Atrial fibrillation (AF) is one of the most common clinical arrhythmias, with a prevalence of about 0.5% in the population and increasing with age, as reported by Framingham’s study, and a prevalence of more than 6% in people over 60 years of age. The treatment of patients with persistent or permanent atrial fibrillation is still based on controlling the ventricular rate and preventing thromboembolism. The 24-hour average ventricular rate of untreated atrial fibrillation tends to be faster than that of sinus rhythm, which can lead to symptoms such as palpitations and shortness of breath, and can exacerbate pre-existing angina pectoris or heart failure, and sustained heart rate increase can also lead to tachycardia. In patients with atrial fibrillation who have no indication for reversion to sinus, ventricular rate control plays a crucial role in improving symptoms and preventing tachycardia. The criteria for satisfactory ventricular rate control in atrial fibrillation are mostly used: a ventricular rate of 60-80 beats/min at rest and 90-115 beats/min during exercise. 24-hour ambulatory electrocardiographic monitoring recordings (Holter) of the frequency trend is a commonly used method of evaluating whether the ventricular rate control is satisfactory or not. With the widespread use of Holter examination, it has been found that patients with atrial fibrillation, who are considered to have satisfactory ventricular rate control clinically, have a significantly increased chance of experiencing long RR intervals of varying degrees during nocturnal sleep. How to correctly determine the clinical significance of atrial fibrillation with long RR intervals is often a matter of clinical confusion. The question that arises from this is whether atrial fibrillation is present with second-degree atrioventricular block. In the past, the criterion for diagnosing atrial fibrillation with second-degree atrioventricular block has been proposed as RR intervals >1.5S in Holter recordings or electrocardiograms, more than three times. This diagnostic criterion has been questioned as the phenomenon of atrioventricular conduction in atrial fibrillation has been recognized, and it has been argued that this diagnosis should be rejected. However, there is no universally recognized criterion for the diagnosis of atrial fibrillation with AV conduction block. By definition, atrioventricular block should be characterized by varying degrees of conduction disturbances in the electrical activity of the atria as it passes through the junction zone to the ventricles. If all atrial electrical activity is transmitted down to the ventricles but with some delay, it is defined as a degree I atrioventricular block. Obviously this condition is not suitable for atrial fibrillation. Atrial fibrillation with degree III atrioventricular block can definitively occur. Partial atrial activity that does not travel down to the ventricles is defined as a degree II AV block. Normally, the electrical activity of the atria in atrial fibrillation reaches 300-400 beats/min or even faster, and certainly not all of it can be transmitted down to the ventricle, which is determined by the electrophysiological characteristics of the ventricular myocardium, and is a physiological protection mechanism against causing an excessively fast ventricular rate. We can say that atrial flutter is accompanied by a 2:1 downbeat, but not a 2:1 block. Based on such a definition, it seems that it is difficult to determine in AF whether the electrical activity that is not transmitted downstream is part of a normal physiologic situation or whether there is atrioventricular block. The perception of a long RR becomes a critical issue. The study of atrial conduction phenomena in atrial fibrillation found that in patients with satisfactory control of ventricular rate in atrial fibrillation and no obvious uncomfortable symptoms, Holter examination showed that the incidence of RR intervals >1.5S ranged from 54.7% to 79.23%, and the longest RR intervals, 1.5-4.6S, appeared most often during nighttime sleep, and disappeared during wakefulness and activity. After 1-4.5 years of follow-up, there was no progressive prolongation of the long RR intervals associated with AF or need for pacemakers.Pitcher et al. looked at the 24-hour Holter performance of a group of asymptomatic patients with chronic persistent AF under satisfactory clinical control, and found that there was a wide range of 24-hour physiologic variability in ventricular rate. The same patient would have a fast ventricular rate of more than 140 beats/min, a bradycardia of less than 50 beats/min, and a long RR interval of up to 4S at night during the day. An electrophysiologic study of a group of 20 patients showed that the longest RR intervals associated with atrial fibrillation were 2.10-3.04 S. After electrical reversal to sinus rhythm, electrophysiologic examination was performed in all 20 patients, except for one who had a first-degree atrioventricular block, with AH intervals of 160 ms, and in 19 who had atrioventricular nodal conduction function, including AH intervals, Hippocampal bundle time frame, HV intervals, atrioventricular nodal effective The conduction functions of the AV node, including AH interval, Hippocampal time limit, HV interval, AV node effective period of inactivity, Vinzel’s point, and 2:1 block point, were within the normal range in the other 19 cases. The mechanism of atrial fibrillation with long RR intervals may not be simply attributable to one cause. Pathological changes in the atrioventricular node of the heart is a possible factor, but there are more likely to be the following reasons: (1) atrial fibrillation in the atrium of the rapid disorganization of the electrical activity of the atrium leads to the atrioventricular junction area of physiological disturbances and the continuity of hidden conduction and produce a long RR interval, is not a pathologic block; (2) the increase in the tension of the vagus nerve can make the myocardial electrical activity of the conduction of the delayed myocardium, the prolongation of myocardial ossufficiency, so that the ventricular rate decreased, the ventricular response slows; (3) some drugs that affect autonomic tone can be affected by Certain drugs affecting cardiac autonomic tone can cause relative or absolute vagal dominance, and drugs with negative frequency can make atrial and ventricular insidious conduction more obvious. Long RR intervals due to nonpathologic AV conduction dysfunction in atrial fibrillation are generally characterized by the use of drugs to control ventricular rate, a normal 24-hour overall heart rate distribution, an average heart rate in the normal range, and the coexistence of a rapid ventricular rate during activity and bradycardia at rest. Long RR intervals occur with a distinct circadian rhythm, mostly appearing at night in the resting state and disappearing in the awake and active states. Although this long RR can reach 4-5 seconds, it is usually not accompanied by clinical symptoms corresponding to bradycardia, especially not symptoms of cardiogenic cerebral ischemia. There is a degree of variability, sometimes significant, in the RR intervals before and after the appearance of the long RR interval, and there are generally no consecutive, relatively regular long RR intervals, so that a 1-minute heart rate is not unacceptably slow if calculated at the moment of the long RR. The above characteristics of this long RR did not change significantly after a certain period of follow-up. It is hypothesized that increased insidious conduction due to changes in cardiac autonomic function should be the main cause of the long RR interval in these patients. Atrial fibrillation with pathologic AV conduction dysfunction is generally characterized by the following features. In addition to drugs and other triggering factors: (1) 24h average heart rate is slow, especially persistent slow. (ii) The presence of multiple long RR intervals that are not related to sleep and have no temporal regularity. Long RR intervals occur frequently during the day, especially during exercise. (iii) Frequent long RR intervals with multiple equal or even consecutive long intervals within a short period of time, which is considered to be junctional escape beats or junctional escape rhythms. (4) Those who have clinical symptoms caused by obvious slow heart rate. (5) If atrial fibrillation is preceded by atrioventricular node lesions or pathological sinus node lesions. Therefore, the clinical significance of atrial fibrillation with long RR intervals should be judged by combining clinical and other data. We certainly cannot miss patients with true atrioventricular block, but it is now more important to be careful not to mistake patients who have been treated satisfactorily for atrioventricular block. Long RR intervals and bradycardia at rest and during sleep are common in patients with AF who have satisfactory ventricular rate control. If the overall heart rate is well distributed, there are no symptoms corresponding to bradycardia. Slow heart rate and long RR intervals at a given moment in time should not be a concern in clinical treatment, and negative frequency drugs for ventricular rate control should be easily reduced or discontinued, resulting in inadequate ventricular rate control and a range of symptoms. Nor should an artificial criterion of RR interval be established to determine the need for a pacemaker, causing unnecessary loss and financial burden to the patient. The idea of “bailing out” the use of ventricular rate control medications with a pacemaker in this situation is not advisable. Truly irreversible, clinically significant bradycardia is a good reason to consider a pacemaker, but long RR and bradycardia are not the same concept, and one-minute heart rate and 24-hour average heart rate are much more important than a few long RRs. A significant majority of patients with persistent or permanent atrial fibrillation have concomitant organic heart disease and cardiac insufficiency. In the case of atrial fibrillation, the only solution to the long RR is to install a VVI pacemaker. The ventricular contraction dyssynchrony that results thereafter can nevertheless be the cause of worsening heart failure, which is something that has to be taken into account when making decisions.