Clinical Study Of The Hyperacute ST-elevated Myocardial Infarction With J Wave Syndrome

Along with change of the dietary structure , ageing of the population, the increasing morbility of hypertension, hyperlipidemia, diabetes mellitus and other disease , the morbility of myocardial infarction (MI) is enhancing year by year . Sudden cardiac death(SCD) caused by AMI is a tremendous chanllenge to human society and the clinical medicine. Study of SCD in China investigated that the incidence is 41.84 per ten thousand persons ,one person has happened in a minute, and the survival outside of the hospital is 5% .The initiating mechanism of SCD is arrhythmia, almost 80% of which is ventricular tachycardia or ventricular fibrillation. In order to reduce the happening of SCD, the study of the non-invasive predictions is paid much attention.Since Bierrdgarrd and Japan's Aizawa separately reported patients with J wave in ECG would happen idiopathic ventricular fibrillation, then J wave had been attached importance in clinical. Subsequently, some examinations confirmed J wave would occur in hyperacute ST-elevated myocardial infarction(STEMI) , and phase 2 reenty led to ventricular fibrillation in STEMI . As a result, an new prediction of ventricular repolarization in ECG of sudden death quietly emerged: ischemic J wave. J point refers to the junction of the QRS and ST-segment, which marks the end of ventricular depolarization and the beginning of repolarization. When its amplitude beyond 0.1mv and its time more than 20ms, J point is called J wave, which is known as the Osborn wave, the dome-shaped or hump-shaped wave along with ST-elevation. J wave could be found in physiological and pathological conditions. In physiological state J wave occurs in the early repolarization syndrome(ERS), which occupies 2.5%-18.2% of the normal electrocaidiogram. Under pathological conditions, it happens in Brugada syndrome, the idiopathic ventricular fibrillation(referred to ventricular fibrillation), and the hyperacute myocardial infarction.Objective:To evaluate the value of J wave in the prediction of malignant ventricular arrhythmia after acute myocardial infarction (AMI) by studying the electrocardiographic characteristics of patients with ST-elevated hyperacute myocardial infarction(STEMI) with J wave syndrome.Methods:112 cases of patients with ST-elevated hyperacute myocardial infarction which received coronary angiography. These cases were divided into two groups, one with J wave, the other without J wave. To analyze the relationships among J wave, the infarction wall, the related coronary, and malignant arrhythmia by observing the polymorphism and dynamic evolution of J wave.Results: J wave has three polymorphism: three cases with clear J wave, 8.8% of the total J wave syndrome; 12 cases with partial fusion of J wave and T wave, 35.3% of the total; 19 cases with fully fusion of J wave and T wave, 55.9% of the total. The J wave group had higher indices than non J wave group, as fellows:â‘ right coronary atherosclerotic stenosis involved;â‘¡acute inferior myocardial infarction;â‘¢incidence of malignant ventricular arrhythmia.Discussion: This study showed that J wave may happen in the early hyperacute stage of STEMI and have dynamic evolution along with ST-elevated segment. J wave usually occurs in inferior ventricular wall involved with right coronary atherosclerotic stenosis and is accompanied with ventricular arrhythmia. Its possible mechanisms are: the interruption of oxygen and the stopping of metabolic conveyor when acute ischemia happened in myocardial cells of AMI, resulted in a series of events in pathological and physiological: because of the reducing of inflow current (ICa, INa) and the increasing of outflow current, particularly of Ito, in addition, the less distribution of Ito in the endocardial cells, the depression of action potential dome is more significant in epicardial cells than the endocardial. Therefore, the transmural potential difference between phase 1and phase 2 brought about J-point elevation and J-wave formation in ECG. If the myocardial ischemia continues, Ito enhances and increases to phase 2 and the J wave and ST-elevated segment will appear at the same time.(2) Because Ito is more in the right ventricle than left, action potential notch mediated by Ito is more significant in the right ventricle. Ito is more in the epicardium than the endocardium. (3)The transmural potential generated by Ito , induced the phase 2 plateau of epicardial cells'action potential to a dome. Ito enhancing, the epicardial action potential notch deepened, as fellowed, Ica-l cound not activated, the dome of action potential lost and the duration significantly shortened. All of these above led to the all-or-none repolarization on the end of phase 1. And the potential duration was shortened 40% to 70%. When the action potential doom completely lost in the epicardial cell, often nonuniformity, the transmural dispersion of repolarization increased obviously. The doom of non-ischemic cells would led ischemic ones which lost the doom to produce a new potential, named phase 2 reentry. a R-on-T ventricular premature contraction would perform on the ECG, which would easily trigger ventricular tachycardia and ventricular fibrillation. The preventions and treatments of ventricular arrhythmia in STEMI involve: open the criminal artery earlier, resile the blood stream; replenish potassium and magnesium; utilize the beta adrenergic receptor blocker earlier if the cardiac function is good; implant the ICD if necessary.Conclusion:1.J wave would occur in the early hyperacute stage of STEMI, and could have three types, the one of fully fusion of J wave and T wave is more common. 2. J wave usually happens in inferior ventricular wall induced by right coronary atherosclerotic stenosis.3.J wave is accompanied with ventricular arrhythmia, and is an effective index in predicting malignant ventricular arrhythmia after AMI in electrocardiogram. 4.The preventions and treatments of ventricular arrhythmia in STEMI involve: open the criminal artery earlier, resile the blood stream; replenish potassium and magnesium; utilize the beta adrenergic receptor blocker earlier if the cardiac function is good; implant the ICD if necessary.