One must apply some caution when pronouncing a heart to be healthy. In the normal heart, fibrosis develops with age, especially in the atria, and this is an important cause for atrial fibrillation. Also, subtle abnormalities may not be detected during routine examination, for example small areas of fibrosis in the right ventricle of patients with the Brugada syndrome, said to occur in structurally normal hearts.
The most common arrhythmias that occur in otherwise normal hearts are premature beats, or extrasystoles, and atrioventricular nodal reentrant tachycardia.
The premature beat (extrasystole)
Scherf and Scott defined an extrasystole in 1973 as “ a contraction of the whole heart, or parts of the heart, due to impulses which are abnormal, either regarding the site of origin-ectopic- or their time of occurrence-premature- or both, interfering with and replacing a dominant rhythm”. In this definition the word “contraction” is used although an extrasystole does not necessarily lead to a contraction. I prefer the term premature beat, because “beat” is used in the context of rhythm. By feeling the pulse, one can detect the premature beat, but it is not the premature beat itself that is felt because the premature contraction, if present, is too weak to lead to the expulsion of blood from the ventricles. The premature beat makes the heart refractory to the next sinus impulse, and only after a so-called compensatory pause does the second sinus impulse elicit a contraction that can be felt at the pulse. There is in fact no “extra” beat.
Engelmann, in 1895, was the first to use the term extrasystole. In 1906, Willem Einthoven, who invented the electrocardiograph that records the electrical activity of the heart, constructed a cable between his laboratory and the Leiden University hospital. According to Snellen (1984): “Occurrence of extrasystoles had the peculiar effect that Einthoven could warn the physician that he was going to feel an intermission of the pulse at the next moment. It seems that this annoyed the physician…and after only a few years he cut the connection”. Thus, a great opportunity to document clinical arrhythmias was lost.
Mechanisms and clinical significance
Premature beats may be caused by every known arrhythmogenic mechanism, but most often this mechanism cannot be identified with certainty.
Single premature beats, atrial or ventricular, are often not perceived by the individual. No treatment is needed. If a person is bothered by frequent, symptomatic premature beats, beta adrenergic blocking agents may be helpful, or even a class III antiarrhythmic agent. In diseased hearts, single or multiple ventricular premature beats may elicit sustained reentrant rhythms, and in such hearts class III agents may be harmful (see section on arrhythmias in various diseases).
Atrioventricular nodal reentrant tachycardia
The atrioventricular (AV) node, normally the only electrical connection between atria and ventricles, has two atrial inputs: a fast pathway with a long refractory period and a slow pathway with a shorter refractory period. An atrial premature beat may be blocked in the fast pathway and slowly conducted in the slow pathway. When the impulse reaches the junction between slow and fast pathways, it may be retrogradely conducted back to the atrium via the fast pathway, which by now has recovered its excitability. The retrograde atrial impulse may excite the slow pathway, thus completing the reentrant circuit, and once the sequence is established it may continue and lead to a sustained reentrant tachycardia.
In 1914 G.R.Mines predicted this sequence of events, but it was not till the 1960s and 1970s that sophisticated mapping of the AV node in animal experiments firmly established this mechanism.
Nowadays, catheter radiofrequency ablation of the slow pathway is the most effective treatment.
Michiel J Janse MD, Amsterdam, The Netherlands