What is ‘valvular’ atrial fibrillation? A reappraisal

Extract

Introduction

Despite the same electrophysiological abnormality, the risk of stroke and systemic embolism in atrial fibrillation (AF) ranges from <1%/year to >20%/year and can be assessed by simple clinical risk factors.¹ This has led to the gradual adoption of vitamin K antagonist (VKA) oral anticoagulation as a preventive strategy for most patients with AF, unless clearly identifiable to be at very-low risk.^2,3 The recent availability of non-VKA oral anticoagulants (NOACs) is likely to increase the number of AF patients treated with these drugs for stroke prevention in the future. In some such patients, atrial appendage occlusion devices are now also a viable alternative.³

All the pivotal trials comparing VKAs with the NOACs in AF have enrolled patients with so-called ‘non-valvular’ AF and excluded patients at particularly high risk of thrombo-embolism, such as those with AF accompanying mitral stenosis or patients with mechanical prosthetic valves.⁴ The reasons for not including these patients in trials testing NOACs also included the possibility that the pathogenesis of thrombo-embolism may be substantially different from other types of AF. The distinction between ‘valvular’ AF ‘non-valvular’ AF, however, still remains uncertain, with variable definitions adopted in the NOAC trials. This has led to therapeutic confusion, well illustrated by a recent web-based survey among over 500 Italian physicians mainly involved in the prescription of anticoagulants to AF patients. Here, only 57.1% of the cardiologists and 67.9% of the internists agreed that the existing definitions of non-valvular AF (e.g. from Guidelines) were sufficiently clear.⁵