Atrial fibrillation (AF) is one of the most common cardiac arrhythmias. According to data published in 2004, the prevalence of atrial fibrillation in China is 0.77% among residents aged 30 to 85 years, with a prevalence of more than 30% among those aged 80 years and older. Thromboembolic complications are the main cause of death and disability in AF, with stroke being the most common type of presentation. In patients with non-valvular AF, the annual incidence of ischemic stroke (approximately 5%) is 2 to 7 times higher than in non-AF patients. Prevention of new and recurrent strokes should be a major component of a comprehensive management strategy for patients with atrial fibrillation. A growing number of studies have confirmed that the rational use of anticoagulants in patients at increased risk of stroke can help to significantly reduce the incidence of ischemic stroke, yet most patients with AF in China do not receive anticoagulation therapy [1,2]. It is important to further increase the awareness of the dangers of AF and its complications and to enhance the prevention of thromboembolic complications (especially stroke) to improve the prognosis of patients and to reduce the socioeconomic and family burden associated with them. Several oral anticoagulants have been used in clinical practice, such as warfarin, dabigatran, rivaroxaban and apixaban. In order to promote and standardize anticoagulation therapy for patients with atrial fibrillation and reduce the incidence of thromboembolic complications in ischemic stroke, the Chinese Society of Cardiovascular Diseases, the Chinese Society of Cardiac Electrophysiology and Pacing, the Cardiovascular and Cerebrovascular Disease Committee of the Chinese Gerontological Society, the Rhythm Branch of Chinese Biomedical Engineering, the Evidence-Based Medicine Committee of the Chinese Physicians Association, and the Arrhythmia Alliance (China) have organized domestic experts to develop this expert consensus. This expert consensus has been developed.
1. Risk stratification of stroke and thromboembolism in patients with atrial fibrillation and principles of anticoagulation therapy
Appropriate anticoagulation therapy is an effective measure to prevent thromboembolic events in patients with atrial fibrillation, but at the same time it increases the risk of bleeding complications. Therefore, the benefit-risk ratio should be assessed before determining whether a patient is suitable for anticoagulation, and anticoagulation should be initiated only if the benefit of preventing thromboembolic events clearly outweighs the risk of hemorrhagic complications. The level of risk of ischemic stroke in patients with atrial fibrillation is closely related to their baseline characteristics, and risk stratification of patients based on baseline characteristics is the basis for the development of a proper anticoagulation strategy [7]. Currently, the CHADS2 scoring system is the most widely used clinical assessment tool, and its scoring method is shown in Table 1 [8]. As the CHADS2 score increases, the risk of future ischemic stroke in patients with atrial fibrillation gradually increases. In the absence of contraindications, all patients with atrial fibrillation with a CHADS2 score ≥2 should undergo long-term oral anticoagulant therapy. Patients with a CHADS2 score of 1 may be treated with aspirin (100 mg-300 mg, qd), and some patients may be considered for oral anticoagulation, while those with a CHADS2 score of 0 generally do not require anticoagulation.
Although there is conclusive research evidence that standardized anticoagulation for patients with atrial fibrillation at increased risk of thromboembolic events can significantly improve patient prognosis, most patients with atrial fibrillation in China are not treated with anticoagulants. In contrast, most of the patients on warfarin are not systematically monitored for international normalized ratio (INR) or the INR remains ineffectively low (1.3-1.5). The reasons for this state of affairs are manifold, among which the lack of awareness of clinicians about the dangers of thromboembolic complications and the excessive concern about the increased risk of bleeding associated with conventional anticoagulant warfarin therapy are probably the main reasons. In fact, the benefits of anticoagulation in patients with atrial fibrillation far outweigh the risks of complications associated with anticoagulation therapy, provided that the relevant guidelines are followed and the indications are properly grasped and coagulation function is monitored as required.
2. Anticoagulation therapy for patients with atrial fibrillation
(1) Application of warfarin in anticoagulation therapy for patients with atrial fibrillation
Warfarin has been widely used in clinical practice for more than 60 years and has been playing an important role in the prevention of ischemic stroke in patients with atrial fibrillation. The drug exerts its anticoagulant effect by reducing the synthesis of coagulation factors II, VII, IX & X, among others. The full anticoagulant effect can only be achieved when all vitamin K-dependent coagulation factors are inhibited, so the maximum efficacy of warfarin is mostly achieved after 4-5 days of continuous dosing, and its anticoagulant effect is completely lost only after 5-7 days of discontinuation.
(2) Research evidence
Several randomized clinical studies have so far demonstrated the role of warfarin in the primary and secondary prevention of stroke in patients with atrial fibrillation, showing that long-term warfarin therapy in patients with moderate-to-high-risk atrial fibrillation, with close monitoring of the INR, is effective in reducing the risk of ischemic stroke and is significantly more effective than placebo, aspirin, and aspirin combined with clopidogrel [9-11]. A meta-analysis of available studies showed [12] that warfarin treatment reduced the relative risk of stroke by 64% and the absolute risk of stroke by 2.7% per year in patients with atrial fibrillation. When only ischemic stroke was calculated, application of dose-adjusted warfarin treatment reduced the relative risk by 67% and the benefit was of the same magnitude in preventing initial and recurrent strokes. Warfarin treatment resulted in a significant 26% reduction in all-cause mortality with a low incidence of intracranial hemorrhage. This meta-analysis also found that interruptions in warfarin therapy or inadequate anticoagulation intensity in patients with atrial fibrillation significantly increased the risk of stroke.
(3) Dosing method
Although guidelines such as those of the United States recommend a starting dose of warfarin of 5 mg/d-10 mg/d [13], the dose of warfarin required to achieve the INR target in our population may be lower than in patients in Europe and the United States due to ethnic and weight differences, so warfarin therapy should be started at a lower dose (e.g., 1.5 mg/d-3.0 mg/d). If the INR does not reach the target with the initial dose, the INR can be gradually increased in the range of 1.0mg/d-1.5mg/d and continuously tested until it reaches the target value. Special populations (e.g., elderly, frail, malnourished, heart failure, liver disease, recent surgical treatment, or those taking drugs that potentiate the effects of warfarin) should start at lower doses (e.g., <1.5 mg/d).
During the course of warfarin therapy, the INR should be monitored periodically and the warfarin dose should be adjusted accordingly to control the INR between 2.0 and 3.0. Although the above target INR values are mainly derived from the results of clinical studies in Europe and the United States, there is no evidence that Chinese patients need to adopt a lower INR target value. If the INR does not reach the above range, it may not be effective in preventing thromboembolic events due to insufficient anticoagulant effect. Some authors have suggested that a lower INR target value (1.8-2.5) is appropriate for warfarin therapy in elderly patients, but evidence from large clinical studies is lacking for this view. Cohort studies suggest that patients with atrial fibrillation treated with warfarin have a 2-fold increased risk of stroke with an INR in the range of 1.5-2.0. Therefore, this consensus recommends that older patients should adopt the same INR target values as the general adult population (2.0-3.0).
The frequency of INR monitoring should be patient-specific. At the beginning of warfarin treatment, INR should be tested at least every 3-5 days, and after the INR reaches the target value and the warfarin dose is relatively fixed, testing every 4 weeks is sufficient. If the patient is treated with drugs that may affect the effect of warfarin or if other disorders occur during the course of warfarin therapy, the frequency of testing should be increased and the warfarin dose should be adjusted as appropriate. Drugs commonly used to enhance the anticoagulant effect of warfarin include: antiplatelet agents, NSAIDs, quinidine, chloral hydrate, chloramphenicol, promethazine, cimetidine, etc. Some broad-spectrum antimicrobials may enhance the effect of warfarin by reducing the synthesis of vitamin K. Common drugs that reduce the anticoagulant effect of warfarin include: phenobarbital, phenytoin sodium, vitamin K, estrogen, acid reducers, laxatives, rifampin, chlorothiazide, spironolactone, etc. Some herbal medicines (e.g. Salvia, Ginseng, Angelica, Ginkgo, etc.) can have a significant effect on the anticoagulant effect of warfarin, so monitoring should be enhanced when receiving concurrent herbal treatment. Some foods (e.g. grapefruit, mango, garlic, ginger, onion, kelp, cauliflower, kale, carrot, etc.) may also enhance or diminish the anticoagulant effect of warfarin, which should be paid attention to in the course of drug administration.
(4) Treatment of increased INR or bleeding complications
If the INR is higher than the target value or bleeding complications occur during warfarin treatment, the patient should be actively treated. See Table 2 for specific treatment.
(5) Contraindications
Warfarin therapy is temporarily contraindicated in the following cases.
Perioperative (including ophthalmic and oral surgery) or traumatic injury.
Obvious hepatic or renal impairment.
Moderate to severe hypertension (blood pressure ≥ 160/100 mmHg).
Coagulopathy with bleeding tendency.
Active peptic ulcer.
Pregnancy.
Other bleeding disorders.
(6) Limitations
Although the anticoagulant effect of warfarin is positive, there are some limitations of this drug. First, the extent to which coagulation mechanisms are affected by warfarin application varies widely and unpredictably among individuals, so the effective dose varies widely. Second, the anticoagulant effect of the drug is susceptible to the effects of various foods and drugs, and frequent monitoring of coagulation and timely adjustment of drug doses are required during the course of administration, which can affect patient compliance with long-term therapy. The establishment of a sound atrial fibrillation clinic or anticoagulation clinic, where experienced specialists systematically manage atrial fibrillation patients receiving anticoagulation therapy, can help to overcome its limitations to a certain extent.
(7) Assessment of bleeding risk when applying oral anticoagulants
Anticoagulation therapy may increase the risk of bleeding complications in patients, therefore, attention should be paid to assessing the bleeding risk of patients before and during treatment, and determining the appropriate treatment plan based on the assessment results. There are several assessment methods used in clinical practice, among which the HAS-BLED scoring system is considered to be the easiest and most reliable option. Patients with a score of 0 to 2 are considered to be at low risk of bleeding, while a score of ≥3 indicates an increased risk of bleeding.
It should be noted that patients at increased risk for bleeding tend to be at increased risk for thromboembolic events, and the static benefit of anticoagulation may be greater in these patients. Therefore, anticoagulant therapy should be administered as long as the patient has an indication for anticoagulation (CHADS2 score ≥2), and an increased HAS-BLED score should not be considered a contraindication to anticoagulation. Care should be taken to screen for and correct reversible factors that increase the risk of bleeding in such patients, and further intensive monitoring is required. The initial dose of warfarin therapy should be lower (1.0 mg/d-1.5 mg/d) and the frequency of monitoring coagulation markers should be increased. INR needs to be tested every 1-2 days when starting warfarin therapy or during dose adjustment, and every 2 weeks after INR reaches the standard.
2. Immediate detection of INR and patient self-management
Monitoring INR as required is an important guarantee of safe and effective anticoagulation therapy for patients with atrial fibrillation. At present, INR testing for patients with atrial fibrillation in China is mainly done in the central laboratory of the hospital. Although this model can ensure the quality of monitoring, it affects patient compliance to a certain extent because of the complicated process, long waiting time and the need to use venous blood specimens and other limitations. Recently, China began to introduce the point-of-care test (POCT), which is easy to operate and requires only a drop of finger blood to report test results instantly, greatly simplifying the testing process for anticoagulation therapy and providing convenience for rapid outpatient and emergency testing of INR and home monitoring of patients. Clinical studies have shown that the application of POCT technology for home self-monitoring in patients taking warfarin is equally effective compared with monthly high-quality clinical testing [14].
The standardized POCT technique is essential to ensure the reliability of the test results, so the necessary technical training should be provided to the users of the POCT instrument to ensure the standardization of its operation. If abnormally high or low POCT results are found, it is recommended that venous blood be collected in a central hospital laboratory to review the test results and make the necessary adjustments to the anticoagulation regimen as appropriate.
Experience in Europe and the United States has shown that the establishment of specialized atrial fibrillation clinics or anticoagulation clinics is an effective measure to improve anticoagulation coverage and prevent thromboembolic complications in patients with atrial fibrillation. At present, some large hospitals in China have made useful attempts and explorations in this regard and achieved good results, which is worth promoting in large and medium-sized hospitals in China.
(3) The role of aspirin in the prevention of thromboembolic events in patients with atrial fibrillation
The value of aspirin for thromboembolic events in patients with atrial fibrillation has been controversial. Although some authors have suggested that aspirin therapy may be considered for those with a low risk of thrombosis (CHADS2 score 0-1), this suggestion lacks sufficient evidence. A new large cohort study including 132,372 patients with non-valvular atrial fibrillation suggested that aspirin, either alone or in combination with warfarin, did not have significant antithrombotic efficacy but increased the risk of bleeding [15]. Therefore, the role of aspirin in the prevention of thrombotic events in patients with atrial fibrillation remains to be further explored.
(4) Novel oral anticoagulants
Novel anticoagulants can specifically block a critical link in the coagulation waterfall and significantly reduce the risk of bleeding while ensuring anticoagulation efficacy. New anticoagulants currently under development or already on the market include direct thrombin inhibitors, factor Xa inhibitors, factor IX inhibitors, tissue factor inhibitors, and new vitamin K antagonists, the representative drugs of which include direct thrombin inhibitor dabigatranate and direct factor Xa inhibitors rivaroxaban and apixaban. The new oral anticoagulants do not require routine monitoring of coagulation function during treatment, making it easier for patients to receive long-term treatment.
①Dabigatran etexilate
The direct thrombin inhibitor dabigatranate acts on prothrombin (i.e., factor IIa) to exert anticoagulant effects [16, 17]. The RE-LY study (Randomized evaluation of long term anticoagulant therapy) provided clinical evidence of dabigatranate in long-term anticoagulant therapy in patients with atrial fibrillation [18]. The aim of this study was to evaluate the efficacy and safety of two doses of dabigatran applied to patients with atrial fibrillation and its comparison with warfarin. A total of 18,113 patients with ECG-confirmed AF within 6 months prior to the study were enrolled, with a mean CHADS2 score of 2.1. Patients were randomized to three groups receiving dabigatranate 110 mg bid, 150 mg bid, and warfarin, with warfarin dose adjusted according to INR values (target 2.0-3.0), and a median follow-up of 2.0 years. The study results showed that the incidence of the primary effectiveness endpoint (stroke or body circulation thrombosis) was 1.53%, 1.11%, and 1.69% in the dabigatranate 110 mg bid, 150 mg bid, and warfarin groups, respectively. The incidence of the primary safety endpoint (major bleeding) was higher in the warfarin group than in the dabigatranate 110 mg group (p=0.003), but there was no statistical difference in the incidence of major bleeding events between the dabigatran 150 mg and warfarin groups (p=0.31). With regard to the secondary endpoint of stroke incidence, the dabigatranate 150 mg group was lower than the warfarin group (p<0.001), but there was no reduction in stroke incidence in the 110 mg group compared with the warfarin group (p=0.41). This study suggests that dabigatranate (150 mg bid) was more effective than warfarin in patients with atrial fibrillation, and its bleeding complication rate was similar to that of the warfarin-treated group; bleeding complications were reduced at the dabigatranate dose of 110 mg bid, while its efficacy was similar to that of the warfarin-treated group.
Routine monitoring of coagulation during dabigatranate therapy is not required, but dose reduction and increased monitoring are needed for those with advanced age (≥75 years), reduced renal function, frailty, and other bleeding risk factors to avoid serious bleeding events [19,20]
②Rivaroxaban
The ROCKET-AF study (Rivaroxaban once-daily oral direct factor Xa inhibition compared with vitamin K) has shown significant anticoagulant efficacy. antagonism for prevention of stroke and embolism trial in atrial fibrillation) evaluated the efficacy of rivaroxaban for the prevention of thromboembolic events in patients with atrial fibrillation [25]. The study used a randomized, double-blind, double-simulation, event-driven design with the aim of demonstrating that rivaroxaban is no less effective than warfarin in preventing stroke events in patients with non-valvular atrial fibrillation. A total of 14,264 subjects were enrolled with a history of stroke, transient ischemic attack, or embolism of the body circulation, or the presence of at least 2 independent risk factors for stroke (including chronic heart failure, hypertension, age ≥75 years, and diabetes mellitus). Subjects were randomly assigned to either the rivaroxaban group (20 mg qd) or the warfarin group (warfarin dose adjusted according to INR [target value of 2.0-3.0]) and followed until the end of the study when a total of 405 primary endpoint events occurred. The results showed a 21% reduction in the rate of the primary effectiveness endpoint (stroke and non-CNS embolic events) in the rivaroxaban group compared with patients in the adjusted-dose warfarin group (p<0.001); a 14% reduction in the rate of vascular death, stroke and non-CNS embolism in the rivaroxaban group (p=0.034), and a significant reduction in the rate of both hemorrhagic stroke and non-CNS embolic events. The incidence of both hemorrhagic stroke and non-CNS embolic events were significantly lower. In terms of safety endpoints, the rates of major bleeding and clinically significant non-major bleeding events in the rivaroxaban group were comparable to those in the warfarin group (p=0.442). Patients in the rivaroxaban-treated group had a 33% reduction in the incidence of intracranial hemorrhage (p=0.019), a 31% reduction in the incidence of critical organ bleeding (p=0.007), and a 50% reduction in bleeding-related deaths (p=0.003). Available evidence suggests that rivaroxaban is no less effective than, or even better than, warfarin in preventing thromboembolic events in patients with non-valvular atrial fibrillation, and has a better safety profile.
(iii) Apixaban
The AVERROES study (Apixaban versus acetylsalicylic acid to prevent strokes in AF patients who have failed or are unsuitable for vitamin K antagonist treatment) showed that apixaban was more effective than aspirin in preventing stroke and systemic thromboembolic events without increasing the risk of severe bleeding in patients who were not suitable for warfarin treatment [26]. A total of 5,599 patients with atrial fibrillation who had at least 1 stroke risk factor and were not suitable for warfarin therapy were randomized to apixaban (5 mg, b.i.d) or aspirin (81-324 mg/d) therapy with a mean follow-up period of 1.1 years. The incidence of the primary endpoint (stroke and embolism of the body circulation) was found to be 1.6% per year in the apixaban group, significantly lower than in the aspirin group (3.7% per year, p<0.001). The incidence of major bleeding was similar in the apixaban and aspirin groups (1.4% versus 1.2% per year, respectively, p=0.57). The ARISTOTLE (Apixaban for reduction in stroke and other thromboembolic events in atrial fibrillation) study was terminated early because the results of the interim analysis showed a significantly greater benefit in the apixaban group than in the aspirin group. The primary objective was to demonstrate that apixaban was no less effective than warfarin in preventing the primary composite endpoint (ischemic or hemorrhagic stroke and circulatory embolism), and the secondary objective was to investigate whether apixaban was more effective than warfarin in preventing the composite endpoint of ischemic or hemorrhagic stroke, circulatory embolism, and all-cause death. A total of 18,201 patients with atrial fibrillation with risk factors for stroke were randomly assigned to either the apixaban (5 mg, bid, with some patients applying a dose of 2.5 mg, bid) treatment group or the dose-adjusted warfarin treatment group (INR target values of 2.0-3.0) for a minimum treatment period of 12 months. After a mean follow-up of 1.8 years, apixaban was shown to reduce the risk of the primary composite endpoint by 21% (p<0.001), the risk of severe bleeding by 31% (p<0.001), all-cause mortality by 11% (p=0.047), hemorrhagic stroke by 49% (p<0.001), and intracranial hemorrhage by 58% (p<0.001) compared to the warfarin group. The results of this study suggest that apixaban is more effective in reducing the incidence of stroke or circulatory thrombosis and the risk of bleeding events, as well as all-cause mortality, compared with adjusted-dose warfarin.
Undoubtedly, the clinical use of new oral anticoagulants provides a safe and effective alternative for the prevention of thromboembolic complications in patients with atrial fibrillation. However, since these drugs have been on the market for a short time, post-marketing safety monitoring and clinical experience are still needed. In addition, clinical evidence to date on new oral anticoagulants is mainly from patients with non-valvular AF, and the value of their use in patients with valvular AF and post-prosthetic valve replacement and valve repair remains to be explored, and dose-adjusted warfarin should still be used for anticoagulation in these patients. In China (especially in economically underdeveloped areas), there are still a large number of patients with valvular atrial fibrillation, so warfarin still has an important clinical status and wide application. At this stage, new oral anticoagulants are mainly used for patients with non-valvular atrial fibrillation.
3.Anticoagulation therapy for special populations
The current evidence on anticoagulation in special populations is mainly from clinical trials on warfarin, and there is a lack of large clinical studies on new oral anticoagulants in this area. Referring to the 2010 European guidelines for the treatment of atrial fibrillation [7], the following recommendations are made for anticoagulation in special populations.
(1) Perioperative anticoagulation
Patients with atrial fibrillation who are receiving warfarin need to be temporarily discontinued before surgery or interventional procedures, and heparin is applied as transitional therapy. For non-emergency procedures, warfarin is usually discontinued about 5 days before surgery (about 5 half-lives) to reduce the INR to below 1.5. If the INR is >1.5 but the patient requires early surgery, the patient may be given a small oral dose (1-2 mg) of vitamin K to bring the INR back to normal as soon as possible. Anticoagulation in the perioperative period for patients with atrial fibrillation who have implanted mechanical heart valves or other thrombotic risk factors is controversial, and it is generally believed that warfarin should be discontinued and low molecular weight heparin or normal heparin should be used for transitional anticoagulation.
(2) Stable angina pectoris and peripheral arterial disease
The optimal anticoagulation strategy for patients with atrial fibrillation in combination with stable angina pectoris, carotid atherosclerotic disease, or peripheral arterial disease has yet to be explored. Although some authors recommend combining antiplatelet agents (especially aspirin) with warfarin for these patients, available studies suggest that adding aspirin to warfarin therapy does not further reduce the incidence of stroke and myocardial infarction, but significantly increases the risk of bleeding events. Warfarin alone is at least as effective as aspirin for secondary prevention in patients with stable coronary artery disease, and therefore warfarin alone is recommended for such patients.
(3) Acute coronary syndromes and/or percutaneous coronary interventions
Dual antiplatelet therapy (aspirin plus clopidogrel; 4 weeks for bare metal stents and 6-12 months for drug-eluting stents) in patients with unstable angina and post-coronary stent placement significantly reduces the risk of adverse cardiovascular events. When these conditions are combined in patients with atrial fibrillation, the addition of dual antiplatelet therapy to warfarin therapy may also reduce the incidence of thromboembolic events. Available evidence suggests that the short-term (e.g., 4 weeks) addition of warfarin does not significantly increase the risk of bleeding events compared with dual antiplatelet agents alone, with an acceptable benefit/risk ratio, but the safety of long-term triple antithrombotic agents remains to be demonstrated. Patients with atrial fibrillation who have a bare metal stent may be treated with a short course (4 weeks) of triple antithrombotic therapy followed by warfarin and an antiplatelet agent (aspirin or clopidogrel), and after 12 months, if the patient is stable, anticoagulation with warfarin only, as is the case in patients with stable coronary artery disease. Drug-eluting stents should be followed by longer triple antithrombotic therapy (sirolimus, everolimus, and tacrolimus-eluting stents should be treated for ≥3 months, and paclitaxel-eluting stents should be treated for at least 6 months), followed by warfarin plus clopidogrel (75 mg/day) or aspirin (75-100 mg/day), combined with a proton pump inhibitor or H2 receptor antagonist if necessary. Warfarin anticoagulation alone may be applied after 12 months if the disease is stable.
If not contraindicated, patients with non-ST elevation myocardial infarction should be treated with dual antiplatelet therapy with aspirin in combination with clopidogrel. Concomitant anticoagulation is also indicated if the patient has atrial fibrillation and is at moderate to high risk of stroke. Patients in the acute phase may be treated with aspirin, clopidogrel, regular or low molecular heparin, or bivalirudin and/or glycoprotein IIb/IIIa inhibitors, followed by triple antithrombotic therapy (warfarin, aspirin and clopidogrel) for at least 3-6 months. If the patient is at low risk of bleeding and high risk of thromboembolism, warfarin with clopidogrel (75 mg/day) or aspirin (75-100 mg/day plus gastric mucosal protector) may be applied for 12 months. Thereafter warfarin alone is applied for long-term treatment.
Acute ST-segment elevation myocardial infarction requires a combination of aspirin, clopidogrel, and heparin. When patients have a high thrombotic load, bivalirudin or glycoprotein IIb/IIIa inhibitors may be given temporarily. Because this combination antithrombotic therapy can significantly increase the risk of bleeding, glycoprotein IIb/IIIa inhibitors or bivalirudin should not be routinely used at INR >2. The principles of medium- and long-term antithrombotic therapy in such patients are the same as for non-ST elevation myocardial infarction.
(4) Acute ischemic stroke
To date, there are few studies on antithrombotic therapy in the acute phase of ischemic stroke. Acute stroke is often the first presentation in patients with atrial fibrillation, and the risk of stroke recurrence is highest in the first 2 weeks after cardiogenic stroke. However, anticoagulation during the acute phase of stroke increases the risk of intracranial hemorrhage or post-infarction hemorrhage, so antithrombotic therapy is not recommended for patients with ischemic stroke within 2 weeks of onset. Antithrombotic therapy should be started after 2 weeks of onset if there are no contraindications, and the principles of treatment are the same as for patients with general atrial fibrillation.
(5) Atrial flutter
Retrospective studies have shown that patients with atrial flutter are at the same risk of thromboembolic complications as patients with atrial fibrillation and should therefore be managed according to the same principles of antithrombotic therapy as patients with atrial fibrillation.
(6) Atrial fibrillation resuscitation
In patients with atrial fibrillation >48 hours or of unknown duration, transesophageal ultrasound is recommended for the presence of left atrial or auricular thrombus before elective cardioversion is proposed. If transesophageal ultrasound is not available, antithrombotic therapy with dose-adjusted warfarin (INR 2.0-3.0) should be administered for at least 3 weeks. Because left atrial dysfunction (atrial stenosis) is often present after reentry, patients are at significantly increased risk of intra-atrial thrombosis and should continue anticoagulation therapy for approximately 4 weeks after reentry. Patients with atrial fibrillation episodes <48 hours can be directly cardioverted with concomitant common heparin for thromboprophylaxis. Oral anticoagulation should be started after cardioversion and continued for life in patients with high risk factors for stroke, but is not required routinely in those without high risk factors for thromboembolism. Cardioversion should be performed immediately if atrial fibrillation occurs >48 hours and is associated with hemodynamic instability (angina, myocardial infarction, shock, or pulmonary edema) and should be preceded by heparin therapy and followed by oral anticoagulant therapy. The duration of oral anticoagulation therapy (4 weeks or lifetime) depends on whether the patient has high risk factors for stroke.
4. Conclusion
Stroke and other thromboembolic complications are the main cause of death and disability in patients with atrial fibrillation, and reasonable anticoagulation therapy is important to improve the quality of life and long-term prognosis of patients with atrial fibrillation. Although relevant guidelines at home and abroad recommend thromboprophylaxis for patients with high-risk atrial fibrillation, most patients have not been treated accordingly so far, therefore, in future clinical work, efforts should be made to strengthen standardized anticoagulation therapy for patients with atrial fibrillation to reduce the risk of thromboembolic events. The clinical application of new oral anticoagulant drugs will provide new tools for the prevention of thromboembolic complications in patients with atrial fibrillation. These drugs have the advantages of easy administration, stable pharmacokinetic properties, no need for routine monitoring of coagulation indexes, and less influence by food and other drugs, which will definitely play a positive role in improving the coverage and compliance of anticoagulation therapy in patients with atrial fibrillation.