Case Studies in Physiology: Using premature ventricular contractions to understand the regulation of carotid artery longitudinal wall motion.

Recent observations have identified a distinct longitudinal motion pattern of the common carotid artery, where the wall oscillates along its length both with (anterograde) and against (retrograde) the direction of blood flow. The regulation of the longitudinal pattern remains largely undetermined, in part due to difficulty uncoupling local pressure and flow stimuli from upstream energy sources. In this case study of a 29-yr-old male, we examine the regulation of longitudinal wall motion from the perspective of spontaneous premature ventricular contractions (PVCs). With respect to the pre-PVC beat, during the PVC, there was an 81% reduction in carotid blood velocity (96.8 to 18.4 cm/s), a 69% reduction in pulse pressure (58 to 18 mmHg), and a 59% reduction in apical left ventricular (LV) rotation (6.9 to 2.8°) as a result of reduced LV filling time. During this time, anterograde longitudinal wall motion was unchanged (0.06 mm), whereas retrograde motion was reduced by 91% (0.75 to 0.07 mm). During the compensated post-PVC beat, there were large increases in all outcomes, except for anterograde wall motion. Taken together, there appears to be little influence of either local or upstream factors on anterograde wall motion. Although retrograde wall motion generally mirrored blood pressure, blood velocity, and upstream cardiac movement, the primary motion regulator remains unclear. In this Case Study, we provide evidence against the role of blood velocity in regulating local wall motion and reinforce the potential importance of cardiac mechanics dictating the unique longitudinal motion pattern at the common carotid artery. Benign arrhythmias can be a useful tool to probe new hypotheses in physiology. We tested the control of longitudinal motion of the common carotid artery wall using observations from spontaneous premature ventricular contractions in a healthy male. Forwards wall motion remained unchanged despite large deviations in local blood velocity and backwards wall motion mirrored changes in pulse pressure, blood velocity, and cardiac motion, thereby revising our original hypothesis of the control of longitudinal wall motion.