PAF is typically a situation where collecting relevant data is a difficult task knowing, in any case, that it is impossible to express the entire data in figures. Quite a few years ago, I suggested a pattern showing that cardiac arrhythmia results from the combination of three factors which can be identified anytime but hardly weighted in percentage.[2] This pattern involves a cardiac arrhythmogenic substrate, influenced by the autonomic nervous system (ANS), with a trigger starting arrhythmia. The arrhythmia may burst, as expressed by the author, into "World War III", or on the contrary, remain unnoticeable. The reasons for these major variances from one patient to another, and even of PAF attacks in a patient, remain unknown. But it is a fact that the symptom is most often assessed differently by the physician and by his patient. For the patient, the symptom is the major issue whereas the physician's main concern is the potential arrhythmia-related risk, in particular stroke rather than discomfort.

Physician and patient points of view may differ. A patient wanting to explore PAF pathophysiology needs specific cardiac electrophysiology and ANS qualifications and knowledge, and this is rarely the case. The patient who focuses on symptoms ignores the invisible part of the iceberg. But the patient may also doubt that his medical issue is really dealt with when medicine considers, only occasionally, his quality of life, whereas this is in fact his main concern. Physician and patient points of view complement one another, even fruitfully, depending on which parameter is involved. Very briefly, this publication shows and confirms that studying the arrhythmogenic substrate is the physician's job, studying the trigger is the patient's job, and studying the ANS is their common job.

Over the last ten years, there has been extensive research on the substrate, in particular in Europe where fundamental and clinical electrophysiological research is a core tradition, particularly in the Netherlands and France. This research led to two notions with major practical consequences: AF's self-maintained nature and the fact that AF originates, often focally, in the left atrium. This is typically the kind of progress expected from professionals and is, I must admit, perfectly understood and accounted for by Hans Larsen through his study of recent medical literature.

Mr Larsen has also well understood my contribution concerning the role of ANS on the onset of PAF attacks, and the percentages he allocates in his surveys to the various vagal, adrenergic or dual forms are indeed those noticed in everyday practice. To analyze these forms, physician-patient cooperation is recommended, even if this goes against the fairly common physician attitude who prefers a patient not to be too knowledgeable, to prevent biased observations. My experience is that the most useful symptomatological details are often provided by the observations of physicians suffering themselves from PAF. All physicians do not necessarily master AF as such, but thanks to their qualifications and experience they know how to observe and analyze clinical signs. I remember the surgeon who noticed that after a stressful surgery morning the evening involved an additional vagal attack risk; until he mentioned this, I had not identified the potential role of the rebound effect. Just the same, when PAF attacks occur at the end of a week, they may often be explained by higher than usual physical activity and/or unusual physical activity, or higher alcohol consumption.

These examples show how the relevance of physician-patient cooperation varies when analyzing PAF clinical signs. The cooperation is highly efficient in the search for triggers, and this is one of the new and interesting points of this publication, usually not considered by physicians. To my knowledge, the survey carried out by the author directly with patients is the best researched that can currently be found in medical literature. When asked what must be done to prevent further attacks, I usually tell my patients it all depends on them and that the answer lies in their own observations. This is, in particular, the case for sports, whether on an occasional basis or with the major issue of professional training; excessive training is harmful when it exaggeratedly modifies the ANS balance beyond the sympathetic and parasympathetic physiological values.[3] It is a major mistake to think that the man in the street must be as trained and fit as the professional sportsman. Any common sense driver knows that if he wants to make his car last he must avoid handling it as a rally or Formula I driver.

I feel no need to comment in detail on the therapeutic advice provided in the book, but I must make a few general remarks. Avoiding as far as possible known triggers is a requirement often treated as anecdotal. The reason may be that for physicians "anecdotal" is slightly deprecatory because it refers to details not covered by a general demonstrated rule. But some anecdotal observations sometimes turn out to be of great interest. For instance, the first patient who led me to describe vagally-mediated PAF was alternately in sinus rythm or AF depending on whether he was standing up or lying down. Changing the ANS balance is only possible when one of the causes of its malfunction is clearly identified, which is rare except with the athlete, or patients with hyperthyroidism or quite exceptional pheochromocytoma. In fact, the substrate is definitely the main arrhythmogenic factor of the above-defined triad and is the true therapeutic target.

As such, it seems to me this target falls mainly under the physician's role rather than the layman's. In this field, it is unsafe to rely on the too many anecdotes or beliefs available, as they sometimes qualify as pure "folk medicine". The issue is not to deny that an infection, or poisoning by mercury contained in dental amalgams may cause the problem, but to acknowledge that this simply cannot be demonstrated in compliance with the rules of evidence-based medicine. Which means that, within a group of randomized patients, statistical efficacy evidence of a therapeutic intervention or of no intervention (placebo), carried out on a blind basis for both the patient and physician, must be demonstrated. Who, among patients suffering from PAF, is prepared to play this game perfectly mastered by physicians and which sometimes irritates physicians themselves when they think their experience gives them the absolute truth ?

Two examples in the book show how drug reputation must be confirmed by "controlled" therapeutic trials performed in compliance with the rules. Sotalol has long been considered a higher efficacy drug than other beta-blockers as it combines with its specific action on beta- adrenergic receptors a "type III" pharmacological effect suggesting "amiodarone-like" properties. Simply, no one had ever taken the time to compare, by the rules, sotalol and beta- blockers on the one hand, sotalol and amiodarone on the other. Recent research has demonstrated that sotalol efficacy is no higher than that of the other beta-blockers, [4] and, on the other hand, lower than that of amiodarone. Physicians can also be misled by beliefs which vary significantly from one country to another, as often noticed in Europe due to its diversity of national practices. How to explain otherwise the variances between countries in the use of such a major antiarrhythmic drug as amiodarone? This drug holds approximately a 50% share on the worldwide antiarrhythmic market, but with significant differences in use: high (probably unreasonably high…) use in France or Belgium, low (probably unreasonably low…) use in Germany, fairly balanced use in Great Britain and the Netherlands. The drug's bad reputation, on its launch in the USA more than ten years after having been launched in Europe, mainly stemmed from the prescription method requiring specific caution not complied with at the time. In fact, it is well-known now that this is the most efficient drug for treating PAF as well as nearly all other cardiac arrhythmias, but that it must only be used when the other drugs have proved inadequate. From there on, I usually say that the most serious complication of amiodarone, in case of troublesome or serious side-effect, is that the patient loses treatment benefit as, after so many years, there is still no new drug truly as efficient as amiodarone on the market. The fact that this book advises against amiodarone is just one of scientific publication drawbacks, which non-professionals may find difficult to identify or of which they simply are not informed. Just as the media sometimes tend to emphasize a single train crash rather than keep up to date with all trains arriving on time, it is much more difficult in our system to publish hundreds of no-problem cases after several years of use than to publish ten cases involving more or less serious short-term complications.

All in all, patients and physicians will read this book differently, but both will find it useful. AF is such a complicated disease that no physician, including cardiologists, can pretend they know everything about its various fundamental, clinical and therapeutic aspects. Patients seeking information about their own case must realize that medicine is not an easy profession, but does attempt to take the right path, even if that path does not always turn out to be the best path. On the other hand, our increasingly evidence-based medicine must not neglect human aspects just because they cannot be easily expressed in figures.

This publication is a highly notable contribution to our knowledge about a disabling disease that can only benefit from physician-patient cooperation.

Philippe Coumel, MD, FESC
Hôpital Lariboisière, Paris, France
January 2003

References

1. Coumel Ph, Wilde AAM. Learning from mistakes: the case of clinical electrophysiology. A perspective on evidence-based rhythmology. Circulation 2001;104 :845-47
2. Coumel Ph. The management of clinical arrhythmias. An overview on invasive versus non-invasive electrophysiology. Eur Heart J 1987;8 :92-99
3. Coumel Ph. Atrial fibrillation: one more sporting inconvenience? Eur Heart J 2002;23 :431-33
4. Coumel Ph. Sotalol: a fool's deal ? Eur Heart J 2001;22:1370-73