Background and Objectives: Coronary heart disease is one the most important diseases that threaten human. There is a high rate of ventricular arrhythmias (VA) in acute myocardial infarction (AMI). Ventricular fibrillations (VF) are the main lethal reason in AMI out of hospital. Primary VF is 60% in all the VF, 80% of which occur during the first 12 hours. Holters show that more than 60% nonsustained or monophasic or multimorphasic VT occurs in 67% patients in the first 12 hours. GISSI test indicated that patients with VT have high mortalities. Studies have demonstrated that the mechanism of VT was very complicated. Many factors play roles in VT partly or totally, directly or indirectly. They affect the normal, ischemic and necrosis myocardium, resulting to variety VA by changing their electrophysiological characteristics. AMI and malignant VA usually occur in the left ventricle which is supplied with blood by LAD mainly. Thus using the LAD in this test is helpful to get some knowledge of the mechanism of VA.In the early AMI, malignant VA (sustained VT, multimorphasic VT and VF) are caused by triggers (PVC, VT) or arrhythmogenic substrates. Many studies showed that triggers located in the border between the ischemic and non-ischemic zones. There is still some debate about the originating of multimorphasic VT. The transition from VT to VF is related to the activating waves splitting in the ischemic zones.MAP mapping technique is widely used in evaluating repolarizing of myocardium, in which much information can be got, such as the local information of polarization and repolarization. It also is helpful to get known to myocardial electrophysiology.Long dispersion of ventricular repolarization plays a critical role in ventricular tachycardia. The CARTO system, which can locate the sites and record MAPs simultaneously, was used in this test. MAP is a very helpful tool. Mapping technique could provide with global information of repolarization by connecting MAP and CARTO , which is useful to get to know where the VA originate and the electrophysiological characteristics of the epicardium. This test connected CARTOsystem with MAP technique to map the epicardium of left ventricle before ligature of LAD and evaluate the repolarization sequence. This may provide some help to treat VF in AMI.Methods: Some definitions to this test: Local activation time (LAT), time from the earliest activation of the ventricle to that of the local depolarization. End Of Repolarization Time (EORT), time from the earliest activation of the ventricle to the end of repolarization. Dispersion of ventricular repolarization (DVR), EORTmax- EORTmin. Making model of AMI in swine: Fix the swine onto the operating table. Pentobarbital is used for induction of anaesthesia by injecting it into the belly. After 15 minutes, trachea cannula was undergone, oxygen was inhaled. Fentanyal, pancuronium bromide and sodium hydroxybutyrate were injected through the ear margin vein. The femoral vein was punctured. Sheathings were implanted. The chest was opened. The heart was uncovered and LAD was ligated. Mapping took place. All the data and images were recorded for later statistics. Map epicardium before and after the ligature of LAD. Keep the temperature constant. Asynchronous defibrillation underwent when VF occurred.Results: All the 5 swines underwent MAP mapping in epicardium of left ventricle before ligating LAD. The data showed that MAPD and AT were in negative linear correlation, while EORT and AT were in positive linear correlation. Linear correlation test lied in statistical significance ( P<0.05) . The gradient of regression line was not exceeding -1 between MAPD and AT by linear regression analysis in all the mapping MAPs, which was at -0.25~-0.68. While as to EORT and AT , the gradient was not exceeding +1, at 0.33~0.89. During the mapping after ligature of LAD, 1 pig died of VF when LAD was being ligated, one swine died at 45min.Others surrived long enough for mapping at 10-minute and 2-hour. Heart rate varied greatly, from 50bpm to 200bpm. VF occurred from time to time. Heart rate and heart rhythm also changed .Thus less site were mapped only when heart rate and heart rhythm were costant than before ligature. So the data couldn't be used for linear correlation and regression analysis, or for evaluating the sequence of depolarization and repolarization. If the negative compensation mechanism between MAPD and AT was same to that before ligature or not , which could not be judged because of the independabledata.The reason that DVR increased cannot be explained. The result of statistical analysis showed that DVR did not vary before and after ligature in non-ischemic zone (P>0.05). But it changed in ischemic zone (P<0.05). DVR did not change from 10-minute to 2-hour (P>0.05).Conclusion: The sequence of repolarization was same to that of depolarization in epicardium before ligature of LAD. That is to say, those who depolarized earlier repolarized earlier. MAPD and AT were in negative linear correlation, while EORT and AT were in positive linear correlation. DVR was increased greatly after ligature of LAD than before. |