Changes in heart beat timing: reactivity, resetting, or perturbation?

Author(s): vanderMolen, M. W., Somsen, R. J. M.

Journal/Book: Biol Psychol. 1998; 47: PO Box 211, 1000 AE Amsterdam, Netherlands. Elsevier Science BV. 227-241.

Abstract: A widely held hypothesis within behavioral medicine is that cardiovascular reactivity is a risk factor for cardiovascular disease. The measurement model for this cardiovascular reactivity is rather simple. A basal level of function is seen to increase while the organism is stressed and then return to basal function. We argue that this model is incomplete and that other forms of 'reactivity' may be relevant to pathophysiology. A pathophysiological hypothesis is discussed which assumes a cyclic heart beat generation mechanism that is sensitive to stimulation only at certain phases of its cycle. Implications of this hypothesis for measurement are developed to illustrate the point that models of normal function can determine the measures most relevant to pathophysiology.

Note: Article Jennings JR, Univ Pittsburgh, Western Psychiat Inst & Clin E1329, 3811 Ohara St, Pittsburgh,PA 15213 USA

Keyword(s): behavioral medicine; cardiovascular reactivity; heart rate; phase sensitivity; cardiac cycle time effect; arrhythmia; cardiac sudden death; WESTERN COLLABORATIVE GROUP; SUDDEN CARDIAC DEATH; PACEMAKER ACTIVITY; A BEHAVIOR; FOLLOW-UP; PHASE; ANNIHILATION; DISEASE; NODE; HYPERTENSION

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