CONTRAST ECHOCARDIOGRAPHY WITH ASSESSMENT OF MYOCARDIAL PERFUSION IN DIAGNOSIS OF NO-REFLOW PHENOMENON IN PATIENT WITH ACUTE MYOCARDIAL INFARCTION

2019 ◽  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Perfusion ◽  
Contrast Echocardiography ◽  
No Reflow ◽  
No Reflow Phenomenon

scholarly journals Assessment of no-reflow phenomenon by myocardial contrast echocardiography in patients with acute myocardial infarction with ST-segment elevation

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
D Krinochkin ◽  
I Bessonov ◽  
E Yaroslavskaya ◽  
V Kuznetsov
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Perfusion ◽  
Contrast Echocardiography ◽  
Left Ventricular ◽  
Myocardial Contrast Echocardiography ◽  
St Segment Elevation ◽  
No Reflow ◽  
St Segment ◽  
No Reflow Phenomenon

Abstract Funding Acknowledgements Type of funding sources: None. Background The noninvasive assessment of myocardial perfusion by echo contrast agents in patients with acute myocardial infarction with ST-segment elevation (STEMI) after successful revascularization is becoming a relevant clinical reality. Perfusion imaging techniques with myocardial contrast echocardiography (MCE) remains the least studied and most promising ultrasound technology for the diagnosis of no-reflow phenomenon. Purpose To study the echocardiographic and angiographic characteristics of the no-reflow phenomenon detected by MCE in patients with STEMI. Methods The study included 43 patients aged from 40 to 82 years in acute stage of myocardial infarction. Patients were divided into two groups: 32 patients characterized by sufficient myocardial reperfusion after revascularization according to MCE results and 11 patients were with the impaired perfusion. Results The patients with impaired perfusion demonstrated a greater size of the left ventricular (LV) asynergy (40.1 ± 2.2% vs 27.4 ± 8.5%, p < 0.001). LV dilatation (LV end-systolic volume 67.3 ± 20.3 ml vs 51.8 ± 17.2 ml, p = 0.015), impaired LV ejection fraction (39.5 ± 3.4% vs 47.2 ± 4.9%, p < 0.001), and significant mitral regurgitation (45.5% vs 3.1%, p = 0.011) with a decrease in DP/DT (979.9 ± 363.4 mmHg/s vs 1565.7 ± 502.8 mmHg/s, p < 0.001) was more often detected in this group. In more than a quarter of these patients, coronary angiography showed no perfusion disorders after revascularization. In the group with impaired perfusion by MCE, the single-vascular lesions (46.9% vs 9.1%, p = 0.033), the lesions of the anterior interventricular artery (90.9% vs 40.6%, p = 0.004), and acute occlusion (100% vs 68.8%, p = 0.043) were more often determined. Conclusion According to the results of MCE, the echo signs of LV dysfunction were more pronounced after successful revascularization in patients with STEMI and myocardial perfusion disorders. The SYNTAX score was twice higher in these patients compared to the patients with recovered perfusion. In addition, no-reflow phenomenon by MCE was observed in the most patients with anterior interventricular artery lesion.

scholarly journals Coronary microvascular reperfusion injury and no-reflow in acute myocardial infarction

2007 ◽  
Vol 30 (3) ◽  
pp. 133 ◽  
Author(s):  
Sheng Kang ◽  
Yuejin Yang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Contrast Echocardiography ◽  
Microvascular Endothelium ◽  
Microvascular Damage ◽  
Microvascular Injury ◽  
No Reflow ◽  
No Reflow Phenomenon

Purpose: To review (1) the mechanisms of coronary microvascular reperfusion injury, particularly in the relationships between microvascular endothelium dysfunction, microstructure damage, microemboli and no-reflow phenomena; (2) the no-reflow presentation and management at ischemia-reperfusion to suggest future direction for no-reflow therapy in acute myocardial infarction. Sources: Original articles and reviews published between 1997 and 2007 and focusing on the no-reflow phenomenon in MEDLINE and PubMed. The search terms used were “no-reflow”, “microvascular injury”, “acute myocardial infarction” and “reperfusion injury”. All papers identified were English-language, full text papers. In addition, the reference lists of identified relevant articles were also searched. Conclusions: The no-reflow phenomenon is characterised by damage to microvascular function and microstructure at ischaemia-reperfusion. Microemboli contribute to no-reflow. Clinical myocardial contrast echocardiography (MCE), scintigraphic and magnetic resonance imaging (MRI) have shown evidence of microvascular damage, eg, perfusion defects are closely related to lack of contractile recovery and irreversible myocyte damage. Clinical agents and devices targeting microvascular injury (especially protection of endothelium and reduction of microemboli) after acute myocardial infarction may be key points to improve no-reflow.

scholarly journals The Predictors of No-Reflow Phenomenon after Primary Angioplasty for Acute Myocardial Infarction

2016 ◽  
Vol 10 (03) ◽  
Author(s):  
Kamran Aeinfar ◽  
Ata Firouzi ◽  
Hossein Shahsavari ◽  
Hamidreza Sanati ◽  
Reza Kiani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Primary Angioplasty ◽  
No Reflow ◽  
No Reflow Phenomenon

Carvedilol reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel

Perfusion ◽  
2008 ◽  
Vol 23 (2) ◽  
pp. 111-115 ◽  
Author(s):  
JL Zhao ◽  
YJ Yang ◽  
WD Pei ◽  
YH Sun ◽  
M Zhai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Channel Blocker ◽  
Contrast Echocardiography ◽  
Study Groups ◽  
K Channel ◽  
Control Group ◽  
Myocardial Tissue ◽  
Endothelin 1 ◽  
No Reflow

It has been verified that carvedilol can attenuate myocardial no-reflow. However, the effects of carvedilol on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown. Forty mini-swines were randomized into 5 study groups: 8 control, 8 carvedilol pretreatment, 8 glibenclamide (KATP channel blocker)-treated, 8 carvedilol and glibenclamide-pre-treated and 8 sham-operated. An acute myocardial infarction(AMI) and reperfusion model was created with a three-hour occlusion of the left anterior descending coronary artery followed by one-hour reperfusion. Compared with the control group, carvedilol significantly decreased the area of no-reflow (myocardial contrast echocardiography: from 78.5±4.5% to 24.9±4.1%, pathological means: from 82.3±1.9% to 25.8±4.3% of ligation area, respectively; all p < 0.01) and reduced necrosis size from 98.5±1.3% to 74.4±4.7% of ligation area, p < 0.05). It also decreased plasma ET-1 and myocardial tissue ET-1. However, glibenclamide abrogated the protective effect of carvedilol. The beneficial effect of carvedilol on myocardial no-reflow could be due to its effect on ET-1 via the activation of the KATP channel.

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