Arrhythmogenic effect of high blood pressure: some observations on its mechanism.

An increase in aortic pressure is a reproducible way of causing ventricular ectopic rhythms. This study sought to determine whether it is the aortic pressure per se or the concommitant increase in afterload or preload that has a direct arrhythmogenic effect. Experiments were carried out in 17 anaesthetised dogs. For each 10 s period the pressure and the presence of a ventricular arrhythmia (at least one ectopic beat) were noted. In nine animals an aortic valve gradient was created (and released). The results were compared to those obtained by impeding the aortic flow at the ascending aorta. The mean systolic left ventricular pressure was significantly higher in the arrhythmia associated periods in 8/9 experiments when there was an aortic valve gradient and in 5/9 experiments when there was not. In 4/9 experiments the mean aortic pressure associated with arrhythmia was significantly lower with an aortic valve gradient than when there was no gradient and no arrhythmia. In 7/9 of these experiments, coronary sinus flow was measured volumetrically during the manoeuvres applied. The coronary flow was significantly lower when there was neither arrhythmia nor aortic valve gradient than when there was an arrhythmia (with or without an aortic valve gradient). In another eight experiments a pressure reservoir in the aorta was either raised or lowered while another pressure reservoir in the left atrium was moved in the opposite direction. Thus the mean aortic pressure could be increased while the left atrial pressure was decreased and vice versa. If the left atrial pressure was taken into account, the mean difference of the aortic pressure from its expected value, derived from the aortic v left atrial pressure regression equation, was significantly higher when there was an arrhythmia than it was when there was no arrhythmia in all eight experiments. On the other hand, the mean difference in the left atrial pressure from its expected value was significantly higher when there was an arrhythmia in 1/8, lower in 2/8 and not significantly different in 5/8 experiments. It is concluded that when the blood pressure is raised, it is the increase in afterload rather than an increase in aortic pressure itself or in the preload that has an arrhythmogenic effect on the ventricles.