Long PR interval and MVP

This patient presented symptoms of exertion that can be at least partially explained by AP-VS intervals that did not shorten during exercise. In the first version of the MVP algorithm, the device did not switch on this type of tracing, the only switching criterion being the presence of 2 blocked atrial activities out of 4. At the request of some physicians faced with patients remaining symptomatic in the setting of long PR on exertion, the algorithm was modified accordingly in the second version to switch to DDD mode. In this example, this new functionality had not been programmed, thus the functioning is similar to that of the old version of the algorithm.

A first-degree atrioventricular block (AV block) corresponds to a simple prolongation of the PR interval which exceeds the physiological values. There are an equal number of P waves and QRS complexes and a fixed constant PR space exceeding 200 ms in adults. If sinus function is normal, there is no bradycardia (ventricles at the same rate as the atria). The term AV block is therefore inappropriate since it is not, strictly-speaking, a block (interruption of conduction) but rather a slowing down of conduction. An extension of the PR space can indicate a slowing down at any level of the "conduction chain" between the first activated atrial cell (onset of the P wave) and the first activated ventricular cell. A long PR may occur as a result of:

1. a delay in atrial conduction (rare); a major prolongation of the intra-atrial conduction time (slowed conduction velocities and/or atrial dilatation) revealed on the electrocardiogram by a very wide P wave can result in a modest prolongation of the PR interval;
2. a conduction delay in the atrioventricular node (the most frequent), such that the longer the PR interval, the greater the probability that the deceleration is located in the atrioventricular node;
3. a delay in distal conduction at the His-Purkinje network; most often associated with the presence of a wide QRS, this reflects the presence of a trifascicular block and justifies the implantation of a pacemaker.

The presence of a very long PR interval can be associated with the occurrence of symptoms, if the response to exertion is not physiological. Indeed, in the absence of reduction of the PR interval in conjunction with the increase in exercise rate, the atrial systole following atrial depolarization occurs too early during ventricular diastole. Atrial systole may even occur at the end of a ventricular systole resulting in a loss of active atrial contribution to cardiac ejection, a shortening of left ventricular filling time, diastolic mitral regurgitation and, in the most marked cases, atrial contraction due to closed mitral valves. This can be accompanied by a more or less prominent symptomatology (exertional dyspnea, sensation of retrograde flow in the jugular veins, palpitations, malaise) very similar to that observed in patients paced in VVI mode with retrograde conduction (pacemaker syndrome). A number of uncontrolled studies suggest that implantation of a pacemaker reduces symptoms and improves functional status in this setting. In the latest European guidelines, there is a hemodynamic indication (class IIA) for pacemaker implantation for this type of presentation: « implantation of a pacemaker should be considered in patients with primary AV block (PR > 300 ms) and symptoms consistent with pacemaker syndrome. »

The number of symptomatic patients in this setting is relatively limited and, as explained above, the first version of the algorithm did not allow an adequate response to this problem.