All arrhythmia cause abnormal heartbeat intervals (HBI or RR intervals) and result in artificially inflated HRV or btbBP results. Based on this fact, HBI-alone analyses are contraindicated for arrhythmia. For HRV technologies, the FDA has allowed a few correction techniques to enable HRV analyses, but only for low-quality (low-density) arrhythmia. In general, if the arrhythmia (ectopy that is not artifact) is isolated as singlets or doublets, these abnormal HBIs are modified (“corrected”) based on an interpolation of the values of neighboring HBIs. However, a run of three or more ectopic beats may not be corrected. These must presented to the physician as an indication of pathology, and they corrupt the HRV results. As shown in the next section on Atrial Fibrillation, the spectral analysis method inherent in P&S monitoring enables ANS assessment even in the presence of high-quality arrhythmia.

Unexplained arrhythmia (palpitations) is a common occurrence. It is often demonstrated in patients with an otherwise healthy normal heart, as determined by a negative cardiac work-up. A typical patient example is a young, healthy, fit woman who reports frequent palpitations after exercise. While the arrhythmia is often a concern to the patient, if it is not malignant or life threatening, it may go untreated. However, unexplained arrhythmia may have a significant impact on quality of life. With P&S monitoring, most unexplained arrhythmia cases are found to have autonomic dysfunction (imbalance). Normalizing their ANS balance (SB) often relieves their arrhythmia. For 10–15 %, of these patients, the relief is complete as confirmed by negative cardiologic or electrophysiologic assessment. P&S imbalances in these cases tend to be corrected using short-term, low-dose therapy. If the P&S imbalance is a resting PE, then titrating anticholinergic therapy relieves the PE and often relieves the arrhythmia. If the imbalance is a Valsalva or PC PE, then carvedilol is recommended (section “Carvedilol Therapy”). If the imbalance is a SE, then titrating sympatholytic relieves the SE and often relieves the arrhythmia.

In the 1990s, Phillipe Coumel wrote that atrial fibrillation (AFib) is not a homogeneous entity, and many factors are responsible for a number of different behaviors, clinical consequences, and reactions to therapy [1]. He observed that the electrophysiological characteristics of atrial cells (action potential duration and refractoriness, conduction speed) are modulated differently by P and S influences. The parasympathetics tend to favor macro-reentry phenomena, whereas the sympathetics favor abnormal automaticity and triggered activity [2].

In normal hearts, vagal influences are predominant, thus explaining that the clinical pattern of vagal-mediated paroxysmal atrial fibrillation is preferentially observed in the absence of detectable heart disease, in young male adults, with an EKG pattern of common flutter alternating with fibrillation. Sympathetically mediated atrial fibrillation is observed in the presence of any heart disease, the first effect of which is to provoke a vagal withdrawal. The clinical history is a guide for suspecting autonomic involvement in arrhythmogenesis. Observing the behavior of sinus rate variability just preceding the onset of the arrhythmia permits documentation of the mechanism. The role of P and S influences should be taken into consideration every time conventional antiarrhythmic treatment is insufficient. Beta-blockers as well as digitalis may be either beneficial or detrimental, according to the causal mechanism. The choice of beta-blockers or digitalis or a combination should be based on more information [2].

Dr. Coumel observed that the conventional evaluation of preventive treatments is not really adapted to provide the correct answers to difficult problems of therapeutic indications, as the benefit–risk relationship is not really known. Like ventricular fibrillation, atrial fibrillation may be primary or secondary to organized tachyarrhythmias, and reentrant flutter or automatic atrial tachycardia may well form the actual target for treatment. The P and S nervous systems are always involved in arrhythmogenesis. P and S action may predominate and explain why a treatment may or may not be effective in situations that are identical only in appearance. The electrophysiologic milieu of atrial tissue probably accounts for the perpetuation of the process of atrial fibrillation or its self-termination. Drugs may contribute to modify the milieu in a way that in the end may be favorable or not. The presence or the absence of heart disease and heart failure largely contributes to the (1) state of SB, (2) hemodynamic consequences of AFib, and (3) proper effects of drugs. The overall consequence of these complex situations is that (1) any precise therapeutic decision algorithm for AFib is overly simplistic and (2) any global evaluation of drug efficacy or toxicity is not really meaningful as long as the category of patients treated is not precisely determined. No drug appears better or worse than others, but simply more or less adapted to various situations [1]. Again, more information is helpful.

A 270-patient atrial fibrillation (AFib) study was first published as an abstract entitled “Altered autonomic activity with atrial fibrillation as demonstrated by non-invasive autonomic monitoring.” The manuscript was accepted at the American Autonomic Society, 17th International Symposium, Kauai, HI, October 2008, and presented as a poster [3]. Later the manuscript was published in the US Cardiology [4]. Excerpts of this manuscript are presented here.