Re: Should we screen for atrial fibrillation? - isn't the right question and doesn't give the right answers
Disease labeling of populations with common phenomena of ageing (Non valvular AF) is indeed a risky business. As is the albeit common view presuming causality in a highly confounded statistical association. The non biased term is to consider stroke as commonly associated with atrial fibrillation and the issue linked to this is the problem of defining where anticoagulation can credibly reduce or defer recurrent injury and death in those at risk.
Any prevalence of atrial fibrillation needs a causal process established and risk factor, for the aetiology of AF (not just the consequences such as stroke or haemorrhage) defined. Stroke associated with atrial fibrillation is clearly not always thromboembolic and anticoagulation reduces but does not eliminate stroke in chronic atrial fibrillation patients. Anticoagulation may defer stroke (again not prevent stroke or death) but also causes deaths in a minority due to unprovoked bleeding. These patients are not easily identified by crude population bleeding risk scores.
The older the sample frame the more prevalent unrecognised and asymptomatic paroxysmal AF will be. What to do about any AF is far from clear. It is not helped by confusing any AF with persistent AF, in a young heart from an old heart, from a structurally normal heart from one with multiple structural abnormalities. Reacting to any AF in any circumstance is fraught with error, bias and confounded by risk to the patient. That 90% of a small sample accepted anticoagulation for any AF in Strokestop is in itself hardly surprising. It does not confirm an informed or even valid choice and actually probably suggests that the risk was grossly over egged and the benefit over simplified. It is critical to remember that CHADS VASC is a risk equation developed in chronic persistent non valvular atrial fibrillation . As with many population scores while helpful in those where it was intended to be used, even in those it will over estimate the stroke rate. Hence new risk scores continue to be tested in different sample frames.
Th ARREST AF trial and many others shows anticoagulated patients continue to have strokes due to poor control of atherosclerotic risk factors (HBP, DM, renal impairment), unchecked obesity/hypo-ventilation/OSA smoking and lack of fitness. This seems sensible as none of these respond to anticoagulation. Equally we know paroxysmal AF patterns can be present for decades without consequences in younger individuals many of whom reach late middle age tolerating brief and frequently uncontrolled periods in AF without any consequences beyond transient irritation for minutes, hours or days. Equally atrial flutter is frequently severely symptomatic yet has reduced thromboembolic risk and the potential for ECG patterns of flutter/fibrillation has been long documented and are seen daily and again likely to have reduced thromboembolic risk. While improving tools for marginally safer and as effective anticoagulation (NOAC agents) have emerged over the last decade these are not effective treatments for ischaemic or atherosclerotic stroke.The mystery of the linkage of AF to thromboemblism is just not as simple as often portrayed.
Thus caution is needed with simple views that screening everyone for anything and treating the majority is as has been seen so often to be the case far from informed. Cost utility of screening is complex but more directly patients choices are not informed to be told a simplistic tale of one size fits all. Unfortunately presuming trials are there to "strengthen the case" reveals confirmation bias exists before any actual data is available. Show us the data first then we might consider its value and truly inform patients. Till then I would advise you use your watch for telling the time?
Competing interests: No competing interests