Posttraumatic Stress and Prolonged Grief After the Sudden Cardiac Death of a Young Relative

The sudden cardiac death (SCD) of a young person is a devastating event often attributed to underlying genetic heart disease.¹ In the absence of a prior diagnosis or symptoms, a grieving family must come to terms with the uncertainty about the cause of death and ongoing genetic risk to the family. Approximately 7% of a bereaved population will develop prolonged grief (PG) for which some risk factors include female sex and sudden unexpected death. Although family members may be particularly vulnerable to PG, psychological assessment is rarely undertaken. We sought to assess psychological functioning, including PG and posttraumatic stress (PTS) symptoms, and to identify factors that correlate with adverse outcomes after the SCD of a young relative.

Between July 2013 and December 2014, participants in a cross-sectional survey study of PG and PTS symptoms were recruited from the national referral program for SCD in the young in Australia. Adults who had a relative 45 years or younger who died suddenly without a premorbid diagnosis and thorough postmortem examination either diagnostic of a genetic heart disease or resulting in an unascertained cause of death and who were first-degree relatives of the decedent were included. Instruments and measures included in the study were the 36-Item Medical Outcomes Study Short-Form, version 2 (SF-36v2, health-related quality of life),² of which the mental component score and physical component score are reported; Depression Anxiety Stress Scale–21 (DASS-21; Cronbach α = .70-.90)³; Impact of Events Scale–Revised (≥24 indicates PTS symptoms; Cronbach α = .94)⁴; and the Prolonged Grief Disorder scale (for which scores were excluded for deaths occurring <6 months previously).⁵ Clinical data about the deceased were collected from their medical records. Participants who witnessed the death of the decedent included those who discovered the decedent’s body. Data were analyzed using the SAS University Edition software package (SAS Studio 3.3, SAS Institute Inc). Scores on the SF-36v2 were converted to Australian weighted T scores.⁶ Comparison with Australian population norms for DASS-21 was done with raw subscale scores.⁷ Logistic regression with generalized estimating equations was used to account for clustering within families. Participants gave written informed consent, and approval for the study was granted by the Sydney Local Health District ethics review committee.

One hundred three participants from 57 families completed the survey (a 44.4% response rate). Characteristics and survey scores are shown in Table 1. Prolonged grief was reported by 19 (20.6%) participants, with a mean (SD) time since death of 5 (3) years (range, 0.5-10 years), and the proportion was higher among mothers of the decedent (10 [35.7%]) and those who were witnesses to the death (10 [41.7%]). Posttraumatic stress symptoms were reported by 44 (44%) participants, and the proportion was higher among mothers of the decedent (19 [59.4%]) and those who were witnesses to the death (18 [66.7%]). Participants reported more severe depression (mean [SD] score, 4.2 [4.5] vs 2.6 [3.9]; P < .001), anxiety (mean [SD] score, 2.9 [3.2] vs 1.7 [2.8]; P < .001), and stress (mean [SD] score, 5.3 [3.9] vs 4.0 [4.2]; P = .004) than the general population.

Witnessing the death was strongly associated with both PG and PTS symptoms after adjusting for family clustering, maternal relationship, and time since death (Table 2). Sixteen respondents reported both PG and PTS symptoms (17.6%, mean [SD] age, 50 [11] years, of whom 6 [37.5%] were males) and were more likely to have witnessed the death (10 [66.7%] vs 14 [19.2%]; P < .001), to have been the mother of the deceased (9 [56.3%] vs 19 [25.3 %]; P = .02), to report lower mean (SD) mental component scores on the SF-36v2 (35.4 [9.3] vs 45.1 [11.4]; P = .003), and to have higher scores on the DASS-21 for depression (6.9 [5.3] vs 3.6 [4.2]; P = .009), anxiety (4.9 [4.0] vs 2.5 [2.9]; P = .005), and stress (7.8 [4.8] vs 4.9 [3.7]; P = .008).

There were no differences observed in the mean (SD) age (44 [16] vs 42 [15] years; P = .26), proportion of females (59 [46.1%] vs 60 [58.3%]; P = .08), or mean (SD) age of the decedent (21 [7] vs 23 [8] years; P = .26) among nonresponders and responders, respectively.

The SCD of a young person is a considerable traumatic stressor, and family members are at increased risk of psychological morbidity. Our study shows that almost 1 in 2 family members reported significant psychological difficulties, particularly PG and PTS symptoms, and suggests that all families of a young person who experiences SCD receive additional support. Both PG and PTS are associated with poor health outcomes, and there is extensive evidence for the efficacy of psychological treatments for persons in need of intervention for these conditions. Current research efforts on SCD focus primarily on clinical and genetic aspects of management of the decedent’s family. We suggest that specialized input from a clinical psychologist who can triage ongoing treatment needs is critical in the multidisciplinary clinic setting. In the setting of the SCD of young, healthy individuals, better support of family members is clearly needed to promote healthy grieving.

Corresponding Author: Christopher Semsarian, MBBS, PhD, MPH, Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Locked Bag 6, Newtown, New South Wales, 2042 Australia (c.semsarian@centenary.org.au).

Published Online: January 25, 2016. doi:10.1001/jamainternmed.2015.7808.

Author Contributions: Dr Ingles had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Ingles, Kasparian, Semsarian.

Acquisition, analysis, or interpretation of data: Ingles, Spinks, Yeates, McGeechan, Semsarian.

Drafting of the manuscript: Ingles, Spinks, Kasparian, Semsarian.

Critical revision of the manuscript for important intellectual content: Ingles, Yeates, McGeechan, Semsarian.

Statistical analysis: Ingles, McGeechan, Semsarian.

Obtained funding: Ingles, Semsarian.

Administrative, technical, or material support: Ingles, Spinks, Yeates, Semsarian.

Study supervision: Ingles, Kasparian, Semsarian.

Conflict of Interest Disclosures: None reported.

Funding/Support: This work was funded by project grant APP1059515 from the National Health and Medical Research Council (NHMRC). Dr Ingles is the recipient of an NHMRC and National Heart Foundation of Australia Early Career Fellowship (APP1036756). Ms Spinks is supported by the Mamma Lena and Dino Gustin Foundation Heart Scholarship. Dr Kasparian is supported by an NHMRC Career Development Fellowship (APP1049238). Dr Semsarian is the recipient of an NHMRC Practitioner Fellowship (APP1059156).

Role of the Funder/Sponsor: The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.