Cardiovascular Reactivity and Its Relation to Cardiovascular Disease Risk
The confluence of factors that lead to the development of cardiovascular diseases such as coronary heart disease (CHD), essential hypertension, and stroke are a consequence of a prolonged period of pathogenesis spanning years and possibly decades (cf. Adams, Bobik, & Korner, 1989; Hulley, Rosenman, Bawol, & Brand, 1980; Lund-Johansen, 1967; MacMahon, Cutler, Furberg, & Payne, 1986; Page, 1949). Preclinical cardiovascular disease may be described as the pathological changes in the heart and arteries and in their central neural regulation that develop early in the course of atherosclerotic cardiovascular disease before symptoms or morbid events occur (Devereux, 1989). The preclinical detection of the progression of these disease states represents a potential for the development of medical and behavioral interventions that would circumvent disease progression before irreversible structural changes have occurred. Psychophysiological endeavor for the past three decades has labored to assess whether cardiovascular reactivity to emotional stress may be a predictor of preclinical pathogenic processes involved in the etiology of cardiovascular disease (see Manuck, 1994; Schneiderman, 1976; Schneiderman & McCabe, 1989). Advances in the use of noninvasive measurement techniques, such as impedance cardiography, to derive a more comprehensive assessment of the underlying hemodynamic and autonomic mechanisms medi-ating cardiovascular reactivity have facilitated this research (Hurwitz, Shyu,
Reddy, Schneiderman, & Nagel, 1990; Hurwitz et al., 1993; Sherwood et al., 1990). Although there are numerous promising and elegant lines of research that appear to support the notion that cardiovascular reactivity may be a marker of cardiovascular disease risk, much of this research was undertaken prior to the establishment of a multifactorial model of the pathogenesis of cardiovascular disease (e.g., Krantz & Manuck, 1984). A rapidly growing literature in the past few years has firmly established a linkage among CHD, hypertension, cardiac structure, baroreceptor and adrenoceptor sensitivity changes, and the insulin metabolic syndrome (insulin resistance, hyperinsulinemia, glucose intolerance, central obesity, dyslipidemia, hemostatic abnormalities, elevated blood pressure, and increased sympathetic activity; see Reaven, 1995; Schneiderman & Skyler, 1996). The theoretical basis for the development of the insulin metabolic syndrome (see Fig. 12.1) suggests that heightened central sympathetic drive is linked to insulin resistance and hyperinsuiinemia in a positive feedback loop that eventually leads to atherogenesis and possibly elevated blood pressure (Schneiderman & Skyler, 1996; Skyler, Marks, & Schneiderman, 1995). Therefore, to the extent that hyperreactivity to a behavioral stressor
FIG. 12.1. Schematic diagram depicting how the positive feedback loop among insulin resistance, sympathetic drive, and hyperinsulinemia may
mediate relationships among genetic, environmental, and lifestyle factors to the development of hypertension and CHD.