EDITORIAL

Atrial fibrillation: What can we do, what should we do, and what must

we do?

KNUT GJESDAL

Department of Cardiology, Ulleval University Hospital and Faculty Division Ulleval, University of Oslo, Oslo, Norway

Cardiologists have been through ‘‘a decade of guide-

lines’’, including those involving atrial fibrillation

(1). However, compliance with the recommenda-

tions is hesitant, and their usefulness is limited when

new treatment modalities appear. The major threat

of atrial fibrillation, i.e. cardio-embolic stroke, can

be prevented in 2/3 of patients when warfarin is

prescribed, however, despite the existence of a well-

defined group of patients at higher risk, too few

receive this treatment (2), and those who do, often

receive suboptimal dosage.

The rate control approach must be refined

In atrial fibrillation anti-dromotropic drugs reduce

AV-conduction. Beta-adrenergic receptor blockers,

calcium-channel blockers like verapamil and diltia-

zem, and digitalis are Class I recommended drugs,

but we know little about which drugs and drug

combinations are best suited for the individual

patient. We often aim at a heart rate at rest of

B/80/min and 110/min at moderate exercise (3), but

these values are not proven to be optimal. Until

recently we have assumed that rate control improves

quality of life and perhaps reduces the shortened life

expectancy of the atrial fibrillation patient, but even

this has been refuted by a recent AFFIRM substudy

(4). The patient group with presumed adequate rate

control did not fare better than those with faster

rates. We do not know whether or not this lack of

benefit from treatment means that heart rate is not

that important, or if adverse drug effects compro-

mise the results. It has also been argued that

selection of patients to the AFFIRM study could

be skewed, favouring inclusion of those who toler-

ated their fibrillation, thus underestimating the

benefits of adequate rate control (5). The results of

the AFFIRM study are in contrast to the good

results of the ultimate rate control provided by

AV-nodal ablation followed by pacemaker treatment

(6). This ‘‘ablate and pace with rate response’’

strategy, which is applied to patients with poor rate

control, also overcomes any problem related to the

irregular rate in atrial fibrillation.

Rhythm control

In persistent atrial fibrillation cardioversion by drugs

or current are frequently offered, but even despite

the use of antiarrhythmic drugs for secondary

prevention, the recurrence rate is depressingly high

(7), and neither quality of life nor life expectancy are

improved by the struggle for rhythm control (4).

However, the final role for cardioversion is far from

established (8).

Lack of efficacy of the current secondary preven-

tive drugs and their potentially life-threatening side

effects, may account for this: both the quality of life

and the life expectancy ought to be higher in those

who regain and maintain sinus rhythm.

Curative ablation

Today, atrial fibrillation can be cured either by maze

surgery, or less invasively by radiofrequency catheter

ablation. The landmark study from Bordeaux

demonstrated that atrial fibrillation often is initiated

by triggering extrasystoles from the pulmonary veins

and that the responsible muscle fibres can be

destroyed by ablation (9). Stricture of the pulmonary

vein(s) is, however, a feared complication. Pappone

et al. chose to avoid the veins and deliver a series of

Correspondence: Knut Gjesdal, Department of Cardiology, Ulleval University Hospital and Faculty Division Ulleval, University of Oslo, Oslo, Norway.

E-mail: knut.gjesdal@medisin.uio.no

Scandinavian Cardiovascular Journal. 2005; 39: 324�/326

(Received 23 October 2005; accepted 23 October 2005)

ISSN 1401-7431 print/ISSN 1651-2006 online # 2005 Taylor & Francis

DOI: 10.1080/14017430500431433

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burns creating lines around the pulmonary ostea,

thereby isolating them (10). The results are further

improved when the encircling lines around the right

and the left pulmonary veins are connected by a roof

line and a line from the left lower vein to the mitral

ring (11). When a right-sided flutter isthmus abla-

tion line finally is added, the resulting atrial com-

partmentalisation resembles that following the maze

procedure. The procedure requires skill and persis-

tence, but in the best hands, success rates are high

and the complication rates are acceptable. Now even

patients with chronic fibrillation and heart failure

can benefit from curative ablation (12).

The huge population with atrial fibrillation

Framingham data suggest that during a life-time,

25% of us will develop atrial fibrillation (13). The

prevalence increases dramatically with age, and is

9% among those �/80 years (14). Among males, the

age-adjusted prevalence has increased over the last

10 years (15). Hospital admissions for atrial fibrilla-

tion have also increased (16). Fifteen percent of all

strokes are ascribed to atrial fibrillation (17). In both

genders there is excess mortality when atrial fibrilla-

tion is present, the relative risk is 1.5 in men and 1.9

in women (18). Thus atrial fibrillation imposes a

heavy burden on public health.

How can we prepare for the future?

It is unthinkable that such vast numbers of patients

can ever be offered the curative treatment of today.

Research is urgently needed to refine the conven-

tional drug treatment, not least establish the aims of

treatment. Prevention of atrial fibrillation should be

sought as in some situations atrial pacing reduces

fibrillation in sick sinus syndrome, compared to

ventricular pacing (19). Drugs (20) and pacing

(21) prevent atrial fibrillation after aorto-coronary

by-pass surgery. Dofetilide prevents fibrillation in

heart failure (22), and ACE-inhibitors and angio-

tensin 2 receptor blockers are advantageous in

hypertensive left ventricle hypertrophy, in heart

failure, after myocardial infarction and after cardio-

version (23). We know that hypertension and cor-

onary heart disease are major risk factors for

fibrillation, and we should systematically look at

the incidence of atrial fibrillation in primary as well

as secondary prevention studies.

In Nordic countries the number of experienced

clinical electrophysiologists is limited, indeed. This

translates into long waiting lists and serious limita-

tions of patient care today. Neither the physicians

nor the patients of tomorrow will accept age limits

not based upon medical reasoning. To the best of my

knowledge, no Nordic hospital has a satisfactory

training program for EP-physicians; we are not

fulfilling the demands of today, and far from the

needs foreseen for tomorrow. This should be our

major challenge.

Conclusions

Today it is possible to cure most cases of recent onset

atrial fibrillation. This work is exciting for the EP-

physicians, and the short-term results are promising

for permanent fibrillation and excellent for the

paroxysmal forms. However, we lack knowledge of

the long-term benefits both for the quality of life and

its prolongation. Lack of staff and restricted financial

resources severely limit our curative ambitions. We

should definitely anticoagulate more patients, and

probably ablate and pace more than we do today. We

should improve tailored rate-controlling drugs, and

we must do research on preventive measures.

Finally, we must train more cardiac electrophysio-

logists to meet the demands of tomorrow: at least a

doubling of experienced clinical electrophysiologists

is needed over the next five years.

References

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