Premium
Affective status following myocardial infarction can predict long‐term heart rate variability and blood pressure reactivity
Author(s) -
Thornton E. W.,
Hallas C. N.
Publication year - 1999
Publication title -
british journal of health psychology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.05
H-Index - 88
eISSN - 2044-8287
pISSN - 1359-107X
DOI - 10.1348/135910799168597
Subject(s) - stressor , anxiety , blood pressure , heart rate , depression (economics) , mood , myocardial infarction , psychology , medicine , ambulatory , cardiology , clinical psychology , psychiatry , economics , macroeconomics
Objectives. The study describes cardiovascular reactivity to challenge 18 months post‐episode in primary myocardial infarct patients. Reactivity during laboratory tests was compared to changes induced by self‐reported stressful events and related to measures of anxiety and depression. Design. Prospective changes of mood states were documented between the postepisode period and an 18‐month follow‐up. Cross‐sectional bivariate correlations and regression analyses were used to relate mood states to cardiovascular responses. Method. Questionnaires were used to document anxiety, depression, more general negative and positive mood status, and patients'general appraisal of stressorsin 30 postmyocardial infarct patients. Responses were collated 4 weeks following their episode and again 18 months post‐episode at psychophysiological assessment. Systolic and diastolic blood pressure and heart rate were measured under four conditions: baseline rest in the laboratory, laboratory challenge tests, ambulation over a 12‐hour period, and self‐reported stressors during this period. A time domain assessment of heart rate variability was also collected over the ambulatory period. Results. Heightened reactivity was significantly greater to self‐reported stressors compared with laboratory challenge. Depression assessed in the immediate post‐episode period proved the best predictor of heightened reactivity to stressors of relevance to patients, and of heart rate variability. Mood status was not a strong predictor of responses to arbitrary laboratory challenge. Conclusions. The data are consistent with the hypothesis that an increased probability of subsequent episodes in post‐myocardial infarct patients suffering depression may be related to reactive vascular responses to self‐perceived stressors and changes in autonomic control.