Symptoms of anxiety and depression and risk of heart failure: the HUNT Study.
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ABSTRACT: Aims
Symptoms of anxiety and depression often co-exist with cardiovascular disease, yet little is known about the prospective risk for heart failure (HF) in people with symptoms of depression and anxiety. We aimed to study these prospective associations using self-reported symptoms of anxiety, depression, and mixed symptoms of anxiety and depression (MSAD) in a large population sample.Methods and results
In the second wave of the Nord-Trøndelag Health Study (HUNT 2, 1995-1997), Norway, baseline data on symptoms of anxiety and depression, socio-demographic variables, health status including cardiovascular risk factors, and common chronic somatic diseases were registered for 62,567 adults, men and women, free of known HF. The cohort was followed for incident HF from baseline throughout 2008. A total of 1499 cases of HF occurred during a mean follow-up of 11.3 years (SD = 2.9), identified either in hospital registers or by the National Cause of Death Registry. There was no excess risk for future HF associated with symptoms of anxiety or MSAD at baseline. For depression, the multi-adjusted hazard ratios for HF were 1.07 (0.87-1.30) for moderate symptoms and 1.41 (1.07-1.87) for severe symptoms (P for trend 0.026). Established cardiovascular risk factors, acute myocardial infarction (AMI) prior to baseline, and adjustment for incident AMI as a time-dependent covariate during follow-up had little influence on the estimates.Conclusion
Symptoms of depression, but not symptoms of anxiety or MSAD, were associated with increased risk for HF in a dose-response manner. The increased risk could not be fully explained by cardiovascular or socio-economic risk factors, or by co-morbid AMI.
SUBMITTER: Gustad LT
PROVIDER: S-EPMC4255780 | biostudies-literature | 2014 Aug
REPOSITORIES: biostudies-literature
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| S-EPMC6443896 | biostudies-literature
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Project description:AimsPatients with heart failure often have under-recognized symptoms, depression, anxiety, and poorer spiritual well-being ('QoL domains'). Ideally all patients should have heart failure-specific health status and quality of life (QoL) domains routinely evaluated; however, lack of time and resources are limiting in most clinical settings. Therefore, we aimed to evaluate whether heart failure-specific health status was associated with QoL domains and to identify a score warranting further evaluation of QoL domain deficits.Methods and resultsParticipants (N = 314) enrolled in the Collaborative Care to Alleviate Symptoms and Adjust to Illness trial completed measures of heart failure-specific health status [Kansas City Cardiomyopathy Questionnaire, KCCQ (score 0-100, 0 = worst health status)], additional symptoms (Memorial Symptom Assessment Scale), depression (Patient Health Questionnaire-9), anxiety (Generalized Anxiety Disorder-7), and spiritual well-being (Facit-Sp) at baseline. Mean ± standard deviation (SD) KCCQ score was 46.9 ± 19.3, mean age was 65.5 ± 11.4, and 79% were male. Prevalence of QoL domain deficits ranged from 11% (nausea) to 47% (depression). Sensitivity/specificity of KCCQ for each QoL domain ranged from 20-40%/80-96% for KCCQ ≤ 25, 61-84%/48-62% for KCCQ ≤ 50, 84-97%/26-40% for KCCQ ≤ 60, and 96-100%/8-13% for KCCQ ≤ 75. Patients with KCCQ ≤ 60 had mean ± SD 4.5 ± 2.5 QoL domain deficits (maximum 12), vs. 1.6 ± 1.6 for KCCQ > 60 (P < 0.001). Similar results were seen for KCCQ ≤25 (6.6 ± 2.4 vs. 3.3 ± 2.4), KCCQ ≤ 50 (4.8 ± 2.6 vs. 2.5 ± 2) and KCCQ ≤ 75 (4.0 ± 2.6 vs. 1.0 ± 1.2) (all P < 00001).ConclusionKCCQ ≤ 60 had good sensitivity for each QoL domain deficit and for patients with at least one QoL domain deficit. Screening for QoL domain deficits should target patients with lower KCCQ scores based on a clinic's KCCQ score distribution and clinical resources for addressing QoL domain deficits.
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Project description:Study objectivesTo assess the association between insomnia symptoms and risk of fatal unintentional injuries.DesignPopulation-based prospective cohort study with a mean follow-up of 14 y, linking health survey data with information on insomnia symptoms to the National Cause of Death Registry.SettingNord-Trøndelag County, Norway.ParticipantsA total of 54,399 men and women 20-89 y of age who participated in the Nord-Trøndelag Health Study between 1995 and 1997.InterventionsN/A.Measurements and resultsThere were 277 unintentional fatal injuries, including 57 fatal motor vehicle injuries during follow-up. There was a dose-dependent association between the number of insomnia symptoms and risk of unintentional fatal injuries (P for trend 0.001) and fatal motor vehicle injuries (P for trend 0.023), respectively. The proportion of unintentional fatal injuries cases that could have been prevented in the absence of difficulties initiating sleep, difficulties maintaining sleep, and having a feeling of nonrestorative sleep were 8%, 9%, and 8%, respectively. The corresponding estimates for motor vehicle injuries were 34%, 11%, and 10%.ConclusionInsomnia is a major contributor to both unintentional fatal injuries in general as well as fatal motor vehicle injuries. Increasing public health awareness about insomnia and identifying persons with insomnia may be important in preventing unintentional fatal injuries.
| S-EPMC4196061 | biostudies-literature
Project description:ImportanceThe research focus on children of parents with alcohol use disorder has eclipsed the potentially wider-reaching detrimental effects of subclinical parental drinking, both alone and in combination with other parental risk factors.ObjectiveTo identify constellations of early parental risk characterized by variations in drinking, mental health, and education in both parents and examine their prospective associations with children's contact with the health care system for anxiety and/or depression (ie, diagnoses or treatment).Design, setting, and participantsThis prospective study was based on linked survey and health registries data. The sample included 8773 children from 6696 two-parent families in Norway who participated in the Nord-Trøndelag Health Study (HUNT) survey in 1995 to 1997 or 2006 to 2008, when the children were aged 13 to 19 years. Data were analyzed from January to September 2018.ExposuresFive constellations of early parental risks, characterized by variations in drinking frequencies and amounts, mental health, and education for both parents, as identified through latent profile analysis.Main outcomes and measuresChildren's diagnoses or treatment of anxiety and/or depression from 2008 to 2016 were recorded in 3 health registries. The primary outcome was the total number of registries where participants presented (ranging from 0 to 3).ResultsOf the 8773 included children, 4404 (50.2%) were boys, and the mean (SD) age at the time of participation in the Nord-Trøndelag Health Study was 16.1 (1.8) years. Prevalence of anxiety and/or depression, as evidenced in at least 1 registry record, was 24.3% (2132 of 8773). Early parental risk profiles risks marked by (1) the lowest parental education (adjusted relative risk, 1.13; 95% CI, 1.01-1.25) and (2) elevated drinking in both parents and elevated mental health symptoms in fathers (adjusted relative risk, 1.52; 95% CI, 1.03-2.22) were associated with a significant increase in risk of anxiety and/or depression in children from those families compared with children from no-risk families.Conclusions and relevanceStudies seeking to understand prospective associations of parental drinking with children's mental health need to consider additional risk factors in combination with one another as well as parental behaviors and characteristics below clinically defined levels. When accumulated at a family level, even seemingly innocuous characteristics contributed to meaningful increases in risk of anxiety and/or depression among children, potentially translating into poorer mental health outcomes for many young people.
| S-EPMC6440260 | biostudies-literature
Project description:Patients with heart failure (HF) have high rates of cognitive impairment and depressive symptoms. Depressive symptoms have been associated with greater cognitive impairments in HF; however, it is not known whether particular clusters of depressive symptoms are more detrimental to cognition than others.The aim of this study was to identify whether somatic and/or nonsomatic depressive symptom clusters were associated with cognitive function in persons with HF.Participants were 326 HF patients (40.5% women, 26.7% non-white race-ethnicity, aged 68.6 ± 9.7 years). Depressive symptoms were measured using a depression questionnaire commonly used in medical populations: the Patient Health Questionnaire-9. Somatic and nonsomatic subscale scores were created using previous factor analytic results. A neuropsychological battery tested attention, executive function, and memory. Composites were created using averages of age-adjusted scaled scores. Regressions adjusting for demographic and clinical factors were conducted.Regressions revealed that Patient Health Questionnaire-9 total was associated with attention (? = -.14, P = .008) and executive function (? = -.17, P = .001). When analyzed separately, the nonsomatic subscale, but not the somatic symptoms subscale (P values ? .092), was associated with attention scores (? = -.15, P = .004) and memory (? = -.11, P = .044). Both nonsomatic (? = -.18, P < .001) and somatic (? = -.11, P = .048) symptoms were related to executive function. When included together, only the nonsomatic symptom cluster was associated with attention (? = -.15, P = .020) and executive function (? = -.19, P = .003).Greater overall depressive symptom severity was associated with poorer performance on multiple cognitive domains, an effect driven primarily by the nonsomatic symptoms of depression.These findings suggest that screening explicitly for nonsomatic depressive symptoms may be warranted and that the mechanisms underlying the depression-cognitive function relationship in HF are not solely related to sleep or appetite disturbance. Thus, interventions that target patients' somatic symptoms only (eg, poor appetite or fatigue) may not yield maximum cognitive benefit compared with a comprehensive treatment that targets depressed mood, anhedonia, and other nonsomatic symptoms.
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