Cardiac mechanoreceptor function implicated during premature ventricular contraction

Abstract

In a premature ventricular contraction (PVC), a systolic blood pressure peak is missing during the affected cardiac cycle, leading to a prolonged reduction in blood pressure which is then followed by a large burst of sympathetic outflow. In a normal ventricular contraction, it is generally believed that peak carotid and aortic distensions associated with systolic pressure is the neural feedback that terminates sympathetic outflow through a baroreflex mechanism. Yet, the characteristically large sympathetic burst following a PVC is terminated without a systolic pressure and evidently without this mechanism. To address this anomaly, we examined the possible role of cardiac receptors in providing an alternative mechanism for the termination of sympathetic outflow in a PVC. For this purpose, recordings of electrocardiogram (ECG), arterial blood pressure (ABP), and muscle sympathetic neural activity (MSNA) were made in a human subject during repeated PVC episodes. The time intervals, or "latencies", from key events within the PVC to the peak of the associated MSNA burst were calculated and compared with the latency in a normal ventricular contraction which is associated with central baroreceptor function. It was found that the only event in a PVC that corresponds with a physiologically plausible latency is that which marks the end of ventricular filling. We conclude with the hypothesis that in the unique circumstances of a PVC, where the systolic pressure peak required to trigger arterial baroreceptors to terminate sympathetic outflow is absent, mechanoreceptors in the heart appear to "step in" to perform this sympathoinhibitory function.