Length Polymorphisms in the Angiotensin I-Converting Enzyme Gene and the Serotonin-Transporter-Linked Polymorphic Region Constitute a Risk Haplotype for Depression in Patients with Coronary Artery Disease.

Journal Article (Journal Article;Multicenter Study)

Genetic variations affecting the course of depressive symptoms in patients with coronary artery disease (CAD) have not yet been well studied. Therefore, we set out to investigate whether distinct haplotypes of the two insertion/deletion polymorphisms in the serotonin-transporter-linked polymorphic region (5-HTTLPR) and the angiotensin I-converting enzyme (ACE) gene located on chromosome 17 can be identified as risk factors for trajectories of depression. Clinical and genotyping data were derived from 507 depressed CAD patients participating in the randomized, controlled, multicenter Stepwise Psychotherapy Intervention for Reducing Risk in Coronary Artery Disease (SPIRR-CAD) trial, of whom the majority had an acute cardiac event before study inclusion. Depression scores on the Hospital Anxiety and Depression Scale (HADS) were assessed at baseline and at five follow-up time points up to 2 years after study entrance. At baseline, depression scores did not significantly differ between patients carrying the risk haplotype ACE D/D, 5-HTTLPR I/I (n = 46) and the non-risk haplotypes (n = 461, 10.9 ± 2.7 versus 10.4 ± 2.5, p = 0.254). HADS-depression scores declined from study inclusion during the first year irrespective of the genotype. At each follow-up time point, HADS-depression scores were significantly higher in ACE D/D, 5-HTTLPR I/I carriers than in their counterparts. Two years after study inclusion, the mean HADS depression score remained 1.8 points higher in patients with the risk haplotype as compared to subjects not carrying this haplotype (9.9 ± 4.2 versus 8.1 ± 4.0, p = 0.009). In summary, the presence of the ACE D/D, 5-HTTLPR I/I haplotype may be a vulnerability factor for comorbid depressive symptoms in CAD patients.

Full Text

Duke Authors

Cited Authors

  • Meyer, T; Rothe, I; Staab, J; Deter, H-C; Fangauf, SV; Hamacher, S; Hellmich, M; Jünger, J; Ladwig, K-H; Michal, M; Petrowski, K; Ronel, J; Söllner, W; Weber, C; de Zwaan, M; Williams, RB; Albus, C; Herrmann-Lingen, C; SPIRR-CAD Investigators,

Published Date

  • August 2020

Published In

Volume / Issue

  • 58 / 4

Start / End Page

  • 631 - 648

PubMed ID

  • 32367400

Pubmed Central ID

  • PMC7378120

Electronic International Standard Serial Number (EISSN)

  • 1573-4927

Digital Object Identifier (DOI)

  • 10.1007/s10528-020-09967-w


  • eng

Conference Location

  • United States