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

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.

Effects of delayed recanalization of an occluded acute myocardial infarction-related artery using coronary angioplasty on late potentials

1995 ◽  
Vol 6 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Antonio G. Hermosillo ◽  
Manuel E. Horna ◽  
Francisco Dfaz ◽  
José Zamora ◽  
Jesus Martinez
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Angioplasty ◽  
Late Potentials

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 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.

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

scholarly journals Conservative Management of Subacute Contained Left Ventricular Rupture after Acute Myocardial Infarction

2018 ◽  
Vol 03 (01) ◽  
pp. 034-038
Author(s):  
Bharat Goud C ◽  
Johann Christopher
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Color Doppler ◽  
Regional Wall Motion ◽  
Left Ventricular ◽  
Mechanical Complication ◽  
Inferior Wall ◽  
Early Reperfusion ◽  
St Segment Elevation ◽  
Myocardial Wall

AbstractLeft ventricular free wall rupture (LVFWR) is a near-fatal mechanical complication of acute myocardial infarction in which an early diagnosis and emergency surgery should be of utmost priority for successful treatment. LVFWR is generally perceived to be universally fatal. Majority of LVFWR patients developing cardiac tamponade die rapidly, while in minority of cases the development of tamponade may be sufficiently slow to allow for diagnosis and successful intervention. In this article, the authors report a case of a 63-year-old male patient diagnosed with an inferoposterior wall myocardial infarction treated with early reperfusion thrombolytic therapy presenting 3 days later with diagnosis of subacute LVFWR. Patient had a history of relapse of chest pain which was severe and prolonged with 2 to 3 mm saddle-shaped ST-segment elevation in lateral leads, detected on a routine electrocardiogram, which led to an urgent bedside transthoracic echocardiogram (TTE). TTE showed regional wall motion abnormality in form of akinetic basal inferior-wall, a small echodense pericardial effusion, and a canalicular tract from endocardium to pericardium, through which color-Doppler examination suggested blood crossing the myocardial wall. A cardiac magnetic resonance imaging further reinforced the possibility of contained LVFWR.

Sign in / Sign up

Export Citation Format

Share Document