CHANGES IN HEART BEAT TIMING - REACTIVITY, RESETTING, OR PERTURBATION

A widely held hypothesis within behavioral medicine is that cardiovasc ular reactivity is a risk factor for cardiovascular disease. The measu rement model for this cardiovascular reactivity is rather simple. A ba sal level of function is seen to increase while the organism is stress ed and then return to basal function. We argue that this model is inco mplete and that other forms of 'reactivity' may be relevant to pathoph ysiology. A pathophysiological hypothesis is discussed which assumes a cyclic heart beat generation mechanism that is sensitive to stimulati on only at certain phases of its cycle. Implications of this hypothesi s for measurement are developed to illustrate the point that models of normal function can determine the measures most relevant to pathophys iology. (C) 1998 Elsevier Science B.V. All rights reserved.