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Reperfusion therapy in acute myocardial infarction saves viable myocardium, but paradoxically reestablishment of coronary artery flow also induces damage and cell death, decreasing the full benefit of reperfusion in terms of reduction of infarct size and preservation of ventricular function . Myocardial reperfusion can in itself produce more damage and cell death, this process defines the phenomenon of reperfusion injury, which could be prevented by applying additional therapies.
During myocardial ischemia, due to lack of O2, the myocyte leaves energy production from the aerobic metabolism of lipids and the production of energy in the form of phosphates will depend, in this situation, on the anaerobic metabolism of glucose. As a result they are consumed muscle glycogen stores that produce little ATP, and also generating acidosis. The cell membrane loses its ability to maintain the fluid's electrolyte balance. Cellular edema is generated by the entry of sodium and water, leading to cell rupture. During ischemia and reperfusion free radicals are produced that stimulate inflammation and consequently release prothrombotic and cytotoxic substances that also produce cellular damage. Due to its osmotic, antithrombotic, anti-inflammatory and rheological effects, dextran could be useful in this scenario.
The administration of a solution in the distal bed, for the protection of the myocardium, before opening the epicardial artery is called by us "controlled reperfusion". The researchers think, using a solution with venous blood, containing less O2 but retaining buffer properties; enriched with Dextran, which has onctic power, anti-inflammatory and anticoagulant properties, and molecules similar to glucose; results in a potentially useful solution for myocardial protection in this scenario.
The group of investigators expect that controlled reperfusion treatment will reduce the incidence of ST correction and infarct size by 20-30%, improving the prognosis in terms of mortality and heart failure.
Acute Myocardial Infarction With ST Elevation
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Centro Cardiovascular Salta
Published on BioPortfolio: 2017-05-12T13:38:21-0400
ST-elevation myocardial infarction is a major cause of morbidity and mortality worldwide. ST-elevation myocardial infarction damages the regional myocardium that undergoes ischemia and nec...
In patients with acute ST-segment elevation myocardial infarction (STEMI), percutaneous coronary intervention (PCI) may cause thrombus dislodgment and impaired microcirculatory reperfusion...
Available data from randomized trials on thrombectomy in patients with ST-elevation myocardial infarction have shown favourable trends on myocardial reperfusion. Better myocardial reperfus...
Standard treatment of patients with acute ST-segment elevation myocardial infarction consist of acute re-opening of the occluded coronary artery (primary PCI). Despite successful treatment...
Early reperfusion therapy has improved the clinical outcomes of patients with acute myocardial infarction (AMI), but these benefits are limited in some patients by reperfusion injuries. T...
The extent of myocardial damage in patients with ST-segment elevation myocardial infarction (STEMI) depends on both the time to reperfusion as well as injury induced by ischaemia-reperfusion resulting...
INTRODUCTION Patients under 40 years of age represent from 1% to 6% of all patients with acute myocardial infarction (AMI). OBJECTIVES We aimed to analyze the recent trends in the clinic...
Thrombolysis in myocardial infarction risk score (TIMI-RS) was designed to predict early mortality in patients with a ST elevation acute myocardial infarction (STEAMI).
Patients with delayed presentation of acute myocardial infarction with ST-segment elevation (STEMI) frequently have a poor prognosis but literature about acute complications in intensive cardiac care ...
Metalloproteinases inhibition by doxycycline reduces cardiac protein degradation at extracellular and intracellular level in the experimental model ischemia/reperfusion injury. Since both extracellula...
A clinical syndrome defined by MYOCARDIAL ISCHEMIA symptoms; persistent elevation in the ST segments of the ELECTROCARDIOGRAM; and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION).
A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction).
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.
Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.