Mismatches between myocardial fatty acid uptake and utilization lead to the accumulation of cardiotoxic lipid species,and cause lipotoxic cardiomyopathy.
Objective:To discuss incidence,clinical significance and result of bradycardic dysfunction of sinoatrial node in inferior wall acute myocardial infarction(AMI).
Objective:To evaluate the myocardial protective effects of HTK solution on immature and cyanosed myocardium in cardiac operation,through comparison with ST.
Objective: To investigate the effect of intramyocardial bone marrow cell injection on myocardial perfusion and LV function in patients with chronic myocardial ischemia.
They play protective roles in cytoprotection in myocardial ischemia reperfusion injury,systemic inflammatory response syndrome and apoptosis,and have more advantages in cytoprotection than drugs.
Expressions of S-adenosylmethionine synthetase gene, arginase gene and oxidant stress related genes in myocardial tissue of normal and diabetic rats were assayed by DNA microarray.
The main aim of the study was to analyze their specific complications, including heart arrhythmia, pulmonary infection, hepatic coma, alienism, myocardial infaction and diabetic ketoacidosis.
Conclusions: The myocardial bridge is an anatomic structure with some functions, such as supporting and fixing aeteria coronaria, increasing arteriotony and raising blood supply of myocardium.
The extent of neutrophilic infiltrates, along with karyolysis and loss of cytoplasmic cross striations, is typical for an acute myocardial infarct of 1 to 4 days in duration from onset.
We recorded the changes of the heart rate the blood pressure, and the left ventricle pressure, and observed Ginkgetin effect on reducing the myocardial infarct death rate of AMI - reperfused rabbits.
The influence of the drug on the cytopathy of the myocardial cells,its effects on virus replication and the content of troponin in the supernatants of the cultured cells were kept under observation.
In response to hypoxia, myocardial cells release signalling molecules called cytokines, which cause dilation of the segment of coronary artery B beyond the blockage.
So we've seen that in ST elevation MI, untreated a complete arterial occlusion may progress to infarction of the full thickness of the affected myocardial wall.