Cardiovascular reactivity refers to the difference in heart rate, blood pressure or other measures of cardiovascular function observed between periods of rest and during the presentation of an external stressor. Reactivity may be conceptualized as a quantitative, physiological variable, such that certain individuals will show greater reactivity than others. The majority of reactivity studies have measured changes in heart rate and systolic blood pressure. To a lesser extent, reactivity has also been studied by measuring changes in ST segment depression of the ECG, rate pressure product, pulse pressure, pulse transit time, cardiac output, total peripheral resistance and left ventricular ejection time, as well as other measures of cardiac performance and circulating levels of catecholamines and cortisol. The paradigms for studying reactivity have involved a broad class of experimental stressors and designs. The evaluation period used to establish resting levels of physiological activity may be a separate relaxation baseline, conducted on a different day than the stress session, or it may be a pre-stress baseline, conducted on the same day as the stress session. The physical stressors may involve the cold pressor test, isometric hand grip and exercise. Cognitive stressors may involve one or more of the following: mental maths, the Stroop Color Word Test, complex analytical or concept formation tasks, a stressful interview, i.e., a structured interview for Type A behaviour, choice reaction time, video games, or naturalistic stress, e.g., job environment. The saliency of the situation for a particular subject may be enhanced by including such factors as pressure to respond quickly, threat of aversive consequences for errors, e.g., shock, incentives for successful completion of the task, competition and harassment. Different methodological permutations of task and measurement characteristics may elicit patterns of arousal, which accentuate reactivity in one or another measure( s). Suffice it to say, however, that the extent of a subject's reactivity to a particular measure, e.g., heart rate (HR) response to mental maths or a video game, is usually reproducible and stable over time. Correlations between different response measures on different tasks are more variable, but moderately high (Krantz and Manuck, 1985). Unless otherwise specified, this review will concentrate on studies of cardiovascular reactivity using cognitive stressors. Cognitive stressors may represent an important laboratory analogue which can be used to assess the effects of acute psychological stress on the cardiovascular system. Laboratory stressors are easily administered and the physiological changes which accompany them may have relevance for the future development of cardiovascular disease. The relationship between laboratory induced cognitive stress and cardiovascular reactivity has been studied in several ways. Early research examined the extent of reactivity in people with manifest cardiovascular disease. These studies typically did rIot involve comparisons to normal controls but were aimed at linking the presence of an abnormal cardiac event, e.g., excessive oxygen consumption or hypertension, to acute cognitive stress. Later studies of reactivity did include comparisons between normals and patients with cardiovascular disease. It soon became clear that the magnitude of stress induced changes in blood pressure or heart rate was not uniform across all subjects and that certain otherwise healthy subjects, as well as some patients, could be described as cardiovascular reactors. The central question, however, is whether the high reactors are at increased risk for the development of future cardiovascular disease. This chapter reviews the pathophysiological and epidemiological significance of acute cardiovascular reactivity as it relates to cardiovascular disease. Long-term prospective studies bridging the gap between the initial observation of excessive reactivity to acute stress and the development of future cardiovascular disease are at present few in number. However, several hypotheses have been advanced which link the acute effects of cognitive stress, e.g., increased heart rate, catecholamines, etc., to known pathogenetic factors in cardiovascular disease. Research on subjects who do not yet have manifest cardiovascular disease, but who are excessively reactive to stress, may be particularly important since it could reveal the mechanisms which link the pathophysiology of future diseae to the episodic stress experienced during the preclinical period of a disorder. The reader is referred to the reviews of Krantz and Manuck (1984, 1985) for an in-depth discussion of reactivity research design and methodological issues.