Increased cardiovascular (CV) reactivity has been associated with worse CV prognosis. Though mood disorders (MDs) have been associated with increased CV reactivity during behavioral stressors, the extent to which MDs and their interaction with coronary heart disease (CHD) influences exercise-induced CV reactivity has not been evaluated.
Five hundred twenty-six patients underwent nuclear exercise stress testing. Cardiovascular parameters were assessed at rest, every 2 minutes during exercise, and at peak exercise. MDs were measured using a structured psychiatric interview, the Primary Care Evaluation of Mental Disorders, and CHD was defined as having a history of myocardial infarction, revascularization, heart failure, and/or cerebrovascular event.
CHD patients exhibited lower peak exercise heart rate (F = 9.40, p = .002) compared with patients without CHD. Submaximal data showed that patients with CHD had a slower rate of increase of heart rate (F = 4.29, p = .04) and diastolic blood pressure (F = 3.27, p = .04). There was an interaction of CHD and MDs, indicating that in patients with CHD, the rate of submaximal increase in systolic blood pressure (F = 3.08, p = .047) and rate-pressure product (F = 5.13, p = .006) was greater in patients with a MD compared with those without a MD. These differences were not observed in patients with no CHD. No other main or interaction effects of MDs and CHD were observed.
Though MDs alone do not seem to be associated with higher levels of stress CV reactivity, their combination with CHD leads to increased submaximal exercise-induced CV reactivity. Prospective studies are needed to explore the causal relationship between these variables.
CV = cardiovascular; HR = heart rate; CHD = coronary heart disease; SBP = systolic blood pressure; MDs = mood disorders; DBP = diastolic blood pressure; RPP = rate-pressure product; BP = blood pressure; SPECT = single photon emission computed tomography; SES = socioeconomic status; BRS = baroreceptor sensitivity; BMI = body mass index; MI = myocardial infarction; MOSMI = Mechanisms and Longitudinal Outcomes of Silent Myocardial Ischemia.
From the Montreal Behavioural Medicine Centre, Montreal Heart Institute- a University of Montreal affiliated hospital, Montréal, Québec, Canada (R.P., K.L.L., J.G., A.A., S.L.B.); Department of Psychology, University of Québec at Montréal (UQAM), Montréal, Québec, Canada (R.P., K.L.L.); Montreal Behavioural Medicine Centre, Hôpital du Sacré-Cœur de Montréal-a University of Montreal affiliated hospital, Montréal, Québec, Canada (K.L.L., S.L.B.); Department of Psychology, McGill University, Montréal, Québec, Canada (J.G.); Department of Psychology, University of Calgary, Calgary, Alberta, Canada (T.S.C.); Department of Exercise Science, Concordia University, Montréal, Québec, H4B 1R6. Canada (S.L.B.).
Address correspondence and reprint requests to Simon L. Bacon, PhD, Montreal Behavioural Medicine Centre, Montreal Heart Institute- a University of Montreal affiliated hospital, Montréal, Québec, H1T 1C8., Canada. E-mail: firstname.lastname@example.org
Received for publication July 16, 2008; revision received October 16, 2008.
Funding for this study was received from the Canadian Institutes of Health Research (MOP79445 and MOP89965), the Heart and Stroke Foundation of Quebec, the Fonds de la recherche en santé du Québec (FRSQ) (to S.L.B. and K.L.L.) and the Social Sciences and Humanities Research Council (SSHRC) (to R.P.).