With the development of science, pacemaker technology is advancing rapidly, becoming smaller and smaller, more and more functional, longer and longer-lasting, and more and more intelligent and automated. The number of patients with a definite efficacy in the treatment of electrical disorders has expanded from the treatment of cardiac disorders to the treatment of non-cardiac disorders. At present, new uses of pacemakers with proven efficacy are mainly as follows. In addition to cardiac arrest and very slow heart rate, ventricular tachycardia, ventricular flutter and ventricular fibrillation are also causes of sudden death, which cannot be solved by ordinary pacemakers and require the installation of an ICD. In case of ventricular tachycardia, 6 to 10 bursts of stimulation above the ventricular tachycardia frequency are delivered to terminate the ventricular tachycardia by overspeed inhibition, and if this is not effective, high-energy defibrillation is delivered to revert the ventricular tachycardia; in case of ventricular flutter and ventricular fibrillation, high-energy discharge defibrillation is performed directly. For patients at risk of sudden death, installation of an ICD is the treatment of choice. Atrial fibrillation is a common clinical arrhythmia with high incidence, high risk, poor efficacy of drug therapy, and high toxic side effects. There are various pacing techniques and methods for the treatment and prevention of atrial fibrillation, such as: dual atrial pacing, atrial multi-part pacing, atrial septal pacing, etc. The use of procedural means such as overspeed inhibition and frequency smoothing to prevent and treat atrial fibrillation is especially suitable for slow-onset arrhythmias with atrial fibrillation. It is particularly suitable for patients with slow arrhythmias with atrial fibrillation. Biventricular synchronous pacing for heart failure In patients with systolic insufficiency heart failure, about 30% to ≥40% are associated with widened QRS time frame, suggesting conduction disturbances between the two chambers or within the ventricles, resulting in intraventricular or interventricular desynchronization during ventricular contraction. In some patients with heart failure with narrow QRS, there may also be ventricular desynchronization, resulting in premature septal contraction, delayed contraction of the left ventricular free wall, and The ventricular wall loses isotropic synchronous contraction, and some blood is trapped in the ventricular cavity and cannot be pumped out, resulting in delayed ventricular relaxation time, shortened effective filling time in diastole, increased left ventricular end-diastolic pressure, increased ventricular wall tension and decreased left ventricular ejection fraction, which further reduces cardiac output. In heart failure, reduced left ventricular contractility and left ventricular enlargement cause mitral regurgitation, and desynchronized contraction of the papillary and peripheral myocardium aggravates mitral regurgitation, resulting in a vicious circle. Biventricular synchronous pacing is the addition of left ventricular pacing to conventional dual-chamber pacing. The left ventricular pacing electrode enters the lateral branch of the posterior left ventricular wall of the coronary vein through the opening of the coronary sinus in the right atrium to pace the left ventricle, and the coordinated interatrial and biventricular contractions are programmed and controlled under ultrasound guidance. Biventricular synchronous pacing improves interventricular mechanical delay, reduces end-systolic volume index and mitral regurgitation, increases left ventricular ejection fraction, improves symptoms, enhances quality of life, and reduces the risk of complications and death.The CARE-HF study demonstrated that in NYHA class III-IV heart failure, the addition of biventricular synchronous pacing to standard pharmacologic therapy reduced hospitalization rates by 37%, all-cause mortality by With 36%, ventricular resynchronization therapy has the potential to become the basic first-line conventional treatment for heart failure. IV. Dual-chamber pacing for hypertrophic obstructive cardiomyopathy In hypertrophic obstructive cardiomyopathy, significant uneven hypertrophy of the ventricular septum is present. When the left ventricle contracts, the hypertrophied septum protrudes into the outflow tract, while the anterior mitral valve leaflet also moves toward the septum (SAM phenomenon), resulting in left ventricular outflow tract obstruction and left ventricular ejection impairment, which leads to a series of clinical manifestations and, in severe cases, patient syncope or sudden death. We placed ventricular pacing electrodes on the apical part of the right ventricle and paced the apical part of the right ventricle to preexcite the right ventricle, artificially creating an asynchronous contraction of the right and left ventricles, which caused a delay in the electrical and mechanical activity of the left ventricular free wall via intraventricular conduction. The obstruction is relieved, and long-term pacing therapy also improves left ventricular remodeling. Therefore, for those with obvious symptoms, significant left ventricular outflow tract obstruction and unable to perform chemical ablation of the septum, a DDD dual-chamber pacemaker can be implanted; for those with combined malignant arrhythmias, a dual-chamber ICD pacemaker can be implanted. Sleep apnea syndrome is a common and easily missed disease. Both central and obstructive sleep apnea syndrome cause hypoxemia and carbon dioxide retention due to apnea and increased vagal tone, leading to bradycardia and decreased blood pressure, resulting in brain and heart system damage, which can lead to sudden death in severe cases. The use of dual-chamber pacing or dual-chamber synchronous pacing can lead to a decrease in the apnea-hypopnea index and an increase in oxygen saturation, significantly reducing the occurrence of sleep apnea, especially for central sleep apnea syndrome, and can be used for patients who do not want surgical treatment and do not receive continuous positive pressure breathing therapy during sleep at night. According to the 2004 European Society of Cardiology guidelines, neurally mediated syncope is classified as vasovagal syncope, carotid sinus syncope, situational syncope, and glossopharyngeal neuralgia, with episodes of syncope causing transient bradycardia and hypotension, which leads to syncope. Pacemaker therapy is suitable for vasovagal syncope and some carotid sinus syncope. Current pacing therapy for neurally mediated syncope is accomplished with procedures such as frequency dips and frequency hysteresis of the pacemaker. When its own frequency drops to the lowest set frequency for a certain period of time, the pacemaker initiates a high pacing frequency for interventional therapy, and after a period of interventional therapy, the pacing frequency gradually returns to the basal rhythm. Pacemaker therapy reduces the onset of syncope or prolongs the time between the onset of aura symptoms and loss of consciousness, giving the patient enough time to take precautions on his own (e.g., lying down, etc.) and thus reducing the occurrence of complications.