EDITOR ’ S CORNER
Alfred A . Bove , MD , PhD
Editor-in-Chief , CardioSource WorldNews
Is AF Contributing to Dementia ?
Over the past few months , Bill has seemed a little forgetful . He is 81-years-old , long retired but active , with a history of hypertension and well-controlled atrial fibrillation ( AF ) for the past 15 years . Because of his wife ’ s diligence regarding his INR , he rarely gets out of range either above or below the therapeutic target .
On their last office visit , his wife asked whether statins can cause dementia . Some of her friends have stopped statin medications because of the ongoing debate regarding a possible link between statins and dementia . Yet , the randomized clinical trials , and the observations from large registries , don ’ t support a connection between statin use and dementia . Because loss of brain function is a common occurrence in an elderly population , we look for relationships that might explain a reduction in cerebral function .
We all accept some reduction in cognitive function with aging and don ’ t call it dementia . Formal testing can define dementia , but most patients don ’ t get too concerned with slight memory loss , balance problems , reduced coordination , or other minor functional changes that occur with advancing age . However , when debate regarding such issues spreads across the medical community — and into the press — patients get concerned .
Lately , there has been concern regarding AF and its relationship with dementia . There are a number of potential mechanisms , one of which is the possibility that small emboli are shed from the atrium and accumulate , limiting blood flow to the brain , and leading to a perceptible reduction in mental function . These have been classified as microstrokes , mini-strokes , and “ whispering ” strokes ; but , whatever you call them , the consequence is a progressive loss of mental function due to embolization from the left atrium .
Avoidance is difficult . With a patient in permanent AF , stopping anticoagulation actually increases the risk of stroke and we all have witnessed a patient who failed to take anticoagulants for their AF
who then experienced a devastating stroke involving a significant portion of their brain . However , when considering dementia , the various etiologies are also important . Vascular dementia due to obstructive cerebral vascular disease could be related to AF from multiple micro-emboli , but that cannot explain Alzheimer ’ s-type dementia . Similarly , microbleeds , which might be the result of excess anticoagulation , might be another contributing factor to cognitive decline .
Consequently , determining all these relationships and their impact on patients cannot be discerned from observational studies . Most studies relate different forms of dementia to a variety of cardiovascular disorders . Look at the research and you ’ ll see patients with heart failure , ischemic heart disease , congenital heart disease , AF , and hypertension , all demonstrating some relationship with dementia .
We are all comfortable with telling a patient with AF that they need an anticoagulant to avoid a stroke . This is true for warfarin and for the nonvitamin K oral anticoagulants ( NOACs ), where the clinical trials indicate that the risk of bleeding and stroke is lower with a NOAC than with warfarin . However , we don ’ t yet have solid data on dementia risk with either warfarin or the NOACs . Small trials comparing NOACs to warfarin in patients with AF suggest a slightly lower risk of dementia with a NOAC , but these data are suggestive and not definitive .
To really answer the questions being debated today , we must wait for larger , randomized trials . Research on dementia is moving forward at a rapid pace because of the increasing number of older adults and the need to reduce risk given the longterm costs of caring for elderly dementia patients .
To fully understand the relationship between AF and dementia , we first need to properly categorize the various forms of dementia . If we are concerned with AF , the most likely link will be between vascular dementia and AF , but other forms of dementia seem to have an association with AF , too , as well as with other forms of chronic heart disease .
Clinical trials are needed that both characterize the dementia clinically , and provide quantifiable measures from standardized tests and vascular images that can be compared over time . Meanwhile , we need to continue anticoagulation to avoid strokes in our AF patients . Whether NOACS are a better choice is still to be determined , but data from small studies suggests that they do lower dementia risk in our AF patients compared to warfarin .
Perhaps the only certainty : offering no anticoagulation therapy in a patient with AF is a much riskier approach . I haven ’ t mentioned aspirin , but there is a growing consensus that what little stroke protection might be gained from aspirin is offset by the considerable risk of bleeding . Indeed , as this issue of CSWN was going to press , a study in JACC indicates that 40 % of people with AF are wrongly prescribed aspirin rather than more effective therapies . 1 Indeed , the analysis of NCDR ® data finds that such an approach in this AF population at moderate- to severe-risk of stroke has a net negative effect . And the role of Watchman ® is still being defined .
At present , treatment of AF focuses on rate or rhythm control and stroke prevention . The strokes we want to prevent are the large ones that cause an abrupt change in function , long-term disability and , often , prolonged supportive care . Our therapeutic goals and clinical trials all focus on prevention of clinically evident strokes , but as we learn more about brain function in AF patients we may need to add microstrokes to our concepts about AF . ■
REFERENCE : Hsu JC , Maddox TM , Kennedy K , et al . J Am Coll Cardiol . 2016 ; 67:2913-23 .
Alfred A . Bove , MD , PhD , is professor emeritus of medicine at Temple University School of Medicine in Philadelphia , and former president of the ACC .
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