Effects of blunt cardiac trauma on coronary vasomotion, perfusion, myocardial mechanics, and metabolism.

Blunt injury to heart muscle can result in a variety of dysrhythmias and mechanical dysfunction. In the present studies of 24 open-chest, working swine hearts with controlled perfusion of the left anterior descending (LAD) coronary artery, changes in proximal and distal coronary vascular resistance (CVR), small-vessel perfusion (using radioactively-labeled microspheres), and regional and global mechanical function and metabolism (myocardial oxygen consumption [MVO2] and lactate extraction) were observed before and for 1 hour following a single impact involving the LAD artery. Trauma caused no spasm, thrombosis, hemorrhage, or laceration of the LAD artery but resulted in significant perfusion redistributions of small vessels. Within minutes of the impact, epicardial/endocadial flow ratios in the myocardial tissue perfused by the traumatized vessel increased (p < 0.005) and were associated with a significant decrease in the distal CVR (p < 0.001). In this same region, significant decreases were also observed in an index of regional work (p < 0.01), shortening (p < 0.005), MVO2 (p < 0.001), and per cent lactate extraction (p < 0.01). Also noted were declines in left ventricular (LV) pressure development and contractility (LV max dp/dt). The regional changes in flow patterns and function in general persisted throughout the course of perfusion. These data suggest that cardiac trauma can induce major changes in vasomotor tone and perfusion distributions of the coronary vasculature, and demonstrate how blunt cardiac-coronary trauma can result in some of the hemodynamic and electrocardiographic abnormalities previously reported.