title: Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease.
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.
authors.affiliation: Yale University School of Medicine, New Haven, Connecticut, USA. amyrschwartz@yahoo.com
authors.forename: Amy R
authors.initials: AR
authors.lastname: Schwartz
authors.forename: William
authors.initials: W
authors.lastname: Gerin
authors.forename: Karina W
authors.initials: KW
authors.lastname: Davidson
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Pickering
authors.forename: Jos F
authors.initials: JF
authors.lastname: Brosschot
authors.forename: Julian F
authors.initials: JF
authors.lastname: Thayer
authors.forename: Nicholas
authors.initials: N
authors.lastname: Christenfeld
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Linden
mesh_terms: D000293:Adolescent; D000818:Animals; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000523:psychology; D002319:Cardiovascular System / Q000503:physiopathology*; D004781:Environmental Exposure; D005260:Female; D020022:Genetic Predisposition to Disease; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D007206:Individuality; D007398:Interpersonal Relations; D008252:Macaca fascicularis; D008297:Male; D008954:Models, Biological; D051381:Rats; D011919:Rats, Inbred Strains; D012107:Research Design; D013312:Stress, Physiological / Q000150:complications* / Q000503:physiopathology; D013315:Stress, Psychological / Q000150:complications / Q000503:physiopathology