Menstrual Factors and Stroke Incidence in Japanese Postmenopausal Women: The Ohasama Study

2016 ◽  
Vol 47 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Keiko Murakami ◽  
Hirohito Metoki ◽  
Michihiro Satoh ◽  
Kei Asayama ◽  
Miki Hosaka ◽  
...  

Background: The association between stroke and menstrual factors, for example, age at the time of menarche and age at the time of menopause, has not been well studied so far and the findings are inconsistent. We sought to examine this association in Japanese postmenopausal women. Methods: We followed 1,412 postmenopausal women aged ≥35 without a history of stroke in Ohasama, Japan. Baseline data were collected using a self-administered questionnaire. Adjusted hazard ratios (HRs) and 95% CIs of each menstrual factor for stroke incidence were calculated using the Cox proportional hazard model. Results: During a median follow-up of 12.8 years, 143 participants developed a stroke for the first time. Women aged ≤13 at the time of menarche had a significantly higher probability of encountering a stroke incidence in their lives compared with women aged 15 at the time of menarche (HR 1.83; 95% CI 1.04-3.22). The same was also true for cerebral infarction (HR 2.34; 95% CI 1.18-4.66). While early menopause was not significantly associated with stroke incidence, women aged ≤45 at the time of menopause faced a higher risk for cerebral infarction compared with women aged 50 years at the time of menopause (HR 3.25; 95% CI 1.54-6.86). Conclusions: Early menarche and its associated features might be a useful tool for future intervention strategies targeting modifiable factors that trigger menstrual onset.

2016 ◽  
Vol 115 (9) ◽  
pp. 1571-1578 ◽  
Author(s):  
Anne M. L. Würtz ◽  
Mette D. Hansen ◽  
Anne Tjønneland ◽  
Eric B. Rimm ◽  
Erik B. Schmidt ◽  
...  

AbstractRed meat has been suggested to be adversely associated with risk of myocardial infarction (MI), but previous studies have rarely taken replacement foods into consideration. We aimed to investigate optimal substitutions between and within the food groups of red meat, poultry and fish for MI prevention. We followed up 55 171 women and men aged 50–64 years with no known history of MI at recruitment. Diet was assessed by a validated 192-item FFQ at baseline. Adjusted Cox proportional hazard models were used to calculate hazard ratios (HR) and 95 % CI for specified food substitutions of 150 g/week. During a median follow-up time of 13·6 years, we identified 656 female and 1694 male cases. Among women, the HR for replacing red meat with fatty fish was 0·76 (95 % CI 0·64, 0·89), whereas the HR for replacing red meat with lean fish was 1·00 (95 % CI 0·89, 1·14). Similarly, replacing poultry with fatty but not lean fish was inversely associated with MI: the HR was 0·81 (95 % CI 0·67, 0·98) for fatty fish and was 1·08 (95 % CI 0·92, 1·27) for lean fish. The HR for replacing lean with fatty fish was 0·75 (95 % CI 0·60, 0·94). Replacing processed with unprocessed red meat was not associated with MI. Among men, a similar pattern was found, although the associations were not statistically significant. This study suggests that replacing red meat, poultry or lean fish with fatty fish is associated with a lower risk of MI.


Author(s):  
Anne-Marie Schjerning Olsen ◽  
Emil L Fosbøl ◽  
Jesper Lindhardsen ◽  
Charlotte Andersson ◽  
Fredrik Folke ◽  
...  

Background: Use of NSAID has shown to be associated with a substantially increased risk of athero-thrombotic adverse events in patients with a history of myocardial infarction. Whether a similar increase in risk is found for VTE is unknown. Methods: Patients aged >30 years admitted with first-time MI during 1997-2009 and their subsequent NSAID use were identified by individual-level linkage of nationwide registries of hospitalization and drug dispensing from pharmacies in Denmark. The risk of VTE associated with NSAID use was analyzed by time-dependent Cox proportional hazard models adjusted for age, gender, calendar year, concomitant drug use, and comorbidity. Results A total of 98,901 patients were included (mean age 68 years (SD 13.0), 64.0% men), 44.0% received NSAIDs during follow-up. There were 1847 VTEs. Relative to no NSAID use, the Cox-analyses showed increased risk of VTE with use of any NSAIDs. Overall NSAID use was associated with increased risk of VTE (Hazard ratio [HR] 1.75 95% confidence interval [CI] 1.52-2.02). In particular use of the selective cyclooxygenase-2 (COX-2) inhibitors rofecoxib and the nonselective NSAID diclofenac was associated with significantly increased risk of VTE (HR 2.56 (CI 1.60-4.08) and HR 2.03(CI.1.50-2.74), respectively). Conclusion: Use of most NSAIDs was associated with an increased risk of VTE. The use of rofecoxib and diclofenac was associated with highest risk. Further studies, preferably randomized clinical studies, are warranted to establish the cardiovascular safety of NSAIDs, however this study suggests that risk of VTE should be considered when prescribing NSAIDs patients with MI.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shoko Aoki ◽  
Kazumasa Yamagishi ◽  
Koutatsu Maruyama ◽  
Rie Kishida ◽  
Ai Ikeda ◽  
...  

AbstractTocopherols, strong antioxidants, may be useful in preventing dementia, but the epidemiological evidence is insufficient. We performed a community-based follow-up study of Japanese, the Circulatory Risk in Community Study, involving 3739 people aged 40–64 years at baseline (1985–1999). Incident disabling dementia was followed up from 1999 through 2020. For subtype analysis, we classified disabling dementia into that with and that without a history of stroke. Dietary intake of tocopherols (total, α, β, γ, and δ) were estimated using 24-h recall surveys. During a median follow-up of 19.7 years, 670 cases of disabling dementia developed. Total tocopherol intake was inversely associated with risk of disabling dementia with multivariable hazard ratios (95% confidence intervals) of 0.79 (0.63–1.00) for the highest versus lowest quartiles of total tocopherol intake (P for trend = 0.05). However, the association was strengthened when further adjusted for α-linolenic acid intake (Spearman correlation with total tocopherol intake = 0.93), with multivariable hazard ratios of 0.50 (0.34–0.74) (P for trend = 0.001) but was weakened and nonsignificant when further adjusted for linoleic acid intake (Spearman correlation with total tocopherol intake = 0.92), with multivariable hazard ratios of 0.69 (0.47–1.01) (P for trend = 0.05). Similar but nonsignificant inverse associations were observed for α-, γ-, and δ-tocopherols but not for β-tocopherol. These results were similar regardless of the presence of a history of stroke. Dietary tocopherol intake was inversely associated with risk of disabling dementia, but its independent effect was uncertain owing to a high intercorrelation of α-linolenic linoleic acids with total tocopherol intake. Even with such confounding, a diet high in tocopherols may help prevent the onset of dementia.


2021 ◽  
Vol 79 (4) ◽  
pp. 1601-1612
Author(s):  
Johan Frederik Håkonsen Arendt ◽  
Erzsébet Horváth-Puhó ◽  
Henrik Toft Sørensen ◽  
Ebba Nexø ◽  
Lars Pedersen ◽  
...  

Background: It is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia. Objective: To assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer’s disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes). Methods: We conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000–2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200–600 pmol/L). We used multivariable Cox regression to compute 0–15-year hazard ratios for dementia. Results: For low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia. Conclusion: We found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Wahrenberg ◽  
P Magnusson ◽  
R Kuja-Halkola ◽  
H Habel ◽  
K Hambraeus ◽  
...  

Abstract Background Despite recent advances in secondary prevention, recurrent cardiovascular events are common after a myocardial infarction (MI). It has been reported that genetic risk scores may predict the risk of recurrent cardiovascular events. Although patient-derived family history is a composite of both genetic and environmental heritability of atherosclerotic cardiovascular disease (ASCVD), it is an easily accessible information compared to genetically based risk models but the association with recurrent events is unknown. Purpose To evaluate whether a register-verified family history of ASCVD is associated with recurrent cardiovascular events (rASCVD) in patients after a first-time MI. Methods We included patients with a first-time MI during 2005 – 2014, registered in the SWEDEHEART SEPHIA registry and without prior ASCVD. Follow-up was available until Dec 31st, 2018. Data on relatives, diagnoses and prescriptions were extracted from national registers. A family history of ASCVD was defined as a register-verified hospitalisation due to MI, angina with coronary revascularization procedures, stroke or cardiovascular death in any parent. Early history was defined as such an event before the age of 55 years in fathers and 65 years in mothers. The association between family history and a composite outcome including recurrent MI, angina requiring acute revascularization, ischaemic stroke and cardiovascular death during follow-up was studied with Cox proportional hazard regression with time from SEPHIA registry completion as underlying time-scale, adjusted for age with splines, gender and year of SEPHIA registry. Regression models were then further adjusted for hypertension, diabetes, smoking and for a subset of patients, LDL-cholesterol (LDL_C) at time of first event. Results Of 25,615 patients, 2.5% and 32.1% had an early and ever-occurring family history of ASCVD, respectively. Patients with early family history were significantly younger than other patients and were more likely to be current smokers and have a higher LDL-C (Median (IQR) 3.5 (1.1) vs 3.3 (1.1) mmol/L). In total, 3,971 (15.5%) patients experienced the outcome. Early family history of ASCVD was significantly associated with rASCVD (Hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.23–1.87), and the effect was sustained when adjusted for cardiovascular risk factors (HR 1.48, 95% CI 1.20–1.83) and LDL-C (HR 1.35, 95% CI 1.04–1.74). Ever-occurring family history was weakly associated with ASCVD (HR 1.09, 95% CI 1.02 – 1.17) and the association remained unchanged with adjustments for risk factors. Conclusions Early family history of cardiovascular disease is a potent risk factor for recurrent cardiovascular events in a secondary prevention setting, independent of traditional risk factors including LDL-C. This is a novel finding and these patients may potentially benefit from intensified secondary preventive measures after a first-time MI. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): This work was funded by grants from The Swedish Heart and Lung Association


2021 ◽  
Vol 23 (Supplement_4) ◽  
pp. iv12-iv12
Author(s):  
Michael T C Poon ◽  
Kai Jin ◽  
Paul M Brennan ◽  
Jonine Figueroa ◽  
Cathie Sudlow

Abstract Aims There is limited evidence on cerebrovascular risks in glioblastoma and meningioma patients. We aimed to compare cerebrovascular risks of these patients with the general population. Method We used population-based routine healthcare and administrative data linkage in this matched cohort study. Cases were adult glioblastoma and meningioma patients diagnosed in Wales 2000-2014 identified in the cancer registry. Controls from cancer-free general population were matched to cases (5:1 ratio) on age (±5 years), sex and GP practice. Factors included in multivariable models were age, sex, index of multiple deprivation, hypertension, diabetes, high cholesterol, history of cardiovascular disease, and medications for cardiovascular diseases. Outcomes were fatal and non-fatal haemorrhagic and ischaemic stroke. We used flexible parametric models adjusting for confounders to calculate the hazard ratios (HR). Results Final analytic population was 16,921 participants, of which 1,340 had glioblastoma and 1,498 had meningioma. The median follow-up time was 0.5 year for glioblastoma patients, 4.9 years for meningioma patients, and 6.6 years for controls. The number of haemorrhage and ischaemic stroke was 154 and 374 in the glioblastoma matched cohort, respectively, and 180 and 569 in the meningioma matched cohort, respectively. The adjusted HRs for haemorrhagic and ischaemic stroke were 3.74 (95%CI 1.87-6.57) and 5.62 (95%CI 2.56-10.42) in glioblastoma patients, respectively, and were 2.42 (95%CI 1.58-3.52) and 1.86 (95%CI 1.54-2.23) in meningioma patients compared with their controls. Conclusion Glioblastoma and meningioma patients had higher cerebrovascular risks; these risks were even higher for glioblastoma patients. Further assessment of these potentially modifiable risks may improve survivorship.


Stroke ◽  
2021 ◽  
Author(s):  
Masayuki Teramoto ◽  
Isao Muraki ◽  
Kazumasa Yamagishi ◽  
Akiko Tamakoshi ◽  
Hiroyasu Iso

Background and Purpose: The effect of green tea and coffee consumption on mortality among cardiovascular diseases survivors is unknown. We examined the association between green tea and coffee consumption and mortality among persons with and without stroke or myocardial infarction (MI). Methods: In the Japan Collaborative Cohort Study, 46 213 participants (478 stroke survivors, 1214 MI survivors, and 44 521 persons without a history of stroke or MI), aged 40 to 79 years at baseline (1988–1990), completed a lifestyle, diet, and medical history questionnaire and were followed up regarding mortality until 2009. The Cox proportional hazard model was used to calculate the multivariable hazard ratios with 95% CIs of all-cause mortality after adjusting for potential confounding factors. Results: During the 18.5-year median follow-up period, 9253 cases were documented. Green tea consumption was inversely associated with all-cause mortality among stroke or MI survivors; the multivariable hazard ratios (95% CIs) for stroke survivors were 0.73 (0.42–1.27) for 1 to 6 cups/wk, 0.65 (0.36–1.15) for 1 to 2 cups/d, 0.56 (0.34–0.92) for 3 to 4 cups/d, 0.52 (0.31–0.86) for 5 to 6 cups/d, and 0.38 (0.20–0.71) for ≥7 cups/d, compared with nondrinkers. A similar inverse association was observed for MI survivors, but not evident for those without a history of stroke or MI. Coffee consumption was inversely associated with all-cause mortality in persons without a history of stroke or MI; the multivariable hazard ratios (95% CIs) were 0.86 (0.82–0.91) for 1 to 6 cups/wk, 0.86 (0.80–0.92) for 1 cup/d, and 0.82 (0.77–0.89) for ≥2 cups/d, compared with nondrinkers. The corresponding hazard ratios (95% CIs) for MI survivors were 0.69 (0.53–0.91), 0.78 (0.55–1.10), and 0.61 (0.41–0.90). No such association was observed for stroke survivors. Conclusions: Green tea consumption can be beneficial in improving the prognosis for stroke or MI survivors, whereas coffee consumption can also be so for persons without a history of stroke or MI as well as MI survivors.


2019 ◽  
Vol 35 (3) ◽  
pp. 295-303
Author(s):  
Sanne A. E. Peters ◽  
◽  
Ling Yang ◽  
Yu Guo ◽  
Yiping Chen ◽  
...  

AbstractPregnancy and pregnancy loss may be associated with increased risk of diabetes in later life. However, the evidence is inconsistent and sparse, especially among East Asians where reproductive patterns differ importantly from those in the West. We examined the associations of pregnancy and pregnancy loss (miscarriage, induced abortion, and still birth) with the risk of incident diabetes in later life among Chinese women. In 2004–2008, the nationwide China Kadoorie Biobank recruited 302 669 women aged 30–79 years from 10 (5 urban, 5 rural) diverse localities. During 9.2 years of follow-up, 7780 incident cases of diabetes were recorded among 273,383 women without prior diabetes and cardiovascular disease at baseline. Cox regression yielded multiple-adjusted hazard ratios (HRs) for the risk of diabetes associated with pregnancy and pregnancy loss. Overall, 99% of women had been pregnant, of whom 10%, 53%, and 6% reported having a history of miscarriage, induced abortion, and stillbirth, respectively. Among ever pregnant women, each additional pregnancy was associated with an adjusted HR of 1.04 (95% CI 1.03; 1.06) for diabetes. Compared with those without pregnancy loss, women with a history of pregnancy loss had an adjusted HR of 1.07 (1.02; 1.13) and the HRs increased with increasing number of pregnancy losses, irrespective of the number of livebirths; the adjusted HR was 1.03 (1.00; 1.05) for each additional pregnancy loss. The strength of the relationships differed marginally by type of pregnancy loss. Among Chinese women, a higher number of pregnancies and pregnancy losses were associated with a greater risk of diabetes.


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