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      Mortality From Myocardial Infarction After the Death of a Sibling: A Nationwide Follow‐up Study From Sweden

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          Abstract

          Background

          Death of a sibling represents a stressful life event and could be a potential trigger of myocardial infarction (MI). We studied the association between loss of an adult sibling and mortality from MI up to 18 years after bereavement.

          Methods and Results

          We conducted a follow‐up study for Swedes aged 40 to 69 years between 1981 and 2002, based on register data covering the total population (N=1 617 010). Sibling deaths could be observed from 1981 and on. An increased mortality rate from MI was found among women (1.25 CI 1.02 to 1.54) and men (1.15 CI 1.03 to 1.28) who had experienced death of an adult sibling. An elevated rate some years after bereavement was found among both women (during the fourth to sixth half‐years after the death) and men (during the second to sixth half‐years after the death), whereas limited support for a short‐term elevation in the rate was found (during the first few months since bereavement). External causes of sibling death were associated with increased MI mortality among women (1.54 CI 1.07 to 2.22), whereas nonexternal causes showed associations in men (1.23 CI 1.09 to 1.38). However, further analyses showed that if the sibling also died from MI, associations were primarily found among both women (1.62 CI 1.00 to 2.61) and men (1.98 CI 1.59 to 2.48).

          Conclusions

          Our study provided the first large‐scale evidence for mortality from MI associated with the death of a sibling at an adult age. The fact that findings suggested associations primarily between concordant causes of death (both died of MI) could indicate genetic resemblance or shared risk factors during childhood. Future studies on bereavement should carefully deal with the possibility of residual confounding.

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          Most cited references 23

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          Genetic susceptibility to death from coronary heart disease in a study of twins.

          A family history of premature coronary heart disease has long been thought to be a risk factor for coronary heart disease. Using data from 26 years of follow-up of 21,004 Swedish twins born between 1886 and 1925, we investigated this issue further by assessing the risk of death from coronary heart disease in pairs of monozygotic and dizygotic twins. The study population consisted of 3298 monozygotic and 5964 dizygotic male twins and 4012 monozygotic and 7730 dizygotic female twins. The age at which one twin died of coronary heart disease was used as the primary independent variable to predict the risk of death from coronary heart disease in the other twin. Information about other risk factors was obtained from questionnaires administered in 1961 and 1963. Actuarial life-table analysis was used to estimate the cumulative probability of death from coronary heart disease. Relative-hazard estimates were obtained from a multivariate survival analysis. Among the men, the relative hazard of death from coronary heart disease when one's twin died of coronary heart disease before the age of 55 years, as compared with the hazard when one's twin did not die before 55, was 8.1 (95 percent confidence interval, 2.7 to 24.5) for monozygotic twins and 3.8 (1.4 to 10.5) for dizygotic twins. Among the women, when one's twin died of coronary heart disease before the age of 65 years, the relative hazard was 15.0 (95 percent confidence interval, 7.1 to 31.9) for monozygotic twins and 2.6 (1.0 to 7.1) for dizygotic twins. Among both the men and the women, whether monozygotic or dizygotic twins, the magnitude of the relative hazard decreased as the age at which one's twin died of coronary heart disease increased. The ratio of the relative-hazard estimate for the monozygotic twins to the estimate for the dizygotic twins approached 1 with increasing age. These relative hazards were little influenced by other risk factors for coronary heart disease. Our findings suggest that at younger ages, death from coronary heart disease is influenced by genetic factors in both women and men. The results also imply that the genetic effect decreases at older ages.
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            Psychological stress and cardiovascular disease.

            There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.
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              Mortality in parents after death of a child in Denmark: a nationwide follow-up study.

              Little is known about the effect of parental bereavement on physical health. We investigated whether the death of a child increased mortality in parents. We undertook a follow-up study based on national registers. From 1980 to 1996, we enrolled 21062 parents in Denmark who had a child who had died (exposed cohort), and 293745 controls--ie, parents whose children were alive, and whose family structure matched that of the exposed cohort. Natural deaths were defined with ICD8 codes 0000-7969 and ICD10 codes A00-R99, and unnatural deaths with codes 8000-9999 and V01-Y98. We used Cox's proportional-hazards regression models to assess the mortality rate of parents up to 18 years after bereavement. We observed an increased overall mortality rate in mothers whose child had died (hazards ratio 1.43, 95% CI 1.24-1.64; p<0.0001). An excess mortality from natural causes (1.44, 1.15-1.78; p<0.0001) was noted in mothers only during the 10th-18th year of follow-up. Mothers had increased mortality rates from unnatural causes throughout follow-up, with the highest rate recorded during the first 3 years (3.84, 2.48-5.88; p<0.0001). Bereaved fathers had only an early excess mortality from unnatural causes (1.57, 1.06-2.32; p=0.04). Mothers who lost a child due to an unnatural death or an unexpected death had a hazard ratio of 1.72 (1.38-2.15; p=0.0040) and 1.67 (1.37-2.03; p=0.0037), respectively. The death of a child is associated with an overall increased mortality from both natural and unnatural causes in mothers, and an early increased mortality from unnatural causes in fathers.
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                Author and article information

                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                ahaoa
                jah3
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                Blackwell Publishing Ltd
                2047-9980
                April 2013
                24 April 2013
                : 2
                : 2
                Affiliations
                [1 ]Centre for Health Equity Studies, Stockholm University/Karolinska Institutet, Stockholm, Sweden (M.R.)
                [2 ]Åbo Akademi University and University of Helsinki, Vasa, Finland (J.S.)
                [3 ]Harvard School of Public Health, Boston, MA (I.K.)
                Author notes
                correspondence to: Mikael Rostila, PhD, Centre for Health Equity Studies (CHESS), Stockholm University/Karolinska Institutet, Sveavägen 160, SE‐106 91 Stockholm, Sweden. E‐mail: mikael.rostila@ 123456chess.su.se
                Article
                jah3158
                10.1161/JAHA.112.000046
                3647267
                23537803
                © 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley-Blackwell.

                This is an Open Access article under the terms of the Creative Commons Attribution Noncommercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Categories
                Original Research
                Epidemiology

                Cardiovascular Medicine

                sweden, bereavement, epidemiology, grief, myocardial infarction

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