Author + information
- Aditya Goyal, MDa,
- Amit K. Dey, MDa,
- Abhishek Chaturvedi, MDa,
- Youssef A. Elnabawi, BSa,
- Tsion M. Aberra, MDa,
- Jonathan H. Chung, MDa,
- Agastya D. Belur, MDa,
- Jacob W. Groenendyk, BAa,
- Joseph B. Lerman, MDa,
- Joshua P. Rivers, MSa,
- Justin A. Rodante, PA-Ca,
- Charlotte L. Harrington, BAa,
- Nevin J. Varghese, BSa,
- Gregory E. Sanda, BSa,
- Yvonne Baumer, PhDa,
- Alexander V. Sorokin, MD, PhDa,
- Heather L. Teague, PhDa,
- Leonard D. Genovese, MDa,
- Balaji Natarajan, MDa,
- Aditya A. Joshi, MDa,
- Martin P. Playford, PhDa,
- David A. Bluemke, MD, PhDb,
- Marcus Y. Chen, MDa,
- Abass Alavi, MDc,
- Roger K. Pitman, MDd,
- Tiffany M. Powell-Wiley, MD, MPHe,
- Ahmed Tawakol, MDf,
- Joel M. Gelfand, MD, MSCEg and
- Nehal N. Mehta, MD, MSCEa,∗ ()
- aSection of Inflammation and Cardiometabolic Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
- bDepartment of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin
- cDepartment of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- dDepartment of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
- eSocial Determinants of Obesity and Cardiovascular Risk Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
- fCardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
- gDepartment of Dermatology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Nehal N. Mehta, Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung and Blood Institute, 10 Center Drive, Clinical Research Center, Room 5-5140, Bethesda, Maryland 20892.
Objectives This study hypothesized that there is an association between chronic stress (as indexed by resting amygdalar activity [AmygA]), hematopoietic system activity (HMPA), and subclinical cardiovascular indexes (aortic vascular inflammation [VI] and noncalcified coronary plaque burden [NCB]) in psoriasis (PSO). The study also hypothesized that treatment of PSO would improve these parameters.
Background PSO is a stress-related chronic inflammatory condition that is associated with increased prevalence of subclinical cardiovascular disease (CVD). In individuals without PSO, stress has been linked to CVD through a serial biological pathway that involves the amygdala, hematopoietic tissues, and atherosclerotic plaques.
Methods A total of 164 consecutive patients with PSO and 47 healthy volunteers underwent 18-flourodeoxyglucose positron emission tomography/computed tomography scans for assessment of AmygA, HMPA, and VI, as well as coronary computed tomography angiography scans for quantifying NCB. Furthermore, a consecutive subset of 30 patients with severe PSO (Psoriasis Area Severity Index Score >10) were followed at 1 year to assess the relationship between skin disease improvement and AmygA, HMPA, VI, and NCB.
Results The PSO cohort was middle-aged (mean age: 50 years), had low cardiovascular risk (Framingham risk score: median: 3) and had mild to moderate PSO activity (median Psoriasis Area Severity Index Score: 5.6). AmygA was higher in patients with PSO compared to volunteer participants. AmygA was associated with HMPA (bone marrow activity: β = 0.20, p = 0.01) and subclinical CVD (VI: β = 0.31, p < 0.001; NCB: β = 0.27, p < 0.001) The AmygA−CVD association was in part mediated by HMPA (VI: 20.9%, NCB: 36.7%). Following 1 year of PSO treatment in those with severe disease, improvement in skin disease was accompanied by a reduction in AmygA, bone marrow activity, and VI, with no progression of NCB.
Conclusions In PSO, a chronic inflammatory disease state, AmygA, which is a manifestation of chronic stress, substantially contributes to the risk of subclinical CVD. Additional studies that use psychometric measures of stress are required to explore therapeutic impact.
This study was supported by the National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, Intramural Research Program (HL006193-01) and NIAMS K24-AR064310. Dr. Gelfand was supported by an NIAMS grant (K24-AR-064310). Dr. Powell-Wiley was supported the National Institutes of Health Intramural Research Program (ZIA HL006168). This research was also made possible through the NIH Medical Research Scholars Program, a public-private partnership supported jointly by the NIH and generous contributions to the Foundation for the NIH from the Doris Duke Charitable Foundation (DDCF Grant #2014194), the American Association for Dental Research, the Colgate-Palmolive Company, Genentech, Elsevier, and other private donors. Dr. Mehta was supported by the National Institutes of Health Intramural Research Program (Z01 HL-06193).
Dr. Gelfand served as a consultant for BMS, Boehringer Ingelheim, GlaxoSmithKline, Janssen Biologics, Menlo Therapeutics, Novartis Corp. Regeneron, Dr. Reddy’s labs, UCB (DSMB), Sanofi, and Pfizer Inc.; has received honoraria and research grants from Abbvie, Janssen, Novartis Corp., Sanofi, Celgene, Ortho Dermatologics, and Pfizer Inc.; and received payment for continuing medical education work related to psoriasis that was supported indirectly by Lilly and Ortho Dermatologics. Dr. Tawakol has been a consultant for Actelion; and has received a research grant from Genentech. Dr. Mehta has received research grants from Abbvie, Janssen, Novartis Corp., and Celgene. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received June 25, 2018.
- Revision received August 13, 2018.
- Accepted August 24, 2018.
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