Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in the United States and the second most common arrhythmia in China after premature ventricular contractions. The incidence of atrial fibrillation in our general population is about 0.4%, in patients with cardiovascular disease it is 4%, and in patients with severe cardiovascular disease it is up to 40%. Therefore, atrial fibrillation is both a hot topic for doctors and a focus of attention for the general population.
”Grandfather of arrhythmias”
Foreign scholars have interestingly called atrial fibrillation (the grandfather of arrhythmia), indicating that the medical community discovered and studied atrial fibrillation earlier and with a longer history than other arrhythmias.
Five years later, at the age of 52, Shakespeare died, and 17 years later, the famous English physiologist and anatomist William Harvey Harvey wrote that “the right atrium of the animal under test underwent a peculiar movement of great irregularity, when the atrium lost its regular contraction and became a kind of crepitus”, and Harvey’s graphic and realistic record is now 381 years old.
It was not until 1906 that Einthoven, the Dutch master of electrocardiology, recorded the first electrocardiogram of atrial fibrillation. The long and storied history of atrial fibrillation research makes it worthy of its title.
”Grandfather’s arrhythmia”
Studies addressing the incidence of atrial fibrillation showed a two-fold jump in the 1990s compared to the 1970s. In-depth studies have found that one of the reasons for the sudden increase in the incidence of atrial fibrillation is the aging of the society’s population. The incidence of atrial fibrillation increases steeply after the age of 60 years in both men and women (Figure 1), and the incidence of atrial fibrillation reaches 80 years of age or older, and the incidence of atrial fibrillation increases with each year of age, making atrial fibrillation today known as “grandfather’s arrhythmia.
Studies have confirmed that as people age, the heart undergoes physiological degenerative changes and atrial myocardial fibrosis progressively increases, with lamellar fibrosis causing a large loss of normal atrial muscle, thus forming the pathological basis for the development of atrial fibrillation. Thus, in a sense, atrial fibrillation can be considered as a degenerative pathology in people of advanced age.
The concatenation phenomenon of atrial fibrillation
”The phrase “a dragon gives birth to a dragon and a phoenix gives birth to a phoenix” is often used to emphasize the influence of family factors on the individual, and it is also used in the same way for atrial fibrillation, which directly translates as “sinus rhythm gives birth to sinus rhythm and atrial fibrillation gives birth to atrial fibrillation.
This statement reflects the concatenation phenomenon after the onset of atrial fibrillation, that is, the longer the duration of atrial fibrillation, the more likely it is to persist, and even if it reverts to sinus rhythm in the middle, atrial fibrillation is likely to occur again. This is because the occurrence of AF can cause electrical and anatomical remodeling of the heart, which is the basis for the persistence and recurrence of AF.
The above-mentioned concatenated phenomena explain the clinical characteristics of AF onset, i.e., as the onset of AF progresses, the more frequent and longer the patient’s AF episodes become, and after a period of time, paroxysmal AF will progress to persistent or chronic AF. This warns clinicians that patients should be converted to sinus rhythm as soon as possible after the initial onset of atrial fibrillation, and the long-term maintenance of sinus rhythm can make the concatenation of atrial fibrillation gradually disappear.
Conversion of coarse fibrillation to fine fibrillation
Coarse fibrillation refers to atrial fibrillation on ECG; 0.2 mV, while amplitude < 0.2 mV is fine fibrillation. At the onset of AF, the ECG often reports the presence of coarse fibrillation waves, which transform into fine fibrillation waves after 1 to 2 years, suggesting that the amplitude of AF waves can decrease as the disease progresses.
The above phenomenon is due to the fact that the frequency of atrial fibrillation waves is relatively low during the initial onset of atrial fibrillation, and the area of atrial muscle involved in each atrial microfold is relatively large, resulting in high amplitude of f waves. As the disease progresses, the f-wave frequency becomes faster, the microfold is more fragmented, and the area of atrial myocardium involved becomes smaller, so the amplitude of the f-wave will become lower.
Similarly, atrial fibrillation often starts as fast AF and changes to slow AF after a few years. Fast AF is defined as ventricular rate; 100 beats/min atrial fibrillation; 100 beats/min as slow AF. The mechanism of progressive change from fast AF to slow AF is that fast and irregular AF waves (350-650 beats/min) try to cross the AV node to agitate the ventricles, and each crossing triggers a ventricular excitation. In fast AF, more AF waves cross the AV node causing a faster ventricular rate, while when the waves become fragmented, their amplitude becomes lower and the number of AF waves increases significantly. It is as if the AV node is a city gate, and when fewer people pass through the gate, there is relatively more order and less crowding, and more people are able to pass through. On the contrary, when too many people are piled up on one side of the gate, the order is disorganized and the number of people passing through the gate decreases instead, which then turns into slow atrial fibrillation.
Atrial fibrillation-ventricular fibrillation-sudden death chain
The ventricular tachycardia-ventricular fibrillation-sudden death disease chain is not new to clinicians, and atrial fibrillation-ventricular fibrillation-sudden death is a newly identified disease chain in recent years in patients placed on buried cardioverter-defibrillators (ICDs).
Data recorded by the ICD show that patients with ventricular fibrillation are the first to develop atrial fibrillation, and that atrial fibrillation with rapid ventricular rate deteriorates cardiac function, activates the patient’s sympathetic nervous system, and triggers ventricular fibrillation through the long and short cycle phenomenon. Therefore, atrial fibrillation is not a benign arrhythmia, and its consequences as a clinical malignant event should be taken seriously.
Difficult brothers of atrial fibrillation
Atrial tachycardia (atrial tachycardia), atrial flutter (atrial flutter) and atrial fibrillation belong to the same type of rapid atrial arrhythmia, and the atrial rates of these three episodes are different, ranging from 150 to 250 beats/min, 250 to 350 beats/min and 350 to 650 beats/min, respectively. In addition to the different atrial rates, the mechanisms of occurrence of the three arrhythmias are also different. Clinically, the same patient may have all three arrhythmias at the same time, and they are often interchangeable and causal. Therefore, the three are often considered as difficult siblings that can be treated with the same antiarrhythmic drugs and radiofrequency surgery.
Labyrinthine surgery and atrial fibrillation
In 1985, Cox proposed and created the surgical Maze technique (Maze) for the treatment of atrial fibrillation. He discovered through animal studies that the foldback waves in atrial fibrillation mainly surround various anatomical openings in the atrial cavity, and that the anatomical integrity of these areas can be prevented by surgically disrupting them. Therefore, by making linear cuts with a scalpel in multiple parts and directions of the atrium, the entire atrium is isolated into interconnected areas of varying sizes by cutting lines, forming a maze-like formation, which allows the f waves after the onset of AF to run only in a small localized area without propagating to other areas (Figure 2), and can achieve the effect of self-generation of AF waves in localized areas of the atrium.
Cox’s labyrinthine procedure has led to a qualitative breakthrough in the surgical treatment of atrial fibrillation, and the results of a group of 346 atrial fibrillation labyrinthine procedures published in 2000 showed an overall success rate and encouraging long-term follow-up results.
The “Rhythm Rate” Debate in Atrial Fibrillation
Atrial fibrillation medications include anticoagulation, ventricular rate control, sinus rhythm reversion, and sinus rhythm maintenance. In recent years, there has been much debate about whether heart rate control or rhythm control is better. Proponents of rhythm control argue that converting AF to sinus rhythm and maintaining it with medication minimizes the risk of disease and achieves the optimal goal of AF medication. In contrast, advocates of rate control argue that the benefits of rhythm control are almost equal to the harms and should not be forced, and that several lines of evidence-based medicine suggest that the ultimate prognosis and cardiovascular event rates for patients with effective ventricular rate control in AF are the same as for those with rhythm control. This suggests that effective ventricular rate control can also lead to a desired clinical outcome.
The two schools of thought have their own views and arguments, and the most scientifically sound theory and method will be the ultimate winner. In other words, when patients with atrial fibrillation can be treated and maintained in sinus rhythm, clinicians should do so without hesitation. When a patient is not easily converted to sinus rhythm after treatment or is not easily maintained after conversion, the physician should not be forced to do so and should choose a treatment strategy that actively controls the ventricular rate. Therefore, individualized treatment based on local and individualized conditions is the philosophy of atrial fibrillation treatment.