Clopidogrel use in patients with AF
The Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE-W) trial 10 compared warfarin with a combination of ASA and clopidogrel. The combination of ASA and clopidogrel remainedinferior to treatment with warfarin and was associated with a similar risk of major hemorrhage (2.4% vs 2.2% per year). The risk of stroke was 41% lower with oral anticoagulation. Results are pending for the ACTIVE-A trial that compares ASA with the combination of ASA and clopidogrel, in patients for whom warfarin is not appropriate.
While clopidogrel does not appear to have a defined role in stroke prophylaxis for AF, the presence of simultaneous coronary artery disease and AF is common, especially in elderly patients with hypertension. A frequently encountered issue in clinical practice is whether or not patients already on warfarin can safely tolerate the additive risks of bleeding conferred by ASA and clopidogrel. This issue occurs in patients already anticoagulated with warfarin for AF, who then need prolonged dual antiplatelet therapy (ASA and clopidogrel) after stent implantation or acute coronary syndrome. A recent registry study in Europe suggests that triple therapy (ASA + clopidogrel + oral anticoagulation) may possibly be preferred over dual antiplatelet therapy alone. Major bleeding in the triple-therapy group was higher (14.9% vs 9% over a median follow-up of 20 months), but the frequency of embolism (1.9% vs 6.9%) and death (17.8% vs 27.8%) was significantly lower in patients on triple therapy. Nevertheless, this study has considerable selection bias and should not be considered definitive. The AHA guidelines acknowledge the lack of adequate data relating to these circumstances that prohibits making strong recommendations.
Strategies to reduce complications of oral anticoagulation
Once a decision is made to pursue oral anticoagulation, several measures can be taken to mini-
mize the likelihood of complications while on therapy. To maintain warfarin therapy within the ther-
apeutic window (INR 2.0-3.0) is a challenging task; in most trials using warfarin, the INR of patients is on target in only 60%-65% of measurements. Table 4 outlines some suggestions for reducing the likelihood of either subtherapeutic anticoagulation or increased bleeding with supratherapeutic INRs. Patient education and the use of a dedicated anticoagulation clinic can help avoid potential problems or identify them at an earlier point.
Anticoagulation before and after cardioversion
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The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) 11 and the Rate Control versus Electrical cardioversion (RACE) 12 trials have established that there is no benefit to converting AF back into sinus rhythm in terms of preventing thromboembolic events. However, a substantial minority of patients with AF will be offered elective cardioversion, using either electrical or pharmacological methods, in an attempt to reduce their symptoms or improve cardiac pump function.
Most physicians are aware of the possibility of pre-existing emboli in the left atrium that can
dislodge upon the return of sinus rhythm. Fewer are aware that cardioversion itself may predispose
patients to developing potential embolic thrombi in the left atrium during the period shortly after a return
to sinus rhythm. This process is thought to occur as a result of “stunning” the atrial myocardium, and can
occur with either electrical or pharmacological cardioversion. The AHA provides guidelines for anticoagulation procedures in the pericardioversion period. Any patient in whom AF may have been present for ≥48 hours (or where the duration of fibrillation is uncertain) should be anticoagulated for at least 3 weeks prior and at least 4 weeks following cardioversion. If cardioversion in such patients is desired ona more urgent (but nonemergent) basis, it is reasonable to consider screening for thrombi in the left atrium using transesophageal echocardiography. If no signs of thrombus formation are identified, the patient can be cardioverted after initiating unfractionated heparin; following cardioversion, at least 4 weeks of anticoagulation is recommended.
Patients with ≥48 hours of AF who require emergent cardioversion (eg, in the setting of heart failure, hemodynamic instability, angina, or myocardial infarction) should be anticoagulated as soon after cardioversion as possible, unless contraindicated.
Cardioversion should not be delayed for the purposes of anticoagulation in these circumstances.
The strategies for prevention of thromboembolic events are less clear for patients with an episode of AF
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lasting <48 hours prior to cardioversion. The AHA guidelines indicate a class IIa recommendation for the
use of a conventional assessment of the risks for thromboembolism (eg, the CHADS 2 score and the
moderate risk factors previously mentioned) as a guide to determine whether ASA, warfarin, or neither
should be used. However, some data suggest that anticoagulation with ASA or warfarin for at least the first 4 weeks would be reasonable. The indication for anticoagulation is strengthened by a CHADS 2 score of ≥1 (in which case anticoagulation would be continued indefinitely in the absence of a reversible cause) or AF where the duration is uncertain.
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