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Cardiovascular responses to a psychological stressor in high versus low reactive women

University of British Columbia

Recent studies have implicated acute reactivity to a psychological stressor as a potential marker in the pathogenesis of cardiovascular disorders. However, only very few well controlled prospective studies necessary to confirm this hypothesis have been conducted. Such studies would need to demonstrate that cardiovascular hyperreactivity is a stable, individual-specific predisposition which is not significantly affected by response habituation to repeated stressor exposures. In the present study the relationship between degree of cardiovascular responsiveness and response habituation as a function of number of stressor repetitions and length of interstressor interval was assessed. Responses to a mental arithmetic task were compared within trials (3 minutes), across trials (3 per session), and across experimental sessions (2 sessions with a 4-week interval) in high versus low cardio-reactive women. Ninety female, normotensive subjects (mean age 24.6 years) participated in the study. Subjects were randomly assigned to one of two experimental conditions: in Condition 1 (repeated exposure) a twenty minute adaptation period was followed by a series of three, 3 minute mental arithmetic tasks with a 90 db white noise interference during the first laboratory session. A three minute rest period followed each task period. Subjects in Condition 2 (single exposure) completed the twenty-minute adaptation period followed by a single 3-minute task and a subsequent fifteen-minute recovery period. During their second visit all subjects completed a series of three mental arithmetic tasks identical to those completed in Condition 1, visit 1. Throughout the experimental sessions heart rate (HR), systolic (SBP), diastolic (DBP), and mean arterial pressure (MAP) were monitored at one minute intervals using an automated, digital Dinamap 845 Vital Signs Monitor. Subjects were classified into heart rate and SBP reactivity terciles on the basis of their response to the first stress task in the initial session. Only those subjects who fell into the lowest and highest reactivity terciles were included in subsequent analyses. Given that not all subjects received all trials three sets of analyses of covariance were necessary to fully examine the 2 (low versus high reactivity) X 2 (conditions) X 2 (visits) X 3 (trials) X 3 (minutes per trial) repeated measures factorial design. Age and respective baselines were employed as covariates. The results consistently indicated main effects (p < .001) for the reactivity groups, visits, trials, and minutes factors on each of the four dependent measures. These findings together with the results of subsequent trend analyses and Newman-Keuls post-hoc tests identified significant decreases in response levels within trials, across trials, and across the two experimental sessions. Decreases from minute 1 to minute 2 of each trial were greater than those from minute 2 to minute 3 on heart rate measures. The same pattern of decreases was observed for the trials factor. Blood pressure responses showed a delayed onset of decreases in response magnitude within experimental trials. All blood pressure measures showed evidence of response decreases from minute 2 to minute 3 of each trial. High reactors showed greater decreases in responses than low reactors across the experimental sessions. For the final stress task the HR, DBP and MAP responses of the high reactivity groups in the repeated stressor condition could not be discriminated from those of the low reactors. The notion of within-individual response specificity and the use of acute cardiovascular reactivity as both a classification and an outcome measure may therefore need to be re-evaluated.

Text

2010-12-04

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http://hdl.handle.net/2429/30284

Psychology

University of British Columbia

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