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Stress-related disorders increase risk for CVD
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Patients with stress-related disorders including PTSD, adjustment disorder, acute stress reaction and other stress reactions had an increased risk for CVD compared with those without disorders, according to a study published in The BMJ.
“These sudden cardiovascular events carry a high risk of a fatal outcome, so increased clinical awareness of these risks among patients with recently diagnosed stress-related disorders deserves further attention,” Huan Song, MD, PhD, postdoctoral fellow at the Center of Public Health Sciences at University of Iceland in Reykjavik and the department of medical epidemiology and biostatistics at Karolinska Institutet in Stockholm, and colleagues wrote.
Swedish patients with stress disorders
Researchers analyzed data from 136,637 patients (median age, 35 years; 38% men) from the Swedish National Patient Register who did not have CVD before their diagnosis of a stress-related disorder between 1987 and 2013. A cohort of 171,314 siblings (median age, 36 years; 51% men) without stress-related disorders or CVD were also included in the study, in addition to 1,366,370 matched patients (median age, 35 years; 38% men) from the general population who were free from stress-related disorders and CVD.
All patients were followed up from the index date to the first primary diagnosis of CVD, emigration, death or Dec. 31, 2013, whichever occurred first.
Patients with stress-related disorders were followed up for a median of 6.2 years. Follow-up for siblings was conducted for a median of 6.9 years and a median of 6.5 years for the matched cohort.
The crude incidence of any CVD was 10.5 per 1,000 person-years in patients with a stress-related disorder, 8.4 per 1,000 person-years for their siblings without the disorder and 6.9 per 1,000 person-years in the matched cohort during up to 27 years of follow-up.
When patients with stress-related disorders and their siblings were compared, the HR for any CVD was 1.64 (95% CI, 1.45-1.84). The highest HR was seen for HF during the first year after a diagnosis of a stress-related disorder (HR = 6.95; 95% CI, 1.88-25.68). Overall HRs decreased after 1 year (HR = 1.29; 95% CI, 1.24-1.34) and ranged from 1.12 for arrhythmia (95% CI, 1.04-1.21) to 2.02 for artery thrombosis/embolus (95% CI, 1.45-2.82).
Results were similar in analyses of the matched cohort for any CVD diagnosis during the first year of follow-up (HR = 1.71; 95% CI, 1.59-1.83) and thereafter (HR = 1.36; 95% CI, 1.33-1.39).
Timing of CVD diagnosis
Stress-related disorders were strongly linked to the diagnosis of CVD before age 50 years (HR = 1.4; 95% CI, 1.32-1.49) compared with a diagnosis after age 50 years (HR = 1.24; 95% CI, 1.18-1.3).
An elevated risk for CVD after a stress-related disorder diagnosis was not modified by the presence of psychiatric comorbidity except for fatal CV events. The risk for fatal CV events significantly increased in the presence of a psychiatric comorbidity.
“One challenge related to this topic of study is how to assess the immediate effect of stress-related disorders on cardiovascular disease,” Song and colleagues wrote. “The main concerns include the risk of reverse causality (that is, cardiac symptoms emerge first and contribute to the diagnosis of stress-related disorders) and surveillance bias (that is, patients with stress-related disorders have more health care visits than others, leading to a higher likelihood of receiving a diagnosis of cardiovascular disease).”
In a related editorial, Simon L. Bacon, MD, co-director of the Montreal Behavioral Medicine Centre and professor in the department of health, kinesiology and applied physiology at Concordia University in Montreal, wrote: “The ultimate test of an underlying unidirectional relation between acute-stress-induced psychiatric disorders and cardiovascular disease will be through intervention studies to treat these disorders. If the association is causal, then effective treatment of the psychiatric disorder should reduce the risk of future cardiovascular disease events.” – by Darlene Dobkowski
Disclosure s : The authors report no relevant financial disclosures. Bacon reports he received investigator-initiated research grants from AbbVie and GlaxoSmithKline, consultant fees from AstraZeneca, Bayer, Merck, Schering-Plough and Sygesa, and speaker fees from Janssen and Novartis.
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