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REACTIVITY SPECIAL SECTION |
From Yale University School of Medicine (A.R.S.), New Haven, Connecticut; Mount Sinai School of Medicine (W.G., K.W.D., T.G.P.), New York, New York; University of Leiden (J.F.B.), Leiden, The Netherlands; National Institute on Aging, National Institutes of Health (J.F.T.), Bethesda, Maryland; University of California, San Diego (N.C.), La Jolla, California; and University of British Columbia (W.L.), Vancouver, British Columbia, Canada.
Address reprint requests to: Amy Schwartz, 100 York St, Apt 17A, New Haven, CT 08511. Email: amyrschwartz{at}yahoo.com
ABSTRACT
OBJECTIVE: Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding.
METHODS: We illustrate current understanding of stress–cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature.
RESULTS: In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship.
CONCLUSIONS: A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.
Key Words: cardiovascular reactivity • blood pressure • stress • hypertension • coronary artery disease.
Abbreviations: ABP = ambulatory blood pressure; ACE = angiotensin-converting enzyme; ADH3 = alcohol dehydrogenase type 3; BHR = borderline hypertensive rat; BMI = body mass index; BP = blood pressure; CAA = coronary artery atherosclerosis; CAD = coronary artery disease; CPT = cold pressor test; CVD = cardiovascular disease; CVR = cardiovascular reactivity; DBP = diastolic blood pressure; EF = endothelial function; ER-
= estrogen receptor alpha; HR = heart rate; HRT = hormone replacement therapy; HRV = heart rate variability; HT = hypertensive; HTN = hypertension; LV = left ventricle; MA = mental arithmetic; MI = myocardial infarction; NO = nitric oxide; NT = normotensive; PNS = parasympathetic nervous system; SBP = systolic blood pressure; SES = socioeconomic status; SHR = spontaneously hypertensive rat; SNS = sympathetic nervous system; WKY = Wistar-Kyoto (rat); 5HTTLPR = serotonin transporter gene.
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