patients with acute ST-elevation myocardial infarction who underwent primary percutaneous intervention  [cached]
Ramazan Topsakal,Mehmet G. Kaya,Ekrem Karakaya,?zgür Günebakmaz
Anadolu Kardiyoloji Dergisi , 2010,
Abstract: Objective: Our aim was to investigate the effects of serotonin, which is a severe vasoconstrictor agent, on the occurrence of no-reflow phenomenon. Methods: In this cross-sectional controlled study, 40 patients, admitted to our clinic with chest pain in the first 12 hours and underwent primary percutaneous coronary intervention because of acute myocardial infarction were enrolled. Patients with TIMI 0 grade basal flow and normal post-procedure flow were included in group 1 and patients with flow grade TIMI ≤were enrolled in group 2. To measure the serotonin levels, blood samples were collected from the coronary ostium before the procedure. Results: In group 1, there were 25 patients (20 males, 5 females) and the mean age was 58±11 years; in group 2 there were 15 patients (13 males, 2 females) and the mean age was 62±8 years. The mean serotonin level in platelet in group 1 was 476±208 ng/109 platelet and in group 2-542±273 ng/109 platelet. The difference was not statistically significant (p=0.39). When we compared the serum serotonin levels, it was 41.4±40.8 ng/ml for group 1, but 66.7±45.7 ng/ml for group 2. Although the serum serotonin levels were higher in group 2, the difference was not statistically significant (p=0.07).Conclusion: There was no effect of serotonin level in the development of no-reflow, in patients to whom primary coronary percutaneous intervention was applied.
TENECTEPLASE AS A NEW MEDICATION IN MANAGING NO-REFLOW  [PDF]
Milan ?ivkovi?,Svetlana Apostolovi?,Milan Pavlovi?,Sonja ?alinger Martinovi?
Acta Medica Medianae , 2012,
Abstract: No-reflow has been defined as “inadequate myocardial perfusion through a given segment of coronary circulation without angiographic evidence of a mechanical obstruction”. Important components of the process are thought to include endothelial ischemic injury producing “blebs” of tissue that directly obstruct the microvasculature, leukocyte plugging of capillaries, and the vascular effects of reactive oxygen species. No-reflow can complicate any percutaneous intervention (PCI), though it is more common following acute myocardial infarctions (MI), particularly with prolonged occlusion times. A 59-year-old woman presented to the hospital after two hours of continuous chest pain. Because of acute myocardial infarction of the inferior and lateral wall, she underwent direct stenting to an occlusion in the right coronary artery. Despite successful implantation of stents revascularization failed. In absence of aspiration devices and other pharmacological agent we decide to apply 30 mg (6000 IU) tenecteplase intracoronary. Three min after administration TIMI flow grade improved from TIMI 0 to TIMI 3. Managing no-reflow can be approached in a number of different ways and needs to be tailored to the type of intervention being performed. As confirmed in practice, prevention is better than cure and both mechanical and pharmacological approaches can be employed in high risk cases. In the setting of acute myocardial infarction the most effective preventative measure is the rapid opening of the vessel and as such the development of a robust and efficient primary PCI service is integral to the avoidance of this complication. Managing no-reflow will become increasingly important with the wider development of primary PCI. Within the setting of acute myocardial infarctions with no reflow as primary percutaneous intervention complication, there are potential important future pharmacological regimens that may become established and one of them can be tenecteplase.
Melatonin Reduces Inflammatory Injury Through Inhibiting NF- B Activation in Rats With Colitis  [PDF]
Jun-Hua Li,Jie-Ping Yu,Hong-Gang Yu,Xi-Ming Xu,Liang-Liang Yu,Jin Liu,He-Sheng Luo
Mediators of Inflammation , 2005, DOI: 10.1155/mi.2005.185
Abstract: Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-κB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-κB in rats with colitis. Rat colitis model was established by TNBS enema. NF-κB p65, TNF-α, ICAM-1, and IκBα in colon tissue were examined by immunohistochemistry, EMSA, RT-PCR, and Western blot analysis. Expression of proinflammatory molecule and activation of NF-κB were upregulated and IκB level decreased in rats with colitis. Melatonin reduces colonic inflammatory injury through downregulating proinflammatory molecule mediated by NF-κB inhibition and blockade of IκBα degradation.
Cholinergic enhancement reduces orientation-specific surround suppression but not visual crowding  [PDF]
Anna A. Kosovicheva,Summer L. Sheremata,Ariel Rokem,Ayelet N. Landau,Michael A. Silver
Frontiers in Behavioral Neuroscience , 2012, DOI: 10.3389/fnbeh.2012.00061
Abstract: Acetylcholine (ACh) reduces the spatial spread of excitatory fMRI responses in early visual cortex and receptive field size of V1 neurons. We investigated the perceptual consequences of these physiological effects of ACh with surround suppression and crowding, two phenomena that involve spatial interactions between visual field locations. Surround suppression refers to the reduction in perceived stimulus contrast by a high-contrast surround stimulus. For grating stimuli, surround suppression is selective for the relative orientations of the center and surround, suggesting that it results from inhibitory interactions in early visual cortex. Crowding refers to impaired identification of a peripheral stimulus in the presence of flankers and is thought to result from excessive integration of visual features. We increased synaptic ACh levels by administering the cholinesterase inhibitor donepezil to healthy human subjects in a placebo-controlled, double-blind design. In Experiment 1, we measured surround suppression of a central grating using a contrast discrimination task with three conditions: (1) surround grating with the same orientation as the center (parallel), (2) surround orthogonal to the center, or (3) no surround. Contrast discrimination thresholds were higher in the parallel than in the orthogonal condition, demonstrating orientation-specific surround suppression (OSSS). Cholinergic enhancement decreased thresholds only in the parallel condition, thereby reducing OSSS. In Experiment 2, subjects performed a crowding task in which they reported the identity of a peripheral letter flanked by letters on either side. We measured the critical spacing between the targets and flanking letters that allowed reliable identification. Cholinergic enhancement with donepezil had no effect on critical spacing. Our findings suggest that ACh reduces spatial interactions in tasks involving segmentation of visual field locations but that these effects may be limited to early visual cortical processing.
Intracoronary Adenosine versus Intravenous Adenosine during Primary PCI for ST-Elevation Myocardial Infarction: Which One Offers Better Outcomes in terms of Microvascular Obstruction?  [PDF]
Gemina Doolub,Erica Dall'Armellina
ISRN Cardiology , 2013, DOI: 10.1155/2013/248476
Abstract: Aims. Previous studies have suggested that intravenous administration of adenosine improves myocardial reperfusion and reduces infarct size in ST-elevation myocardial infarction (STEMI) patients. Intracoronary administration of adenosine has shown conflicting results. Methods. In this retrospective, single-centre, blinded clinical study, we assessed whether selective intracoronary administration of adenosine distal to the occlusion site immediately before initial balloon inflation reduces microvascular obstruction (MVO) as assessed with cardiac magnetic resonance imaging (MRI). Using contrast-enhanced sequences, microvascular obstruction (MVO) was calculated. We found 81 patients presenting with STEMI within 12?h from symptom onset who were eligible for the study. In 80/81 (100%) patients receiving the study drug, MRI was performed on Day 1 after primary angioplasty. Results. The prevalence of MVO was reduced in the patients treated with intracoronary adenosine, (45%) compared to 85% of patients who were administered intravenous adenosine ( ). We found that the size of MVO in patients receiving intracoronary adenosine was significantly reduced compared to 0.91?g in the intravenous-treated group ( ). There was no statistically significant difference in TIMI flow and clinical outcomes after primary PCI. Conclusion. We found significant evidence that selective high-dose intracoronary administration of adenosine distal to the occlusion site of the culprit lesion in STEMI patients results in a decrease in microvascular obstruction. 1. Introduction The concept of “no reflow” refers to a state of myocardial tissue hypoperfusion in the presence of a nonoccluded epicardial coronary artery. The underlying cause of no reflow is microvascular obstruction, which may be produced by various mechanisms [1, 2]. “Reperfusion no reflow” [2] occurs after primary percutaneous coronary intervention (PCI) for reperfusion of an infarct artery in the setting of acute myocardial infarction (AMI) and may be asymptomatic or may present clinically with continued chest pain and ST-segment elevation [3]. Reperfusion no reflow is an independent predictor of adverse clinical outcome after AMI, regardless of infarct size. Despite successful recanalization, perfusion of the ischaemic myocardium is either unrestored or incompletely restored in up to 30% of patients as a result of microvascular obstruction (MVO) [4], which is associated with higher incidence of left ventricular (LV) dysfunction, complications, and death. Multiple therapies [5] for no reflow have been tested in animals and
The Relationship Between Leukocyte Number And No-Reflow Phenomenon Developed After Primary Coronary Intervention
Erden I et al.
Konuralp Tip Dergisi , 2011,
Abstract: No-reflow phenomenon is the absence of myocardial perfusion despite adequate dilatation of the infarct related coronary artery during percutaneous coronary intervention. Microvascular leukocyte plugs are suggested as one of the mechanism of this phenomenon in previous literature. In this study, we aimed to compare absolute leukocyte number of ST segment elevated MI patients groups whith no-reflow phenomenon and normal miyocardial perfusion after primary coronary intervention. 47 patients was enrolled consecutively to this study. During hospital admission, patients blood samples were taken for leukocyte count. Patients was grouped as no reflow and normal perfusion groups according to myocardial blush grades (MBG). Patient with myocardial blush grades 0-1 were accepted as no-reflow group, patients with MBG 2-3 normal perfusion group. When the absolute leukocyte numbers of no-reflow and normal perfusion groups was compared, there was statistificaly significant difference (respectively 14055,56±3818,87 vs. 11503,45±3419,74, p=0,022). In ST segment elevated MI patients with higher leukocyte number before primary coronary intervention, no-reflow phenomenon is developed more frequently. Leukocyte may play important role in mechanism of no-reflow phenomenon.
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