The changing concept of cardiovascular reactivity

Abstract

Cardiovascular reactivity has long been measured in laboratory responses to a wide variety of cognitive and physical stressors, with the hypothesis that exaggerated reactivity plays a pathogenetic role in the development of essential hypertension. However there are few data to support the belief that behavioural differences of cognitive perception of stressors account for observed differences of reactivity. Cardiovascular reactivity in the laboratory does not predict hypertension or account for differences of blood pressure variability in the natural environment. Hypertensives do not exhibit increased blood pressure variability. Antihypertensive therapy consistently fails to lower cardiovascular reactivity in either the laboratory or natural milieu, supporting the dual and largely independent regulation of the basal and reactive blood pressures. It is concluded that there is little support for the use of laboratory stress testing to delineate either the pathogenesis of hypertension, the evaluation of hypertensive subjects, or the efficacy of antihypertensive therapy.

Type a Behaviour, Anxiety and Neuroticism: Reconceptualizing the Pathophysiological Paths and Boundaries of Coronary-Prone Behaviour

“…First, the evidence causally linking acute and non-specific sympathetic arousal to risk or incidence of CHD is not strong. 47 Second, many individuals exhibit both competitiveness and the host of manifest Type A behaviours which it is suggested arise from it, and few of these go on to experience a clinical event of CHD. Indeed, it seems that under some circumstances and in particular environments, many individuals not only show no sign of distress or disease, but report the experience in positive terms.…”