Atrial Fibrillation: A Theoretical Assumption and a New Perspective

The most common cardiac arrhythmia in clinical practice is atrial fibrillation (AF). The cause for the development of AF has been investigated by many studies, however, the question remains unanswered. A recently published hypothesis suggested that atrial fibrillation is a physiological mechanism, of protective value, based on the discontinuation of atrial mechanical systole. This lowers the pressure within the system of the pulmonary veins and alveolar capillaries, in pathological situations, and as a result reduces the probability for development of pulmonary congestion and edema. This hypothesis explains the connection between left ventricle (LV) dysfunction and AF, helps with designing algorithms of relationships between AF and LV dysfunction, and with various diseases and conditions, suggests a new approach to the location of the source of AF and shows a protective function of the atriums in the development of LV dysfunction. There is a correlation between this hypothesis and the known facts and phenomenons associated with AF.

It is known that the most common arrhythmia in clinical practice is atrial fibrillation (AF) and is very often associated with LV dysfunction / heart failure (HF). It is called the epidemic of the century. An arrhythmia that is particulary common in the elderly, AF is growing in prevalence with the ageing of the population. In addition to age, there are many types of cardiac and medical conditions that are also closely linked to AF. These include hypertention, coronary artery disease, heart failure, valvular heart diseases, hyperthyroidism and so on. Despite the fact that there have been many studies carried out on the subject of “AF-a cause or consequence?”, the question remains unanswered.

In the years 2015-2016 the new hypothesis was proposed, which assumes that AF is a protective physiological mechanism in the cases of LV dysfunction/heart failure and it answers many questions related to the AF. The reasoning of the hypothesis is as follows. The end diastolic pressure (EDP) is the algebraic sum of the left ventricle diastolic pressure (LVdp) and left atrial systolic pressure (atrial kick pressure, AKp). EDP=LVdp+AKP. Normal range of EDP is 8-12 mm Hg, AKp is 2-6 mm Hg. At the end of the diastole when the mitral valve(MV) is still open, EDP immediately transmitted and equalized (according to hydrodynamic law) throughout the communicating system of the LV, LA, pulmonary veins(PV), and alveolar capillaries(AC), as there are no obstacles to the spread of the EDP wave. EDP is thus equal to pulmonary wedge pressure (PWP) with a normal range of 8-12 mm Hg. In the conditions of LV dysfunction (HF varying degrees), EDP increases due to failure of the LV (i.e. LV diastolic pressure component increases). EDP = LVsp + AKp. This increased EDP at the end of diastole with opened MV transmits to the entire communicating system of the LA-PV-AC and with the increased PWP, but with the threat of exit of fluid through the alveolar-capillary membrane. When PWP increases to 20 mm Hg, pulmonary edema is usually present.