Stroke Prevention Drugs May Reduce Dementia Risk
Patients with atrial fibrillation could reduce the risk of dementia by taking stroke prevention medications, according to recommendations published online ahead of print March 18 in EP Europace and presented at the conference. The international consensus document was also published in Heart Rhythm, the official journal of the Heart Rhythm Society (HRS), and Journal of Arrhythmia, the official journal of the Japanese Heart Rhythm Society (JHRS) and the Asia Pacific Heart Rhythm Society (APHRS).
The expert consensus statement on arrhythmias and cognitive function was developed by the European Heart Rhythm Association (EHRA), a branch of the European Society of Cardiology (ESC); HRS; APHRS; and the Latin American Heart Rhythm Society (LAHRS).
Arrhythmias, as well as some procedures undertaken to treat them, can increase the risk of cognitive decline and dementia. The international consensus document was written for doctors specializing in arrhythmias and aims to raise awareness of the risks of cognitive impairment and dementia and of methods to reduce them.
Atrial fibrillation is associated with a higher risk for cognitive impairment and dementia, even in the absence of apparent stroke, according to the document. This increased risk may arise because atrial fibrillation is linked with a more than twofold risk of silent strokes. The accumulation of silent strokes and the associated brain injuries over time may contribute to cognitive impairment.
Stroke prevention with oral anticoagulant drugs is the main priority in the management of patients with atrial fibrillation. Oral anticoagulation may reduce the risk of dementia, according to the consensus document.
Adopting a healthy lifestyle also may reduce the risk of cognitive decline in patients with atrial fibrillation. This lifestyle includes not smoking and preventing or controlling hypertension, obesity, diabetes, and sleep apnea.
The document also reviews the association between other arrhythmias and cognitive dysfunction, including postcardiac arrest, in patients with cardiac implantable devices such as implantable cardioverter defibrillators and pacemakers, and ablation procedures.
Treatment of atrial fibrillation with catheter ablation can itself lead to silent strokes and cognitive impairment. To reduce this risk, physicians should follow recommendations for performing ablation and for the management of patients before and after the procedure, according to the document.
Physicians may suspect cognitive impairment if a patient’s appearance or behavior changes (eg, if appointments are missed). Family members should be asked for collateral information. If suspicions are confirmed, the consensus document recommends tools to conduct an objective assessment of cognitive function.
The paper highlights gaps in knowledge and areas for further research. These gaps include, for instance, how to identify patients with atrial fibrillation at increased risk of cognitive impairment and dementia, the effect of rhythm control on cognitive function, and the impact of cardiac resynchronization therapy on cognitive function.
EHRA Updates Guide on NOACs
A new version of the European Heart Rhythm Association (EHRA) Practical Guide on the use of non-vitamin K antagonist oral anticoagulants (NOACs) in patients with atrial fibrillation was published online ahead of print March 19 in European Heart Journal and presented at the meeting.
“European Society of Cardiology guidelines state that NOACs should be preferred over vitamin K antagonists, such as warfarin, for stroke prevention in patients with atrial fibrillation, except those with a mechanical heart valve or rheumatic mitral valve stenosis, and their use in clinical practice is increasing,” said Jan Steffel, MD, Head of the Department of Cardiology at University Heart Center Zurich.
The guide gives advice about how to use NOACs in specific clinical situations. While companies provide a Summary of Product Characteristics for a drug, there are legal restrictions on the content, and the information is often not detailed enough for doctors.
The 2018 edition of the guide has several new chapters. One outlines how to use NOACs in particular groups of patients, including those with very low body weight, the very obese, athletes, frail patients for whom there is concern about bleeding, and patients with cognitive impairment who may forget to take their pills.
Another new chapter briefly summarizes the correct dosing of NOACs in conditions other than atrial fibrillation, such as prevention of deep venous thrombosis, treatment of venous thromboembolism, and treatment of ischemic heart disease. The dosing for each condition is different, which underscores the need for clarity.
Updated advice is given on the combined use of antiplatelets and NOACs in patients with coronary artery disease, particularly those with an acute coronary syndrome or patients scheduled for percutaneous coronary intervention with stenting.
The guide also offers scientific evidence about the use of anticoagulants around cardioversion. The authors give detailed advice about what to do in patients on long-term NOAC treatment who need cardioversion versus patients newly diagnosed with atrial fibrillation and started on a NOAC before cardioversion.
Since the previous edition of the guide was published, the first NOAC reversal agent has received market approval. The authors provide advice about using idarucizumab, which reverses the anticoagulant effect of dabigatran, when there is acute bleeding, when urgent surgery is required, or when the patient has a stroke. Guidance is also included on andexanet alfa, another reversal agent expected to receive market approval, with the caveat that the instructions on the label should be followed.
Unlike warfarin, NOACs do not require monitoring of plasma levels followed by dose adjustments. The guide describes rare scenarios in which physicians might want to know the NOAC plasma level. One scenario concerns patients undergoing major surgery in whom it is unclear, for example because of other drugs or renal dysfunction, whether the usual practice of stopping the NOAC 48 hours in advance is sufficient. The plasma level of the NOAC could be measured just before surgery to confirm that the anticoagulant effect has waned.
The chapter on drug–drug interactions has been expanded with information about anticancer and antiepileptic drugs. “While this is mostly based on potential pharmacokinetic interactions and case reports, it is the first of its kind. This is likely to be adapted and become more complete over the years as our experience increases at this new frontier,” said Dr. Steffel.