Coronary—Ventricular Interaction: The Gregg Phenomenon

Abstract

Despite some negative reports, especially from experiments in pig hearts, there is considerable evidence that changes in coronary perfusion pressure alter myocardial contractile function and oxygen consumption. The mechanism of this Greeg phenomenon has not been delineated; howerver, pressure-induced changes in coronary vascular volume, associated with ineffective coronary pressure-flow autoregulation, are instrumental in producing the Gregg phenomenon. Although changes in coronary vascular volume alter ventricular end-diastolic wall thickness, myocardial fiber length is unchanged. Thus, the Gregg phenomenon does not result from Starling’s law. Inotropic factors released from endothelium appear not to be responsible for the Gregg phenomenon. Changes in coronary perfusion pressure alter myocardial stiffness, both in diastole and in systole; this may alter the ratio of internal to external work and modulate myocardial oxygen demand. Because effective coronary autoregulation prevents perfusion pressure-mediated changes in vascular volume, autoregulation protects myocardium from increased oxygen demand when perfusion pressure is elevated. Failure of autoregulation at reduced perfusion pressure reduces myocardial oxygen demand and improves myocardial oxygen utilization efficiency. The Gregg phenomenon may be the initial step in the process of myocardial hibernation.