Influence of microvascular dysfunction on regional myocardial deformation post-acute myocardial infarction: insights from a novel angiographic index for assessing myocardial tissue-level reperfusion

2016 ◽  
Vol 32 (5) ◽  
pp. 711-719 ◽  
Author(s):  
Ben He ◽  
Song Ding ◽  
Zhiqing Qiao ◽  
Lincheng Gao ◽  
Wei Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Microvascular Dysfunction ◽  
Tissue Level ◽  
Myocardial Deformation ◽  
Myocardial Tissue

Microvasculature Recovery by Angiogenesis After Myocardial Infarction

2018 ◽  
Vol 24 (25) ◽  
pp. 2967-2973 ◽  
Author(s):  
Lina Badimon ◽  
Maria Borrell
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Microvascular Dysfunction ◽  
Repair Process ◽  
Therapeutic Strategies ◽  
Myocardial Tissue ◽  
Microvascular Network ◽  
Early Reperfusion ◽  
Cellular Processes ◽  
High Prevalence

Advances in early reperfusion therapies focused on the revascularization of the ischemic tissues, in the last decades, lead to reduced mortality in acute myocardial infarction (MI) patients. However, a large proportion of patients show inadequate myocardial perfusion because of dysfunction of the microcirculation. The high prevalence of microvascular dysfunction after reperfusion therapies and the negative prognostic of this procedure justify the search for therapeutic strategies that aim to restore the microvascular network. It is well known that the size of the initial infarct, the duration of ischemia and the efficiency of reperfusion determine myocardial tissue damage and cardiomyocyte loss after myocardial infarction. Therefore any advancement on the mechanisms that induce the repair process of microvascular dysfunction after reperfused MI is of great interest. Here, we will review the different proteins and cells known to participate in angiogenesis induction post-MI and we will also discuss the potential pharmacological and cellular processes that promote the recovery of microvasculature by angiogenesis stimulation after MI.

CARDIOVASCULAR DISEASES: PREVALENCE, RISK FACTORS (LITERATURE REVIEW)

Vestnik ◽  
2021 ◽  
pp. 84-92
Author(s):  
М.О. Мустафина ◽  
А. Телжанов ◽  
З.Н. Лигай
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plaque Rupture ◽  
Young Patients ◽  
Microvascular Dysfunction ◽  
Artery Dissection ◽  
Variant Angina ◽  
Coronary Artery Dissection ◽  
Plaque Erosion

Мы провели поиск в PubMed статей, опубликованных с 1980 по 2020, используя термины «острый инфаркт миокарда», «молодой», «разрыв бляшки», эрозия бляшки, спонтанное расслоение коронарной артерии (SCAD), коронарный вазоспазм», «вариантная стенокардия или стенокардия Принцметала», «лекарственный инфаркт миокарда», «миокардит», «коронарная эмболия», «микрососудистая дисфункция», «MINOCA», а также обзор всех опубликованных исследований. Используя данные этого поиска, мы стремимся проинформировать читателей о распространенности, факторах риска, проявлениях и лечении острого инфаркта миокарда у молодых пациентов, а также подробно рассказать о специальных подгруппах с диагностическими и терапевтическими проблемами. We searched PubMed for articles published from 1980 to 2020 using the terms acute myocardial infarction, young, plaque rupture, plaque erosion, spontaneous coronary artery dissection (SCAD), coronary vasospasm, variant angina or angina pectoris. Prinzmetal, drug myocardial infarction, myocarditis, coronary embolism, microvascular dysfunction, MINOCA, and a review of all published studies. Using the data from this search, we aim to inform readers about the prevalence, risk factors, manifestations and treatment of acute myocardial infarction in young patients, as well as detail the special subgroups with diagnostic and therapeutic problems.

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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