Clinical Research Papers:
Predictive value of homocysteine for depression after acute coronary syndrome
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2313 views | HTML 2376 views | ?
Abstract
Hee Ju Kang1, Robert Stewart2, Kyung Yeol Bae1, Sung Wan Kim1, Il Seon Shin1, Hyuno Kang3, Won Jin Moon3, Young Joon Hong4, Youngkeun Ahn4, Myung Ho Jeong4, Jin Sang Yoon1 and Jae Min Kim1
1 Department of Psychiatry, Chonnam National University Medical School, Gwangju, Korea
2 King’s College London, Institute of Psychiatry, London, UK
3 Gwangju Center, Korea Basic Science Institute, Gwangju, Korea
4 Department of Cardiology, Chonnam National University Medical School, Gwangju, Korea
Correspondence to:
Jae Min Kim, email:
Keywords: depression; homocysteine; MTHFR C677T polymorphism; acute coronary syndrome; biomarkers
Received: July 13, 2016 Accepted: September 06, 2016 Published: September 10, 2016
Abstract
We investigated roles of plasma homocysteine and MTHFR gene in relation to risks and treatment responses of depression in ACS. A sample of 969 patients with recent ACS were recruited and 711 followed 1 year later. In addition, of 378 baseline participants with depressive disorder, 255 were randomized to a 24-week double blind trial of escitalopram (N = 127) or placebo (N = 128). A higher homocysteine concentration was independently associated with prevalent depressive disorder at baseline irrespective of MTHFR genotype; and with both incident and persistent depressive disorder at follow-up only in the presence of TT genotype. MTHFR genotype was not itself associated with depressive disorder after ACS. No associations were found with 24-week antidepressant treatment responses. Plasma homocysteine could be a biomarker for depressive disorder particularly in the acute phase of ACS. Focused interventions for those with higher homocysteine level and MTHFR TT genotype might reduce the risk of later depressive disorder.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 11966