Objective: Depression is a risk factor for mortality after acute myocardial infarction (AMI), possibly as a result of altered autonomic nervous system (ANS) modulation of heart rate (HR) and rhythm. The purposes of this study were to determine: a) whether depressed patients are more likely to have an abnormal HR response (i.e., abnormal turbulence) to premature ventricular contractions (VPCs), and b) whether abnormal HR turbulence accounts for the effect of depression on increased mortality after AMI.
Methods: Ambulatory electrocardiographic data were obtained from 666 (316 depressed, 350 nondepressed) patients with a recent AMI; 498 had VPCs with measurable HR turbulence. Of these, 260 had normal, 152 had equivocal, and 86 had abnormal HR turbulence. Patients were followed for up to 30 (median = 24) months.
Results: Depressed patients were more likely to have abnormal HR turbulence (risk factor adjusted odds ratio = 1.8; 95% confidence interval [CI] = 1.0–3.0; p = .03) and have worse survival (odds ratio = 2.4; 95% CI = 1.2–4.6; p = .02) than nondepressed patients. When HR turbulence was added to the model, the adjusted hazard ratio for depression decreased to 1.9 (95% CI = 0.9–3.8; p = .08), and to 1.6 (95% CI = 0.8–3.4; p = .18) when a measure of HR variability (LnVLF) was added. The hazard was found to differ over time with depression posing little risk for mortality in year 1 but greater risk in years 2 and 3 of the follow up.
Conclusion: ANS dysregulation may partially mediate the increased risk for mortality in depressed patients with frequent VPCs after an AMI.
ANS = autonomic nervous system; HR = heart rate; VPC = premature ventricular contraction; AECG = ambulatory electrocardiography; AMI = acute myocardial infarction; LnVLF = natural log of very low frequency; LVEF = left ventricular ejection fraction; TO = turbulence onset; TS = turbulence slope.
From the Departments of Psychiatry (R.M.C., W.B.H., J.A.B., K.E.F., L.L.W., B.S.), Medicine (P.K.S., J.H., P.P.D., M.M.B., A.S.J.), and Epidemiology (L.F.B.), Washington University School of Medicine, St. Louis, MO (R.M.C., W.B.H., K.E.F., P.K.S., B.S., P.P.D.); Duke University Medical Center, Durham, NC (J.A.B., L.L.W.); Harvard University, Boston MA (L.F.B.); National Heart, Lung, and Blood Institute, Bethesda, MD (S.M.C.); Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan (J.H.); Yale University School of Medicine, New Haven, CT, and Columbia University School of Medicine, New York, NY (M.M.B.); and the Mayo Clinic, Rochester, MN (A.S.J.).
Address correspondence and reprint requests to Robert M. Carney, PhD, Behavioral Medicine Center, 4625 Lindell Blvd., Suite 420, St. Louis, MO 63108. E-mail: firstname.lastname@example.org
Received for publication January 6, 2006; revision received August 9, 2006.
This research was supported in part by grant no. 2 RO-1HL58946 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Because co-author Kenneth E. Freedland is an Associate Editor of this journal, the review of this paper was overseen by a guest editor, Lawson R. Wulsin, who was chosen by other editors of the journal. Dr. Freedland was not involved in the decision-making process and like all authors was blinded to the identity of the peer reviewers.