Robert Lemery MD, MA
From the AZ Heart Rhythm Center
and St-Joseph Hospital, Dignity Health, Phoenix, Arizona.
Address for correspondence:
robert.lemery1@gmail.com
The author reports no funding or conflict of interest.
Word count: 1, 500
Why don’t all patients with atrial fibrillation (AF) have symptoms? In
this issue of the Journal, Fukuhara et al (1) report on 110 patients
with paroxysmal AF who underwent invasive hemodynamic measurements at
the time of catheter ablation. Asymptomatic patients with AF, as defined
by an EHRA score of 1 (no symptoms) for AF related symptoms (2), was
documented in 19 patients. Catheter ablation involved either a Tacticath
catheter and use of the Verismo software, or Cryoballoon ablation with a
28 mm balloon. Following catheter ablation, transseptal measurements of
left atrial pressure and arterial pressure were obtained in sinus rhythm
as well as during high right atrial pacing from the lateral wall of the
RA using a multipolar catheter inserted from the right internal jugular
vein. The pressures were obtained through the sheath, which was
connected to a pressure transducer and recorded on a Fukuda Denshi
hemodynamic monitoring system (FCL-2000). The average of three
heartbeats at the end of expiration was used to measure LA pressure and
arterial pressure.
Following measurements in sinus rhythm, the pacing protocol consisted of
pacing at 100 beat/min, increased by 10 beats/min until Wenckebach block
at higher than 120 beats/min. Fukuraha et al (1) demonstrated that the
peak LA pressure and the rate of change of pressure measurements with
pacing were significantly less in asymptomatic patients with AF. In
addition, those patients also had significantly lower mean arterial
pressure during sinus rhythm, as well as significantly lower peak
arterial pressure during sinus rhythm or with atrial pacing. The
multivariate analysis revealed that asymptomatic patients with AF had
significantly lower rates of change of peak LA pressure in SR or while
pacing at 100 bpm, and a lower E/e on echo, suggestive of less diastolic
dysfunction (3).
The etiology of symptoms in patients with AF has generally been
attributed to the irregularity of AVN conduction in AF, rapid
ventricular rates during AF, autonomic effects, loss of AV synchrony and
decreased cardiac output with lack of left atrial appendage contraction,
and perhaps more importantly to uncovering underlying diastolic
dysfunction (4, 5). As clinicians, we have all been baffled by patients
with AF who have symptoms that appear out of proportion to the burden or
perceived severity of AF. Patients with unrelenting and persistent AF
with rapid ventricular rates may not be aware of their AF, and
conversely patients with infrequent paroxysmal AF may be extremely
symptomatic at the time of recurrence of AF. The report by Fukuhara et
al (1) suggests that asymptomatic patients with AF are thus
characterized by preserved diastolic function, with significantly less
increase in peak LA pressure during AF, unrelated to ventricular rates.
There have been several reports (8-11) highlighting the absence of
symptoms in subgroups of patients with AF. In previous studies of
patients with persistent AF (9), or both paroxysmal and persistent AF
(10), ischemic thromboembolic complications were not significantly
different between patients with or without AF symptomatology. As
observed by Fukuhara et al (1), studies of asymptomatic patients with AF
have generally been shown to include significantly more males or
patients with diabetes (8-11). Overall, approximately one-fourth of
patients with AF were previously estimated to be asymptomatic. But with
changing definitions and new means of monitoring AF, significant
clinical readjustments in patient management are emerging. Subclinical
AF, in the new era of increased use of portable and implantable devices,
has shown up to 60% of asymptomatic episodes over 5 years (12-14).
The percentage of patients with asymptomatic AF in the report by
Fukuhara et al (1) was only 17%, likely related to the patient
population studied, which consisted of patients undergoing catheter
ablation. In asymptomatic patients with AF, catheter ablation has been
considered a class IIb indication (15). The justifications for
performing AF ablation in the asymptomatic patients with AF by Fukuhara
et al (1) were not unlike the usual reasons most interventional
electrophysiologists currently perform ablation in patients with
symptomatic AF. These include patient preference of AF ablation over
long-term treatment with AVN blocking or antiarrhythmic agents, concerns
of new onset or worsening of systolic or diastolic heart failure,
patient hope of being able to stop anticoagulation with maintenance of
sinus rhythm, and the risk of bleeding complications with use of
anticoagulants. Clinically, these are all strong deterrents towards a
laisser-faire attitude in the asymptomatic patient.
Nonetheless, after more than twenty years of worldwide experience at
performing AF ablation, the clinical outcome of AF ablation remains a
work in progress. Recurrence of AF post ablation or various ablation
related complications are still somewhat expected or accepted in the
symptomatic patient with AF. Arguably however, it is more difficult to
accept an unfavorable outcome following AF ablation in the asymptomatic
patient. While evidence-based reports are lacking for performing AF
ablation in such patients (15). percutaneous occlusion of the left
atrial appendage has rapidly emerged as a safe and effective
interventional procedure to supplant long-term use of anticoagulants.
Randomized trials comparing the clinical outcome of patients with
subclinical AF treated with Apixaban vs. Aspirin (16) or Edoxaban vs.
Aspirin or placebo (17) will be available over the next year. Numerous
randomized trials comparing percutaneous occlusion of the left atrial
appendage with direct oral anticoagulants will also become available
over the next few years (18). Percutaneous occlusion of the left atrial
appendage could emerge as the treatment of choice for subgroups of
asymptomatic patients with AF. While we need to continue to research the
pathophysiology of why an irregularly irregular heart rhythm may not be
perceived clinically, and adjust our monitoring tools accordingly, as
interventional electrophysiologists we are confronted with an arrhythmia
that has been and remains a lesson in humility.