Means for intravenous administration. With recent atrial fibrillation (AF) (ejection fraction (AF) up to 7 days old), sinus rhythm can be restored with the help of intravenous administration of flekine, propafenone, sotalol or amiodarone. In patients with heart failure or drastically reduced pumping function of the ventricles, only amiodarone must be used for this purpose: other drugs may worsen myocardial contractility and cause ventricular arrhythmias. Sinus rhythm recovery is possible in no more than 2/3 of cases. The relief effect of amiodarone may require waiting up to 24 hours.
Flankaine and propafenone in some cases do not restore sinus rhythm, but reduce the frequency of atrial activity and, thus, transform AF in TP or atrial tachycardia. Paradoxically, the lower frequency of atrial activity can lead to a noticeable increase in the frequency of ventricular contractions due to the fact that the AV node is able to conduct most or all of the atrial impulses on the ventricles, which sometimes makes it necessary to perform emergency electrical cardioversion.
Dofetilide and ibutilide are newer drugs with class III antiarrhythmic drugs. They are moderately effective as a means of stopping a newly emerging AF (there are more chances for success with TA). However, when they are used, there is a significant risk of developing tirade de pointes. In the UK, these drugs are currently unavailable.
One of the means of a new group of drugs that have a selective effect on the electrophysiological properties of atrial myocardium is vernacalant. It has been shown that with recent AF, intravenous administration of the drug restores sinus rhythm within a few minutes in about 50% of patients.
It should be borne in mind that almost half of the episodes of recent atrial fibrillation (AF) for 8 hours spontaneously stop. Therefore, strictly speaking, the introduction of antiarrhythmic drugs is not necessary in order to restore sinus rhythm in each case!
Ineffective drugs. Digoxin is ineffective as a means of restoring sinus rhythm, and there is evidence that it can actually contribute to the preservation of arrhythmia by shortening the refractory period of atrial myocardium. BAB and calcium channel blockers, although they have the ability to effectively reduce the frequency of ventricular contractions in AF, do not restore sinus rhythm.
Drugs for oral administration. Flekainid and propafenone have moderate efficacy in preventing recurrences of AF and have the same contraindications for use as with intravenous administration. They should not be prescribed to patients with myocardial dysfunction or ischemic heart disease, and if TP occurs, which can lead to a significant increase in the frequency of ventricular contractions, ideally should be combined with BAB or calcium channel blockers. The author of these lines gives preference to flekainid and, with normal ventricular function, recommends it as a first-line agent.
BAB rarely prevent atrial fibrillation (AF), but if the medical history suggests that arrhythmia is provoked by exercise or due to hyperthyroidism, they are the drugs of choice. Some (but not all) studies have shown that sothalol, a class III antiarrhythmic drug, is more effective in preventing AF, compared with other BABs, but should be avoided in patients with a prolonged QT interval.
The most effective means of preventing recurrence of atrial fibrillation (AF) is amiodarone, but due to the high incidence of undesirable effects, the drug should only be used as a backup for treating patients with severe symptoms if the other drugs listed above have been ineffective or cannot be prescribed. Amiodarone is the drug of choice in treating patients with heart failure.
Dronedarone, a derivative of amiodarone, due to reports of a large number of cardiac and extracardiac adverse effects, is currently recommended only as a second-line drug for maintaining sinus rhythm in adult clinically stable patients with paroxysmal AF or persistent AF after successful cardioversion.
For the prevention of paroxysmal atrial fibrillation for many years used quinidine. However, a meta-analysis of research data showed that taking the drug is associated with a significant increase in mortality (presumably due to its proarrhythmic action), so it is no longer used to prevent recurrence of AF.
Digoxin shortens the refractory period of the atrial myocardium and thus increases the susceptibility to AF. There is no evidence that it prevents arrhythmia.
A number of drugs slow down AV conduction (the so-called negative dromotropic effect) and thereby reduce heart rate with persistent AF.
1. Calcium channel blockers in atrial fibrillation Intravenous verapamil quickly and effectively suppresses AV conduction, and thus within a few minutes helps to reduce the frequency of ventricular contractions against the background of persistent AF. At the same time, however, it is unlikely that the sinus rhythm will be restored. In fact, there is good reason to believe that verapamil may contribute to the persistence of arrhythmias. Ingestion of verapamil (120-240 mg / day) usually also allows for effective control of the frequency of ventricular contractions in the background of AF both at rest and during exercise. Diltiazem (but not dihydropyridine calcium channel blockers nifedipine and amlodipine) has a verapamil-like effect. Inside the drug is prescribed in a long-acting dosage form at a dose of 200-300 mg / day. Patients with heart failure are advised to avoid prescribing these drugs or use them with caution.
2. Beta-blockers in atrial fibrillation BAB have an effect similar to that of calcium channel blockers.
3. Digoxin in atrial fibrillation The administration of digoxin orally is widely used to control the frequency of ventricular contractions in the background of atrial fibrillation (AF). Its advantages are the long duration of action and the presence of a positive inotropic effect. However, digoxin often does not allow for adequate control of heart rate at rest and rarely provides rhythm control during physical activity, despite adequate plasma concentration. Side effects are often observed. Old age, renal or electrolyte disorders, the appointment of other drugs can contribute to the development of digitalis intoxication in patients taking the drug in an adequate therapeutic dose. Intravenous administration of digoxin is usually ineffective in rapidly reducing the frequency of ventricular contractions during atrial fibrillation (AF). As indicated below, digoxin does not allow to stop or prevent AF. Due to the many restrictions on the use of the drug and the possibility of reducing the frequency of ventricular contractions with AF, using calcium channel blockers or BAB, digoxin may no longer be used for this purpose.
4. Assessment of the adequacy of rhythm frequency control It is important to remember that although monitoring the frequency of ventricular contractions may seem satisfactory at rest, it is often possible to inadequately increase the heart rate during exercise. To ensure that adequate heart rate control is achieved against the background of FP, outpatient ECG monitoring should ideally be used. Standard, although arbitrarily chosen values, indicating effective control of heart rate, are 60-80 beats / min at rest and 90-115 beats / min during moderate exercise. A “soft frequency control” strategy, aimed at maintaining the ventricular rate at less than 110 beats / min at rest, has recently been compared with the standard “strict frequency control” strategy. It was shown that the first of the mentioned strategies is not inferior to the latter. Although asymptomatic patients “mild frequency control” may be considered acceptable, in patients with severe symptoms (such as shortness of breath and palpitations), as well as in individuals with significantly reduced ventricular pumping function, it is important to achieve good control over the frequency of their contractions.
5. High and low frequency of ventricular contractions during atrial fibrillation Some patients with atrial fibrillation (AF) have both very high and low frequency of ventricular contractions during daytime (with AF, a low frequency during sleep is considered normal). In some cases, to suppress high frequencies with the help of drugs that block AV-conduction, the ventricular ECM may be required. In some patients with atrial fibrillation (AF), probably due to impaired AV conduction, there is no adequate increase in heart rate in response to exercise (chronotropic insufficiency). To improve tolerance to a physical load will allow EX- with function of frequency adaptation.
6. Heart failure in atrial fibrillation. Particular attention should be given to patients with heart failure and atrial fibrillation (AF). Persistently high frequency of ventricular contractions may worsen the course of heart failure or be its true cause. As mentioned above, in some patients, due to a violation of AV conduction (both spontaneous and medically caused by drugs, such as BAB), chronotropic insufficiency can be observed. Therefore, it is important to ensure that the patient’s tolerance to physical exertion is not limited by the inability of the heart to adequately increase heart rate during its implementation.
The choice of treatment depends on whether the goal is to control the frequency of ventricular contractions while maintaining atrial fibrillation (AF) or maintaining sinus rhythm. These two strategies are called “rate control” and “rhythm control” (rhythm control), respectively. In general, frequency control is easier than rhythm control.
Atrial fibrillation (AF) results in a loss of mechanical atrial systole before ventricular contraction and often inadequately high heart rate. This leads to a decrease in cardiac output. Therefore, one would expect that the patient’s condition would be better while maintaining normal sinus rhythm than while maintaining persistent or paroxysmal AF.
Nevertheless, several large studies have revealed that in terms of mortality, hospitalization rate and quality of life, the rhythm control strategy is no better than the strategy aimed at controlling heart rate. Patients who participated in these studies were predominantly elderly, and many of them suffered from cardiovascular disease.
Therefore, the results obtained cannot be applied without fail to all patients with atrial fibrillation (AF). For example, young people with paroxysmal idiopathic AF often have more pronounced symptoms, and maintaining sinus rhythm in them is more appropriate.
Although studies have shown that treatment strategies aimed at maintaining sinus rhythm are not better than the “frequency control” strategy, it is important to note that a stable preservation of the normal heart rhythm was not achieved in many patients from the “rhythm control” group. Therefore, it is highly likely that maintaining a normal rhythm still leads to a therapeutic outcome.
This assumption is confirmed by the results of both long-standing and recent studies that indicate that maintaining sinus rhythm improves the quality of life and tolerance to physical exertion. If a safe and relatively cheap way to maintain sinus rhythm is found, the “frequency control” strategy can, of course, be abandoned.
Some patients with atrial fibrillation (AF), despite effective heart rate control, experience very uncomfortable symptoms and feel much better with normal sinus rhythm. Others, including those who did not experience symptoms prior to treatment, feel quite well when pursuing a “frequency control” strategy. Thus, the treatment must be selected individually.
Often the strategy of “rhythm control” ends in failure, which makes it necessary to use the strategy of “frequency control”. However, in patients with severe clinical symptoms, an “aggressive” approach to maintaining sinus rhythm is justified.
It was shown that dabigatran in a dose of 150 mg 2 times a day is more effective in preventing ischemic stroke than warfarin, and in a dose of 110 mg 2 times a day is not inferior to warfarin in effectiveness. Unlike warfarin, therapeutic levels of the drug are observed already 2 h after administration, and the state of stable equilibrium plasma concentration is reached within 2 days. Dabigatran is excreted primarily by the kidneys and is therefore contraindicated for severely impaired renal function or continued massive bleeding.
The dose of the drug should be reduced to 110 mg 2 times a day if the patient is over 80 years old or if the patient is receiving verapamil or when a high risk of bleeding is assumed. In moderate renal insufficiency, the drug is recommended to be administered at a dose of 75 mg 2 times a day.
In the UK, according to the latest changes in recommendations, it is allowed to use new oral anticoagulants (such as dabigatran) after talking with the patient about the advantages and disadvantages of these drugs compared to warfarin. However, these recommendations do not apply to women aged 65-74 without other cardiovascular risk factors that have up to 2 points inclusive on the CHA2DS2VASc scale.
The main adverse effects are relatively rare dyspeptic disorders, diarrhea. Simultaneous systematic use of ketoconazole, cyclosporine, itraconazole or tacrolimus is contraindicated. It was also reported on the interaction of the drug with dronedarone and amiodarone.
Reception of dabigatran should be suspended 2 days before the planned operation, and if the clearance of the drug is reduced due to renal failure, 3-4 days. There is no specific antidote. If the patient switches from warfarin to dabigatran, the reception of the latter should be started with an MHO of less than 2.0.
Warfarin, an antagonist of vitamin K, is well known in clinical practice, but it has significant drawbacks. To regulate the dose of the drug in order to maintain an internationally normalized ratio (MHO) at the therapeutic level (between 2.0 and 3.0), regular blood tests are required. In a significant proportion of patients, maintenance of anticoagulation at a therapeutic level cannot be achieved.
Many drugs affect the metabolism of warfarin and can lead to excessive anticoagulation (these include antibiotics, anticonvulsants, some statins, amiodarone, tamoxifen, and alcohol). The risk of bleeding may increase while taking aspirin. In connection with these shortcomings of the drug, doctors are often reluctant to prescribe warfarin, and patients in some cases refuse to take it.
Before surgery, it may be necessary to stop taking warfarin, which was prescribed to prevent systemic thromboembolic complications in patients with AF. In such cases, it is customary to prescribe heparin as a temporary bridge, but the use of heparin often creates the problem of bleeding and the formation of postoperative hematomas. In fact, the need for such a “heparin bridge” rarely arises: you can stop taking warfarin 3 days before the operation and resume 3 days after it.
More modern drugs. Recently, thrombin and factor Xa inhibitors have become available, which are prescribed in fixed dosages and therefore do not require regular blood tests to monitor their effectiveness. It has been shown that they are at least as effective as warfarin, and their use is associated with less or at least a similar risk of bleeding (especially intracranial hemorrhage), in addition, they interact to a lesser extent with other drugs. Nevertheless, although the results of clinical studies are promising, the experience of using these tools in clinical practice is still small.
Atrial fibrillation classification
Isolated (ie, idiopathic) atrial fibrillation (AF), which occurs in patients younger than 60 years of age, is very common. Although the prognosis is good and the risk of systemic embolism is low (approximately 1.3% over a 15-year period), idiopathic AF can cause very serious symptoms and patient anxiety. Like a “secondary” OP, an isolated OP can be paroxysmal or persistent.
Paroxysmal isolated atrial fibrillation
Only one or several very rare episodes of arrhythmia are possible, but in some cases atrial fibrillation (AF) often recurs, sometimes several times a day.
Paroxysms can last for many hours or end in a few seconds. Over time, some patients (but not all) of AF become persistent.
Studies show that an episode of atrial fibrillation (AF) can lead to changes in the electrical properties of the atria that help to maintain arrhythmias — this process is referred to as “electrical remodeling.”
Often, patients have very serious symptoms. In other cases, including frequent relapses occurring with a high frequency of ventricular contractions, arrhythmia may be asymptomatic or accompanied only by the sensation of arrhythmia, without any discomfort due to high heart rate.
Only some patients can name the factors immediately preceding the arrhythmia and, possibly, provoking it (such as physical exertion, vomiting, alcohol intake or fatigue). One of the forms of paroxysmal idiopathic AF is caused by an increase in the tone of the vagus nerve: an arrhythmia always begins during rest or sleep.
Causes of atrial fibrillation and their prognosis
The most common causes are damage to or impairment of the function of the heart muscle as a result of myocardial infarction, hypertension or cardiomyopathy, as well as valvular heart disease, hyperthyroidism, and SSS. In many cases, AF is idiopathic, i.e. without any obvious reason.
IHD (i.e., stenosing atherosclerosis of the coronary arteries) is not in itself a cause of atrial fibrillation (AF). However, arrhythmia often complicates myocardial infarction in both acute and long-term periods and serves as an indicator of extensive myocardial damage.
Many of the listed causes of atrial fibrillation (AF) can be identified or excluded by clinical examination, ECG and echocardiography. To exclude hyperthyroidism, it is necessary to determine the level of thyroxine and thyroid-stimulating hormone in the serum. If an SSS is suspected, outpatient ECG monitoring may be required.
Prevalence of Atrial Fibrillation (AF)
The prevalence of atrial fibrillation (AF) increases with age. In the UK, when examining male civil servants, FP was found at 0.16, 0.37 and 1.13% of people aged 40–49, 50–59 and 60–64 years, respectively. Among patients monitored by British general practitioners, arrhythmia was detected in 3.7% of patients over 65 years of age.
According to the Framingham study, it was found that 7.8% of men aged 65-74 years suffer from atrial fibrillation (AF). The prevalence of arrhythmias among men aged 75-84 increases to 11.7%. It is estimated that the probability of occurrence of AF in a person’s life is 26%.
Even among those who do not have heart failure and do not tolerate myocardial infarction, this risk is about 15%. In men, arrhythmia occurs 1.5 times more often than in women.
Atrial fibrillation (AF) prognosis
The main factor determining the prognosis is the presence or absence of organic heart disease. For example, with MI, the prognosis is unfavorable, since AF is usually the result of extensive myocardial damage. Many studies have shown that with idiopathic AF, the prognosis is favorable.
AV conduction
AV conduction increases with an increase in sympathetic activity and is suppressed with an increase in the tone of the vagus nerve. Usually, during periods of patient activity, the frequency of ventricular contractions is high (up to 200 beats / min), while at rest or during sleep it decreases.
Absolutely irregular ventricular rhythm indicates the presence of AF, no matter how small or large the frequency of ventricular contractions.
Intraventricular conduction. Ventricular complexes with FP have a normal duration, except for cases of blockade of the bundle of the His, WPW syndrome or aberrant intraventricular conduction, i.e. frequency-dependent blockade of the bundle branch block. Aberrant intraventricular conduction.
Aberrant conduction is the result of different lengths of the recovery period (i.e. the exit period from the refractoriness state) in the two legs of the His bundle. An early atrial impulse can reach the ventricles at a time when one of the legs of the bundle of His is still refractory to activation after the previous cardiac cycle, while the other is already capable of conduction.
As a result, the ventricular complex will have a configuration characteristic of the blockade of the corresponding bundle of the His. Since the right leg usually has a longer refractory period, aberrant conduction usually leads to blockade of PNPG. The duration of the refractory period of the feet of the bundle of His depends on the duration of the previous cardiac cycle. Therefore, an aberration of conducting is more likely to occur when a short cycle follows a long one (the “Ashman phenomenon”). Sometimes a series of aberrant complexes can be mistakenly interpreted as paroxysmal ventricular tachycardia.
However, even if the frequency of ventricular contractions is very high, it is possible to reveal a distinct irregularity of the cardiac cycle; In addition, the question is legitimate: why during AF, there must be “jogging” of another arrhythmia?
The occurrence of atrial fibrillation. AF is usually initiated by atrial extrasystole. Sometimes TP or ABPT is transformed into fibrillation.
Atrial fibrillation
Atrial fibrillation (AF) is the most common arrhythmia. Indeed, due to the increase in life expectancy in the population as a whole, and among patients with heart disease, its prevalence is constantly increasing.
It is important to know the various causes and clinical manifestations of arrhythmia and to understand that the tactics of treatment should be individualized depending on the etiology associated with the risk of arrhythmia and the symptoms present.
When atrial fibrillation (AF), the atria are activated with a frequency of 350 to 600 imp./min. Arrhythmia is caused by the existence of numerous excitation waves circulating in random directions within the atrial myocardium. A very high frequency of electrical activity leads to the loss of effective mechanical atrial systole.
1) Atrial activity in atrial fibrillation. High-frequency and chaotic electrical activity of the atria during AF leads to the appearance of very frequent, low-amplitude and irregular waves f. The amplitude of these waves varies in different patients and in different ECG leads: in some leads, the f waves may be imperceptible, whereas in other leads (especially in lead V1) they can be so pronounced that it is possible to assume the presence of TP, although atrial activity has more high frequency, than it usually happens when trembling. Teeth P, of course, absent.
2) Atrioventricular conduction during atrial fibrillation. Fortunately, the AV-node is not able to conduct all the atrial impulses on the ventricles: if this were possible, the VF would develop as a result! Some impulses are completely blocked, others only partially penetrate the AV node and therefore do not excite the ventricles, but can block or delay the passage of subsequent impulses. This process of “latent holding” is responsible for the irregular rhythm of the ventricles, which is the hallmark of this arrhythmia.
The absence of P-waves (even in the absence of noticeable f waves) and an irregular ventricular rhythm indicate the presence of AF. AF with a high frequency of ventricular contractions is often not diagnosed. Errors can be avoided by remembering that an irregularity of ventricular rhythm is a characteristic feature of arrhythmia. However, if against the background of AF, complete AV block develops, then the ventricular rhythm, of course, becomes slow and regular. The frequency of ventricular contractions in AF depends on the conductive ability of the AV node, which, in turn, is affected by the autonomic nervous system.
ECG in atrial fibrillation (AF)
Atrial fibrillation (AF) is characterized by an absolutely irregular ventricular rhythm and the absence of teeth R. It can be paroxysmal, persistent or permanent (in the Russian-language literature in relation to permanent AF, the terms “permanent” or “chronic” are often used). Causes may include hypertension, MI, cardiomyopathy, valvular heart disease, hyperthyroidism, SSS, and alcohol use. Often, arrhythmia is idiopathic. Its prevalence increases with age, the probability of its occurrence throughout life is 26%.
An individual approach to treatment is necessary, taking into account the etiological factors, clinical manifestations and risks of the arrhythmia itself. Although in most cases it is possible to restore sinus rhythm using cardioversion, quite often the arrhythmia recurs. You can stop and / or prevent the recurrence of OP using flekainid, amio-daron and sotalol, but not digoxin. The frequency of ventricular contractions in AF can be controlled using calcium channel blockers or BAB; use of digoxin may not be enough to control the rhythm, especially during physical exertion.
Stratification of the risk of systemic emboli using the CHA2DS2VASc scale allows you to choose how to prevent these complications with non-valvular AF: taking aspirin, indirect anticoagulants (for example, warfarin or dabigatran) or performing an intervention to occlude the left atrium (LP) using a special device.