scholarly journals Sibling history is associated with heart failure after a first myocardial infarction

Open Heart ◽  
2020 ◽  
Vol 7 (1) ◽  
pp. e001143
Author(s):  
Charlotte Glinge ◽  
Louise Oestergaard ◽  
Reza Jabbari ◽  
Sara Rossetti ◽  
Regitze Skals ◽  
...  

ObjectiveMorbidity and mortality due to heart failure (HF) as a complication of myocardial infarction (MI) is high, and remains among the leading causes of death and hospitalisation. This study investigated the association between family history of MI with or without HF, and the risk of developing HF after first MI.MethodsThrough nationwide registries, we identified all individuals aged 18–50 years hospitalised with first MI from 1997 to 2016 in Denmark. We identified 13 810 patients with MI, and the cohort was followed until HF diagnosis, second MI, 3 years after index MI, emigration, death or the end of 2016, whichever occurred first. HRs were estimated by Cox hazard regression models adjusted for sex, age, calendar year and comorbidities (reference: patients with no family history of MI).ResultsAfter adjustment, we observed an increased risk of MI-induced HF for those having a sibling with MI with HF (HR 2.05, 95% CI 1.02 to 4.12). Those having a sibling with MI without HF also had a significant, but lower increased risk of HF (HR 1.39, 95% CI 1.05 to 1.84). Parental history of MI with or without HF was not associated with HF.ConclusionIn this nationwide cohort, sibling history of MI with or without HF was associated with increased risk of HF after first MI, while a parental family history was not, suggesting that shared environmental factors may predominate in the determination of risk for developing HF.

Neurology ◽  
2017 ◽  
Vol 88 (17) ◽  
pp. 1642-1649 ◽  
Author(s):  
Frank J. Wolters ◽  
Sven J. van der Lee ◽  
Peter J. Koudstaal ◽  
Cornelia M. van Duijn ◽  
Albert Hofman ◽  
...  

Objective:To determine the association of parental family history with risk of dementia by age at onset and sex of affected parent in a population-based cohort.Methods:From 2000 to 2002, we assessed parental history of dementia in participants without dementia of the Rotterdam Study. We investigated associations of parental history with risk of dementia until 2015, adjusting for demographics, cardiovascular risk factors, and known genetic risk variants. Furthermore, we determined the association between parental history and markers of neurodegeneration and vascular disease on MRI.Results:Of 2,087 participants (mean age 64 years, 55% female), 407 (19.6%) reported a history of dementia in either parent (mean age at diagnosis 79 years). During a mean follow-up of 12.2 years, 142 participants developed dementia. Parental history was associated with risk of dementia independently of known genetic risk factors (hazard ratio [HR] 1.67, 95% confidence interval [CI] 1.12–2.48), in particular when parents were diagnosed at younger age (<80 years: HR 2.58, 95% CI 1.61–4.15; ≥80 years: HR 1.01, 95% CI 0.58–1.77). Accordingly, age at diagnosis in probands was highly correlated with age at diagnosis in their parents <80 years (r = 0.57, p = 0.001) but not thereafter (r = 0.17, p = 0.55). Among 1,161 participants without dementia with brain MRI, parental history was related to lower cerebral perfusion and higher burden of white matter lesions and microbleeds. Dementia risk and MRI markers were similar for paternal and maternal history.Conclusions:Parental history of dementia increases risk of dementia, primarily when age at parental diagnosis is <80 years. Unexplained heredity may be attributed in part to cerebral hypoperfusion and small vessel disease. We found no evidence of preferential maternal compared to paternal transmission.


PEDIATRICS ◽  
1987 ◽  
Vol 80 (5) ◽  
pp. 743-744
Author(s):  

Family history of convulsions is not presently a contraindication to the use of pertussis vaccine.1,2 It was suggested in a recent report that there might be an increased risk of seizures following diphtheria, tetanus, pertussis (DTP) vaccination in individuals who have a "family history of convulsions." Unfortunately, the degree of relatedness was not specified in the questionnaire from which these results were derived.3 A subsequent questionnaire specifying relatedness only to siblings and parents also indicated an increased risk. A family history of convulsions was obtained in 17.3% and 16.7% of children who had febrile and nonfebrile convulsions, respectively, following DTP vaccine as compared with 4.8% in vaccinees who had nonneurologic complications following DTP vaccination (Centers for Disease Control, unpublished data, 1987). The risk of seizures following DTP vaccination is approximately one in 1,750 doses. These are usually febrile seizures.4,5 Follow-up of these patients had indicated that they rarely, if ever, have sequelae.5 Convulsions of this type (DTP vaccination induced) are differentiated from encephalopathy which occurs once in about 1:140,000 doses, one third of which result in permanent sequelae.6 Recent studies have demonstrated that the administration of acetaminophen, 15 mg/kg per dose, at the time of immunization with DTP and four and eight hours later, reduces febrile reactions.7 Although this study was too small to allow determination of the effect on seizures following DTP, it is reasonable to expect that reduction in fever also would decrease the likelihood of febrile seizures following DTP. Local pertussis epidemics in the United States occur in unpredictable fashion.


PEDIATRICS ◽  
1986 ◽  
Vol 78 (5) ◽  
pp. 956-957
Author(s):  
CHARLES J. GLUECK

In Reply.— Because the anatomic, biochemical, epidemiologic, nutritional, genetic, and clinical genesis of atherosclerosis is in childhood,1,2 it is important to consider models for sampling in childhood for the dyslipoproteinemias. At a minimum, I would recommend a family history-triggered high-risk strategy with sampling of all children whose parents had sustained premature (≤age 60 years) myocardial infarction, angina, cerebrovascular accident, or peripheral vascular disease.1,2 Second, all children with known parental dyslipoproteinemia should be sampled, as should all children with parental history of essential hypertension gout/hyperuricemia, and/or diabetes.


Author(s):  
Gui He ◽  
Xuanke Ji ◽  
Yali Yan ◽  
Kunyan Wang ◽  
Chunhua Song ◽  
...  

Background: Family history may inform individuals that they are at risk of gastric cancer (GC). However, it is too extensive to conduct intensive screening strategies for all individuals with family history of GC instead of average-risk screening. To establish more precise prevention strategies, accurate risk estimates are necessary for individuals with family history of GC. Methods: We searched PubMed, EMBASE and Cochrane for all relevant studies from their inception to May 21, 2020, for cohort and case-control studies investigating the association between family history of GC and its risk. Relative risk (RR) and 95% confidence interval (CI) were pooled from studies using random-effects or fixed effects. Results: The RR of GC was 2.08 (95% CI=1.86-2.34) in individuals with family history of GC according to twenty-nine case-control studies and 1.83 (95%CI=1.67-2.01) from six cohort studies. The increased risk was higher in individuals with sibling history of GC than those with parental history of GC (RR=3.18, 95% CI=2.12-4.79 vs. RR=1.66, 95% CI=1.46-1.89, P=0.021). For individuals with 2 or more first-degree relatives (FDRs) with GC, the RR was 2.81(95% CI=1.89-3.99). Subjects with both family history and Helicobacter pylori (H. pylori) infection confer a higher risk of GC (RR = 4.03, 95%CI=2.46-6.59). Conclusion: The RR of GC among FDRs is lower than in previous studies. However, the risk of GC is markedly increased in individuals having a sibling with GC, more than 2 FDRs with GC. Intensified screening and eradication therapy for H. pylori could be considered for these individuals.  


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1378-P
Author(s):  
JANAKI D. VAKHARIA ◽  
SUNGEETA AGRAWAL ◽  
JANINE BACIC ◽  
LISA S. TOPOR

2021 ◽  
Vol 9 (1) ◽  
pp. e001948
Author(s):  
Marion Denos ◽  
Xiao-Mei Mai ◽  
Bjørn Olav Åsvold ◽  
Elin Pettersen Sørgjerd ◽  
Yue Chen ◽  
...  

IntroductionWe sought to investigate the relationship between serum 25-hydroxyvitamin D (25(OH)D) level and the risk of type 2 diabetes mellitus (T2DM) in adults who participated in the Trøndelag Health Study (HUNT), and the possible effect modification by family history and genetic predisposition.Research design and methodsThis prospective study included 3574 diabetes-free adults at baseline who participated in the HUNT2 (1995–1997) and HUNT3 (2006–2008) surveys. Serum 25(OH)D levels were determined at baseline and classified as <50 and ≥50 nmol/L. Family history of diabetes was defined as self-reported diabetes among parents and siblings. A Polygenic Risk Score (PRS) for T2DM based on 166 single-nucleotide polymorphisms was generated. Incident T2DM was defined by self-report and/or non-fasting glucose levels greater than 11 mmol/L and serum glutamic acid decarboxylase antibody level of <0.08 antibody index at the follow-up. Multivariable logistic regression models were applied to calculate adjusted ORs with 95% CIs. Effect modification by family history or PRS was assessed by likelihood ratio test (LRT).ResultsOver 11 years of follow-up, 92 (2.6%) participants developed T2DM. A higher risk of incident T2DM was observed in participants with serum 25(OH)D level of<50 nmol/L compared with those of ≥50 nmol/L (OR 1.72, 95% CI 1.03 to 2.86). Level of 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in adults without family history of diabetes (OR 3.87, 95% CI 1.62 to 9.24) but not in those with a family history (OR 0.72, 95% CI 0.32 to 1.62, p value for LRT=0.003). There was no effect modification by PRS (p value for LRT>0.23).ConclusionSerum 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in Norwegian adults. The inverse association was modified by family history of diabetes but not by genetic predisposition to T2DM.


2021 ◽  
Author(s):  
Gema Ariceta ◽  
Fadi Fakhouri ◽  
Lisa Sartz ◽  
Benjamin Miller ◽  
Vasilis Nikolaou ◽  
...  

ABSTRACT Background Eculizumab modifies the course of disease in patients with atypical hemolytic uremic syndrome (aHUS), but data evaluating whether eculizumab discontinuation is safe are limited. Methods Patients enrolled in the Global aHUS Registry who received ≥1 month of eculizumab before discontinuing, demonstrated hematologic or renal response prior to discontinuation and had ≥6 months of follow-up were analyzed. The primary endpoint was the proportion of patients suffering thrombotic microangiopathy (TMA) recurrence after eculizumab discontinuation. Additional endpoints included: eGFR changes following eculizumab discontinuation to last available follow-up; number of TMA recurrences; time to TMA recurrence; proportion of patients restarting eculizumab; and changes in renal function. Results We analyzed 151 patients with clinically diagnosed aHUS who had evidence of hematologic or renal response to eculizumab, before discontinuing. Thirty-three (22%) experienced a TMA recurrence. Univariate analysis revealed that patients with an increased risk of TMA recurrence after discontinuing eculizumab were those with a history of extrarenal manifestations prior to initiating eculizumab, pathogenic variants, or a family history of aHUS. Multivariate analysis showed an increased risk of TMA recurrence in patients with pathogenic variants and a family history of aHUS. Twelve (8%) patients progressed to end-stage renal disease after eculizumab discontinuation; 7 (5%) patients eventually received a kidney transplant. Forty (27%) patients experienced an extrarenal manifestation of aHUS after eculizumab discontinuation. Conclusions Eculizumab discontinuation in patients with aHUS is not without risk, potentially leading to TMA recurrence and renal failure. A thorough assessment of risk factors prior to the decision to discontinue eculizumab is essential.


1997 ◽  
Vol 12 (3) ◽  
pp. 149-151 ◽  
Author(s):  
D Sarantidis ◽  
A Thomas ◽  
K Iphantis ◽  
N Katsaros ◽  
J Tripodianakis ◽  
...  

SummaryIn this study we investigated 1) the changes in anxiety, depression and denial from admission to discharge in patients admitted to the intensive care unit following an acute myocardial infarction and 2) the effect of smoking habits, time lapsed from the appearance of symptoms to seeking help behavior, presence of a person that motivated the patient to seek help, previous myocardial infarction (MI) and family history of MI, on these changes. The results indicated that 1) the levels of both anxiety and depression increased from admission to discharge, while denial decreased; 2) positive family history of MI was associated with lower difference of denial between admission and discharge.


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