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1.
Eur J Psychotraumatol ; 15(1): 2366055, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38912597

RESUMEN

Background: Emerging evidence has linked childhood maltreatment with cardiovascular disease risk; however, the association between childhood maltreatment and cardiac arrhythmias remains unclear. Moreover, any genetic predispositions to atrial fibrillation (AF), a common cardiac arrhythmia associated with an elevated risk of stroke, heart failure, and mortality, that modify such associations have been undocumented.Purpose: To examine the associations between childhood maltreatment and incident arrhythmias, and whether a genetic predisposition to arrhythmias modifies these associations.Methods: This prospective analysis included 151,741 participants from the UK Biobank (mean age 55.8 years, 43.4% male). Childhood maltreatment, including five types, was measured using the Childhood Trauma Screener (CTS). Incident arrhythmias (AF, ventricular arrhythmias [VA], and bradyarrhythmia [BA]) were documented through linked hospital admission and death registry. Weighted AF genetic risk score was calculated. Cox proportional hazard models were conducted to test for associations between childhood maltreatment and incident arrhythmias.Results: During a median follow-up of 12.21 years (interquartile range, 11.49-12.90 years), 6,588 AF, 2,093 BA, and 742 VA events occurred. Compared with the absence of childhood maltreatment, having 3-5 types of childhood maltreatment was associated with an increased risk of incident AF (HR, 1.23; 95%CI 1.09-1.37), VA (HR, 1.39; 95%CI 1.03-1.89), and BA (HR, 1.32; 95%CI 1.09-1.61) after adjusting demographic, socioeconomic and lifestyle factors. The associations between cumulative type of childhood maltreatment and the risk of AF (Poverall < .001; Pnonlinear = .674) and BA (Poverall = .007; Pnonlinear = .377) demonstrated a linear pattern. There was a gradient association between childhood maltreatment and AF risks across the intermediate and high genetic risk groups (both Ptrend < .05) but not within the low genetic risk group (Ptrend = .378), irrespective of non-significant interaction effect (Pinteraction = .204).Conclusion: Childhood maltreatment was associated with higher risks of incident arrhythmias, especially AF and BA. Genetic risk of AF did not modify these associations.


Previous studies indicate that childhood maltreatment is associated with cardiovascular disease risk.Childhood maltreatment was associated with an increased risk of incident arrhythmias, particularly atrial fibrillation and bradyarrhythmia. Genetic predisposition to atrial fibrillation did not significantly modify these associations.Childhood maltreatment could be a new psychological risk factor for cardiac arrhythmias in later life. Inquiries into childhood maltreatment and subsequent referral to psychological services may be helpful.


Asunto(s)
Arritmias Cardíacas , Humanos , Masculino , Femenino , Estudios Prospectivos , Arritmias Cardíacas/epidemiología , Arritmias Cardíacas/genética , Persona de Mediana Edad , Reino Unido/epidemiología , Factores de Riesgo , Predisposición Genética a la Enfermedad , Adulto , Estudios de Cohortes , Adultos Sobrevivientes del Maltrato a los Niños/estadística & datos numéricos , Maltrato a los Niños/estadística & datos numéricos
2.
JACC Heart Fail ; 11(3): 334-344, 2023 03.
Artículo en Inglés | MEDLINE | ID: mdl-36737310

RESUMEN

BACKGROUND: Social isolation and loneliness have emerged as important risk factors for cardiovascular diseases, particularly during the coronavirus disease pandemic. However, it is unclear whether social isolation and loneliness had independent and joint associations with incident heart failure (HF). OBJECTIVES: This study sought to examine the association of social isolation, loneliness, and their combination with incident HF. METHODS: The UK Biobank study is a population-based cohort study. Social isolation and loneliness were assessed using self-reported questionnaires. HF cases were identified by linking hospital records and death registries. The weighted polygenic risk score associated with HF was calculated. RESULTS: Among the 464,773 participants (mean age: 56.5 ± 8.1 years, 45.3% male), 12,898 incident HF cases were documented during a median follow-up of 12.3 years. Social isolation (most vs least: adjusted HR: 1.17; 95% CI:1.11-1.23) and loneliness (yes vs no: adjusted HR: 1.19; 95% CI: 1.11-1.27) were significantly associated with an increased risk of incident HF. The association between an elevated risk of HF and social isolation was modified by loneliness (Pinteraction = 0.034). A gradient of association between social isolation and the risk of incident HF was found only among individuals without loneliness (Ptrend < 0.001), but not among those with loneliness (Ptrend = 0.829). These associations were independent of the genetic risk of HF. CONCLUSIONS: Social isolation and loneliness were independently associated with a higher likelihood of incident HF regardless of genetic risk. The association between social isolation and incident HF was potentially modified by loneliness status.


Asunto(s)
Insuficiencia Cardíaca , Soledad , Masculino , Humanos , Persona de Mediana Edad , Femenino , Estudios de Cohortes , Insuficiencia Cardíaca/epidemiología , Aislamiento Social , Factores de Riesgo
3.
J Am Heart Assoc ; 11(20): e026536, 2022 10 18.
Artículo en Inglés | MEDLINE | ID: mdl-36196897

RESUMEN

Background We aimed to determine the associations of childhood maltreatment with incident heart failure in later life and explore the potentially modifying effects of genetic risk for heart failure on the associations. Methods and Results This cohort study included adults free of heart failure at baseline enrolled between 2006 and 2010 in the UK Biobank. Childhood maltreatment was retrospectively assessed with the online Childhood Trauma Screener in 2016. Five types of childhood maltreatment (range, 0-5), including physical abuse, physical neglect, emotional abuse, emotional neglect, and sexual abuse, were combined into a total score. A weighted polygenic risk score for heart failure was constructed. Incident all-cause heart failure was prospectively ascertained via hospital inpatient and death records, followed up to May 31, 2021. A total of 153 287 adults (mean [SD] age, 55.9 [7.7] years; 43.6% male) were included. Over a median of 12.2 years (interquartile range, 11.5-12.9 years) of follow-up, 2352 participants had incident heart failure. Childhood maltreatment was associated with a greater risk of incident heart failure in a dose-response manner. One additional type of childhood maltreatment was associated with a 15% increase in the risk of developing heart failure (hazard ratio [HR], 1.15 [95% CI, 1.07-1.23]). There was no statistically significant interaction between genetic risk and childhood maltreatment (Pinteraction=0.218). Among participants with high genetic risk, those with 3 to 5 types of childhood maltreatment had a double hazard (HR, 2.00 [95% CI, 1.43-2.80]) of developing heart failure when taking those without any childhood maltreatment as the reference. Conclusions Irrespective of genetic risk for heart failure, childhood maltreatment was associated with an increased risk of incident heart failure in a dose-dependent manner.


Asunto(s)
Maltrato a los Niños , Insuficiencia Cardíaca , Adulto , Niño , Humanos , Masculino , Persona de Mediana Edad , Femenino , Estudios de Cohortes , Estudios Retrospectivos , Encuestas y Cuestionarios , Factores de Riesgo , Insuficiencia Cardíaca/epidemiología , Insuficiencia Cardíaca/genética
4.
Scand J Work Environ Health ; 48(5): 372-379, 2022 07 01.
Artículo en Inglés | MEDLINE | ID: mdl-35411403

RESUMEN

OBJECTIVES: The aim of this study was to investigate whether melatonin receptor type 1B (MTNR1B) rs10830963 polymorphism interacts with night shift work on the risk of incident stroke. METHODS: This study included individuals free of stroke at baseline from the UK Biobank. Night-shift work was assessed by the self-reported questions. MTNR1B rs10830963 was directly genotyped (CC, GC, and GG). Incident stroke was ascertained through hospital records and death registries. Cox proportional hazards models were employed to examine the associations of night shift work and MTNR1B rs10830963 with the risk of incident stroke. RESULTS: A total of 242 194 participants were finally included (mean age: 52.95 years; 51.63% women). Over 12-year follow-up, 3287 incident stroke events occurred. Night shift work increased the risk of incident stroke [hazard ratio (HR) 1.13, 95% confidence interval (CI) 1.00-1.28] after adjusting for socio-demographics, and this association attenuated after additional adjustment for lifestyle factors (HR 1.06, 95% CI 0.94-1.20). MTNR1B rs10830963 polymorphism modified the association between night shift work and incident stroke (Pfor interaction =0.010). In the Cox models adjusted for socio-demographics and lifestyle factors, among night-shift workers, minor allele G was associated with a reduced risk of incident stroke (GC versus CC, HR 0.74, 95% CI 0.58-0.95; GG versus CC, HR 0.65, 95% CI 0.40-1.06; P for trend=0.010); while night shift work was associated with a higher stroke risk only among MTNR1B rs10830963 CC carriers (HR 1.23, 95% CI 1.05-1.44) but not GC/GG carriers. CONCLUSIONS: These results suggest that MTNR1B rs10830963 may potentially modify the associations between night shift work and incident stroke.


Asunto(s)
Receptor de Melatonina MT2 , Horario de Trabajo por Turnos , Accidente Cerebrovascular , Alelos , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Receptor de Melatonina MT2/genética , Horario de Trabajo por Turnos/efectos adversos , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/genética
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