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.

Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery

1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Early Reperfusion ◽  
Vast Number ◽  
Beneficial Effects ◽  
Infarct Related Artery ◽  
Cardioprotective Effects ◽  
Collateral Vessels

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.

Early Reperfusion Assessment and Repeated Thrombolysis in Acute Myocardial Infarction Estimated by Repeated Standard Electrocardiography

Cardiology ◽  
2000 ◽  
Vol 94 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Sabine Gill ◽  
Benedikte Haastrup ◽  
Torben Haghfelt ◽  
Mikael Dellborg ◽  
Peter M. Clemmensen
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Early Reperfusion

scholarly journals Thrombolysis related early reperfusion reduces ECG late potentials after acute myocardial infarction

1991 ◽  
Vol 17 (2) ◽  
pp. A312 ◽  
Author(s):  
Fidela Moreno ◽  
Labros Karagounis ◽  
Steven Ipsen ◽  
Hiram Marshall ◽  
Jeffrey L. Anderson
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Late Potentials ◽  
Early Reperfusion

scholarly journals High risk electrocardiographic patterns in patients with acute coronary syndrome.

2020 ◽  
Vol 2 (1) ◽  
pp. 25-34
Author(s):  
Diego Echeverri- Marín ◽  
Cristhian Felipe Ramirez Ramos ◽  
Andrés Miranda-Arboleda ◽  
Gustavo Castilla-Agudelo ◽  
Clara Saldarriaga-Giraldo
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Reperfusion Therapy ◽  
Early Reperfusion ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Acute Coronary Occlusion ◽  
St Segment ◽  
St Elevation ◽  
Electrocardiographic Findings

Acute myocardial infarction is the leading cause of death in the world and the electrocardiogram remains the diagnostic tool for determining an acute myocardial infarction with ST-segment elevation. In spite of this, only half of the patients present classic electrocardiogram findings compatible with the ST-elevation infarction criteria. There is a spectrum of electrocardiographic findings that may reflect a phenomenon of acute coronary occlusion, which should be promptly recognized by the clinician to offer early reperfusion therapy.

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.

scholarly journals S100a8/a9 Signaling Causes Mitochondrial Dysfunction and Cardiomyocyte Death in Response to Ischemic/Reperfusion Injury

Circulation ◽  
2019 ◽  
Vol 140 (9) ◽  
pp. 751-764 ◽  
Author(s):  
Yulin Li ◽  
Boya Chen ◽  
Xinying Yang ◽  
Congcong Zhang ◽  
Yao Jiao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Cardiovascular Events ◽  
Ischemia Reperfusion ◽  
Coronary Intervention ◽  
Major Adverse Cardiovascular Events ◽  
Mouse Heart ◽  
Early Reperfusion ◽  
Percutaneous Coronary

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515

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