Disease description: Pre-excitation syndrome refers to a syndrome in which, in addition to the normal conduction system, there is an additional conduction pathway between the atria and the ventricles in the heart, causing electrical impulses from the atria to excite some or all of the ventricular muscle in advance. The syndrome was first reported by Wolff, Parkinson and White in 1930 and is therefore also known as W-P-W syndrome. The prevalence of preexcitation syndrome ranges from 0.15% to 1.6%, with a male predominance. Ventricular pre-excitation itself does not produce symptoms and generally has a good prognosis. Pathogenesis: In addition to the normal interatrial conduction pathway, the presence of additional bypasses is the pathologic basis of the preexcitation syndrome. These bypasses consist of atrial muscle-like bundles that can be present almost anywhere around the atrioventricular valve annulus. The common bypasses are atrioventricular bypass; atrial bundle bypass; and junctional ventricular bypass. Patients with preexcitation syndrome are prone to tachycardia due to the presence of two or more conduction pathways between the atria and ventricles. The syndrome occurs in patients without other cardiac anomalies, but a few patients may have congenital heart disease such as Ebstein malformation and mitral valve prolapse. The ECG characteristics of typical preexcitation syndrome (Kent’s bundle preexcitation syndrome) are: (1) P-R interval of sinus beats <0.12s; (2) coarse stuttering at the beginning of QRS wave group (called delta wave or delta wave), but normal at the end; (3) QRS time limit ≥0.12s; (4) secondary changes in ST-T band, the direction of which is opposite to that of the main QRS wave; (5) clinically typical preexcitation syndrome. (5) Clinically, typical pre-excitation syndrome can be divided into the following two types: type A, in which all the δ waves and QRS main waves in the anterior chest leads are directed upward, and the ventricular end of the bypass is at the base of the posterior left ventricular wall; type B, in which the δ waves and QRS main waves in leads V1-V2 are directed downward, and the δ waves and QRS main waves in leads V5-V6 are directed upward, and the bypass is estimated to be located in the anterolateral wall of the right ventricle. The typical preexcitation syndrome ECG preexcitation wave may appear intermittently (clinically known as intermittent preexcitation). 2, L-G-L syndrome (Jame bundle preexcitation syndrome) ECG manifestations: (1) P-R interval <0.12s; (2) QRS wave group time frame is normal; (3) no δ wave at the beginning of QRS. 3, Mahaim bundle syndrome: this type is rare, ECG performance: (1) P-R interval > 0.12s; (2) QRS wave group start with δ wave; (3) QRS wave group widening, excitation ST-T changes. Clinical manifestations: Pre-excitation alone does not cause symptoms, and those with concomitant underlying heart disease may have related symptoms and signs. However, preexcitation syndrome often leads to a variety of arrhythmias, of which atrial fold tachycardia is the most common (about 80%). Because rapid atrial fibrillation or atrial flutter waves can be transmitted down the bypass, preexcitation syndrome combined with atrial fibrillation or atrial flutter can produce rapid ventricular excitation (most ventricular rates are particularly fast, up to 180-200 beats/min, and when the ventricular rate is greater than 200 beats/min, there is a risk of ventricular fibrillation, sudden death). (risk of sudden death). Diagnosis: The diagnosis is not difficult in patients with typical ECG manifestations of the pre-excitation syndrome. In intermittent preexcitation syndrome, the diagnosis is often difficult. Multiple electrocardiograms, ambulatory electrocardiograms, and exercise tests can help to detect preexcitation waves. Treatment: Patients who simply have preexcitation waves and never have episodes of tachycardia, or who have occasional episodes but mild symptoms generally do not require treatment. If accompanied by frequent tachyarrhythmias should be given medication, transcatheter radiofrequency ablation or surgical treatment. Drug therapy: When preexcitation syndrome is complicated by narrow QRS tachycardia (mostly cis-reflex tachycardia, in which atrial excitation is transmitted down to the ventricles through the atrioventricular node, then back to the atria via the bypass, and the cycle repeats, forming tachycardia), it can be treated with atrioventricular node blockers such as stimulation of the vagus nerve, intravenous adenosine and verapamil. Adenosine and AV node blockers are contraindicated when the pre-excitation syndrome is complicated by wide QRS tachycardia. In this rhythm, the ventricles are mostly excited by the anterior transmission of the bypass (which can also manifest as wide QRS waves when combined with bundle branch block). Because the bypass does not have the protective decremental conduction properties of the AV node, rapid excitation such as atrial flutter/atrial fibrillation can be conducted 1:1 to the ventricle, thus risking ventricular fibrillation and cardiac arrest. In these patients, drugs that prolong both the AV node and the AV bypass tract under-phase (propafenone, amiodarone, etc.) may be considered, and in hemodynamically unstable patients, DC electric cardioversion is preferred. Catheter ablation: Transcatheter radiofrequency ablation is currently the best treatment for preexcitation syndrome. Since radiofrequency ablation removes the anatomical basis for the development of arrhythmias in preexcitation syndrome cases, it is curative and has a success rate of more than 95% in a single procedure in experienced centers.