scholarly journals Smoking Causes Fatal Subarachnoid Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (10) ◽  
pp. 3018-3022 ◽  
Author(s):  
Ilari Rautalin ◽  
Miikka Korja ◽  
Jaakko Kaprio
Keyword(s):  
Risk Factor ◽  
Subarachnoid Hemorrhage ◽  
Causal Effect ◽  
Twin Studies ◽  
Hazard Ratio ◽  
Discordant Pair ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Discordant Twin

Background and Purpose: One of the largest twin studies to date suggested that subarachnoid hemorrhage (SAH) is mainly of nongenetic origin, but the causal effect of environmental factors on SAH is yet unknown. We hypothesized that if only one of the twins experience fatal SAH, they do not share the most important environmental risk factor for SAH, namely smoking. If true, such finding would suggest that smoking causes SAH. Methods: Through the nationwide cause-of-death register, we followed 16 282 same-sex twin pairs of Finnish origin from the older Finnish Twin Cohort between 1976 and 2018 and identified all participants who died from SAH. For the baseline, we collected risk factor information about smoking, hypertension, physical activity, body mass index, alcohol consumption, and education. We classified the pairs as monozygotic, dizygotic, or of unknown zygosity. We examined the within-pair risk factor differences in the pairs discordant for SAH, that is, where one twin died from SAH and the other did not. We computed both individual (whole cohort) and pairwise (discordant pair) hazard ratios and 95% CIs. Results: During the 869 469 person-years of follow-up, we identified 116 discordant and 2 concordant (both died from SAH) twin pairs for fatal SAH. Overall, 25 of the discordant twin pairs were monozygotic. For the whole cohort, smoking (occasional/current) was associated with increased risk of SAH death (hazard ratio, 3.33 [CI, 2.24–4.95]) as compared with nonsmokers (never/former). In the pairwise analyses for discordant twin pairs, we found that the twin who smoked had an increased risk of fatal SAH (hazard ratio, 6.33 [CI, 1.87–21.4]) as compared with the nonsmoking twin. The association remained consistent regardless of the twin pairs’ zygosity or sex. Conclusions: Our results provide strong evidence for a causal, rather than associative, role of smoking in SAH.

scholarly journals C-reactive protein and venous thromboembolism

2009 ◽  
Vol 102 (10) ◽  
pp. 615-619 ◽  
Author(s):  
Pamela L. Lutsey ◽  
Brad C. Astor ◽  
Mary Cushman ◽  
Aaron R. Folsom
Keyword(s):  
Venous Thromboembolism ◽  
Hormone Replacement ◽  
Hazard Ratio ◽  
C Reactive Protein ◽  
Atherosclerosis Risk In Communities ◽  
Reactive Protein ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Aric Study

SummaryThe role of inflammation in the causation of venous thromboembolism (VTE) is uncertain. In 10,505 participants of the Atherosclerosis Risk in Communities (ARIC) Study, we assessed the association of the systemic inflammation marker, elevated C-reactive protein (CRP), with incidence of VTE (n=221) over a median of 8.3 years of follow-up. Adjusted for age, race, and sex, the hazard ratios of VTE across quintiles of CRP were 1.0, 1.61, 1.16, 1.56, and 2.31 (p for trend p<0.0007). For CRP above the upper 10 percentile (≥8.55 mg/L), compared with the lowest 90% of CRP values, the hazard ratio of VTE was 2.07 (95% CI 1.47, 2.94). Further adjustment for baseline hormone replacement therapy, diabetes, and body mass index attenuated the hazard ratios only slightly. For example, the adjusted hazard ratio of VTE was 1.76 (95% CI 1.23, 2.52) for CRP above versus below the 90th percentile. In conclusion, this prospective, populationbased study suggests elevated CRP is independently associated with increased risk of VTE.

scholarly journals Osteoarthritis: Insights Offered by the Study of Bone Mass Genetics

2021 ◽  
Vol 19 (2) ◽  
pp. 115-122
Author(s):  
A. Hartley ◽  
C. L. Gregson ◽  
L. Paternoster ◽  
J. H. Tobias
Keyword(s):  
Bone Mass ◽  
Causal Effect ◽  
Mendelian Randomisation ◽  
Mineral Density ◽  
High Bone Mass ◽  
Increased Risk ◽  
High Bone ◽  
Genetic Mechanisms ◽  
Additional Support

Abstract Purpose of Review This paper reviews how bone genetics has contributed to our understanding of the pathogenesis of osteoarthritis. As well as identifying specific genetic mechanisms involved in osteoporosis which also contribute to osteoarthritis, we review whether bone mineral density (BMD) plays a causal role in OA development. Recent Findings We examined whether those genetically predisposed to elevated BMD are at increased risk of developing OA, using our high bone mass (HBM) cohort. HBM individuals were found to have a greater prevalence of OA compared with family controls and greater development of radiographic features of OA over 8 years, with predominantly osteophytic OA. Initial Mendelian randomisation analysis provided additional support for a causal effect of increased BMD on increased OA risk. In contrast, more recent investigation estimates this relationship to be bi-directional. However, both these findings could be explained instead by shared biological pathways. Summary Pathways which contribute to BMD appear to play an important role in OA development, likely reflecting shared common mechanisms as opposed to a causal effect of raised BMD on OA. Studies in HBM individuals suggest this reflects an important role of mechanisms involved in bone formation in OA development; however further work is required to establish whether the same applies to more common forms of OA within the general population.

scholarly journals Plasma Branched-Chain Amino Acids and Incident Cardiovascular Disease in the PREDIMED Trial

2016 ◽  
Vol 62 (4) ◽  
pp. 582-592 ◽  
Author(s):  
Miguel Ruiz-Canela ◽  
Estefania Toledo ◽  
Clary B Clish ◽  
Adela Hruby ◽  
Liming Liang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Amino Acids ◽  
Cardiovascular Death ◽  
Branched Chain Amino Acids ◽  
Control Group ◽  
Cvd Risk ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Branched Chain

Abstract BACKGROUND The role of branched-chain amino acids (BCAAs) in cardiovascular disease (CVD) remains poorly understood. We hypothesized that baseline BCAA concentrations predict future risk of CVD and that a Mediterranean diet (MedDiet) intervention may counteract this effect. METHODS We developed a case-cohort study within the Prevención con Dieta Mediterránea (PREDIMED), with 226 incident CVD cases and 744 noncases. We used LC-MS/MS to measure plasma BCAAs (leucine, isoleucine, and valine), both at baseline and after 1 year of follow-up. The primary outcome was a composite of incident stroke, myocardial infarction, or cardiovascular death. RESULTS After adjustment for potential confounders, baseline leucine and isoleucine concentrations were associated with higher CVD risk: the hazard ratios (HRs) for the highest vs lowest quartile were 1.70 (95% CI, 1.05–2.76) and 2.09 (1.27–3.44), respectively. Stronger associations were found for stroke. For both CVD and stroke, we found higher HRs across successive quartiles of BCAAs in the control group than in the MedDiet groups. With stroke as the outcome, a significant interaction (P = 0.009) between baseline BCAA score and intervention with MedDiet was observed. No significant effect of the intervention on 1-year changes in BCAAs or any association between 1-year changes in BCAAs and CVD were observed. CONCLUSIONS Higher concentrations of baseline BCAAs were associated with increased risk of CVD, especially stroke, in a high cardiovascular risk population. A Mediterranean-style diet had a negligible effect on 1-year changes in BCAAs, but it may counteract the harmful effects of BCAAs on stroke.

scholarly journals Supper Timing and Cardiovascular Mortality: The Japan Collaborative Cohort Study

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3389
Author(s):  
Jingyun Tang ◽  
Jia-Yi Dong ◽  
Ehab S. Eshak ◽  
Renzhe Cui ◽  
Kokoro Shirai ◽  
...  
Keyword(s):  
Hemorrhagic Stroke ◽  
Proportional Hazards ◽  
Cox Proportional Hazards ◽  
Stroke Mortality ◽  
Hazard Ratios ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Study Participants

Evidence on the role of supper timing in the development of cardiovascular disease (CVD) is limited. In this study, we examined the associations between supper timing and risks of mortality from stroke, coronary heart disease (CHD), and total CVD. A total of 28,625 males and 43,213 females, aged 40 to 79 years, free from CVD and cancers at baseline were involved in this study. Participants were divided into three groups: the early supper group (before 8:00 p.m.), the irregular supper group (time irregular), and the late supper group (after 8:00 p.m.). Cox proportional hazards regression models were used to calculate hazard ratios (HRs) for stroke, CHD, and total CVD according to the supper time groups. During the 19-year follow-up, we identified 4706 deaths from total CVD. Compared with the early supper group, the multivariable HR of hemorrhagic stroke mortality for the irregular supper group was 1.44 (95% confidence interval [CI]: 1.05–1.97). There was no significant association between supper timing and the risk of mortality from other types of stroke, CHD, and CVD. We found that adopting an irregular supper timing compared with having dinner before 8:00 p.m. was associated with an increased risk of hemorrhagic stroke mortality.

Headache as a risk factor for dementia: A prospective population-based study

Cephalalgia ◽  
2013 ◽  
Vol 34 (5) ◽  
pp. 327-335 ◽  
Author(s):  
Knut Hagen ◽  
Eystein Stordal ◽  
Mattias Linde ◽  
Timothy J Steiner ◽  
John-Anker Zwart ◽  
...  
Keyword(s):  
Risk Factor ◽  
Cohort Study ◽  
Cox Regression ◽  
Subsequent Development ◽  
Population Based ◽  
Health Study ◽  
Cox Regression Analysis ◽  
Hazard Ratios ◽  
Increased Risk

Background Headache has not been established as a risk factor for dementia. The aim of this study was to determine whether any headache was associated with subsequent development of vascular dementia (VaD), Alzheimer’s disease (AD) or other types of dementia. Methods This prospective population-based cohort study used baseline data from the Nord-Trøndelag Health Study (HUNT 2) performed during 1995–1997 and, from the same Norwegian county, a register of cases diagnosed with dementia during 1997–2010. Participants aged ≥20 years who responded to headache questions in HUNT 2 were categorized (headache free; with any headache; with migraine; with nonmigrainous headache). Hazard ratios (HRs) for later inclusion in the dementia register were estimated using Cox regression analysis. Results Of 51,383 participants providing headache data in HUNT 2, 378 appeared in the dementia register during the follow-up period. Compared to those who were headache free, participants with any headache had increased risk of VaD ( n = 63) (multivariate-adjusted HR = 2.3, 95% CI 1.4–3.8, p = 0.002) and of mixed dementia (VaD and AD ( n = 52)) (adjusted HR = 2.0, 95% CI 1.1–3.5, p = 0.018). There was no association between any headache and later development of AD ( n = 180). Conclusion In this prospective population-based cohort study, any headache was a risk factor for development of VaD.

Pathogenesis of atherosclerosis: lipid metabolism

2017 ◽  
Author(s):  
Olov Wiklund ◽  
Jan Borén
Keyword(s):  
Risk Factor ◽  
Current Data ◽  
Atherosclerotic Cardiovascular Disease ◽  
Causative Role ◽  
Receptor Ligands ◽  
Increased Risk ◽  
Low Hdl ◽  
Arterial Intima ◽  
Coa Reductase

Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.

scholarly journals Prediction of incident diabetes mellitus by baseline IGF1 levels

2011 ◽  
Vol 164 (2) ◽  
pp. 223-229 ◽  
Author(s):  
Harald Jörn Schneider ◽  
Nele Friedrich ◽  
Jens Klotsche ◽  
Sabine Schipf ◽  
Matthias Nauck ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Parameters ◽  
Incident Diabetes ◽  
Large Prospective Study ◽  
Prospective Cohort Studies ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Hba1c Levels

ObjectiveIGF1 is associated with metabolic parameters and involved in glucose metabolism. Low-IGF1 has been implicated in the etiology of glucose intolerance and subjects with pathological causes of either low- or high-IGF1 are at risk of diabetes. We hypothesized that both low- and high-IGF1 levels increase the risk of diabetes and aimed to assess the role of IGF1 in the risk of developing diabetes in a large prospective study.DesignAn analysis of two prospective cohort studies, the DETECT study and SHIP.MethodsWe measured IGF1 levels in 7777 nondiabetic subjects and assessed incident diabetes mellitus during follow-up.ResultsThere were 464 cases of incident diabetes during 32 229 person-years (time of follow-up in the DETECT study and SHIP: 4.5 and 5 years respectively). There was no heterogeneity between both studies (P>0.4). The hazard ratios (HRs) of incident diabetes in subjects with IGF1 levels below the 10th or above the 90th age- and sex-specific percentile, compared to subjects with intermediate IGF1 levels, were 1.44 (95% confidence interval (CI) 1.07–1.94) and 1.55 (95% CI 1.06–2.06) respectively, after multiple adjustment. After further adjustment for metabolic parameters, the HR for low-IGF1 became insignificant. Analysis of IGF1 quintiles revealed a U-shaped association of IGF1 with risk of diabetes. Results remained similar after exclusion of patients with onset of new diabetes within 1 year or with borderline glucose or HbA1c levels at baseline.ConclusionsSubjects with low- or high-IGF1 level are at increased risk of developing diabetes.

Prediction of Cardiovascular Events in Patients with Ankylosing Spondylitis and Psoriatic Arthritis: Role of Lipoproteins in a High-risk Population

2012 ◽  
Vol 39 (7) ◽  
pp. 1433-1440 ◽  
Author(s):  
ANNE GRETE SEMB ◽  
TORE K. KVIEN ◽  
DAVID A. DeMICCO ◽  
RANA FAYYAD ◽  
CHUAN-CHUAN WUN ◽  
...  
Keyword(s):  
Psoriatic Arthritis ◽  
Ankylosing Spondylitis ◽  
Density Lipoprotein ◽  
High Risk Population ◽  
Proportional Hazard ◽  
Mortality And Morbidity ◽  
Cox Proportional Hazard ◽  
Hazard Ratios ◽  
Increased Risk

Objective.To evaluate lipids and apolipoproteins as predictors of cardiovascular mortality and morbidity (CVD) in patients with spondyloarthritis (SpA).Methods.In the pooled cohort of participants in the IDEAL, TNT, and CARDS trials, 50 had ankylosing spondylitis (AS), 36 had psoriatic arthritis (PsA), and 21,641 did not have AS or PsA (non-SpA). We compared lipid levels at baseline between AS or PsA and non-SpA, and hazard ratios (HR) for CVD were calculated in a Cox proportional hazard model.Results.Atherogenic lipids were lower in samples from AS, but not in PsA, compared to non-SpA. The HR for 1 SD increase in baseline lipids for future CVD was for total cholesterol 1.39 (95% CI 0.82, 2.36) in AS, 1.01 (95% CI 0.44, 2.31) in PsA, and 1.10 (95% CI 1.07, 1.14) in non-SpA. Both high-density lipoprotein (HDL) and apolipoprotein (ApoA-1) were significantly associated with CVD in AS (HR 3.67, 95% CI 1.47, 9.06, and HR 1.89, 95% CI 1.02, 3.54, respectively), in contrast to PsA (HDL: HR 1.03, 95% CI 0.49, 2.15; ApoA-1: HR 0.79, 95% CI 0.34, 1.89) and non-SpA (HDL: HR 0.86, 95% CI 0.84, 0.89; ApoA-1: HR 0.88, 95% CI 0.85, 0.91).Conclusion.HDL and ApoA-1 were surprisingly associated with increased risk of future CVD in patients with AS, whereas these lipids were protective in non-SpA.

Primary prevention of cardiovascular disease in patients with systemic lupus erythematosus: case series and literature review

Lupus ◽  
2017 ◽  
Vol 26 (14) ◽  
pp. 1463-1472 ◽  
Author(s):  
S Fasano ◽  
D P Margiotta ◽  
L Navarini ◽  
L Pierro ◽  
I Pantano ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cardiovascular Disease ◽  
Cardiovascular Event ◽  
Lupus Erythematosus ◽  
Cardiovascular Events ◽  
Hazard Ratio ◽  
Systemic Lupus ◽  
Increased Risk

Background Systemic lupus erythematosus is associated with an increased risk of cardiovascular disease. Low-dose aspirin, hydroxychloroquine and statins have been suggested to play a prophylactic role of cardiovascular events. This study is devoted to reviewing the literature on the topic and assessing the effects of these drugs in preventing a first cardiovascular event in a two-centre Italian series. Methods A PubMed search on cardiovascular prevention in systemic lupus erythematosus was performed. Moreover, systemic lupus erythematosus patients admitted to two centres from 2000–2015, who at admission had not experienced any cardiovascular event, were investigated. Aspirin, hydroxychloroquine and statin use, and the occurrence of any cardiovascular event, were recorded at each visit. Kaplan-Meier and Cox regression analyses were performed to evaluate the role of traditional, disease-related cardiovascular risk factors and of each of the three drugs in the occurrence of new cardiovascular events. Results The literature search produced conflicting results. Two hundred and ninety-one systemic lupus erythematosus patients were included in the study and followed for a median of eight years. During follow-up, 16 cardiovascular events occurred. At multivariate analysis, taking aspirin (hazard ratio: 0.24) and hydroxychloroquine for more than five years (hazard ratio: 0.27) reduced, while antiphospholipid antibody positivity (hazard ratio: 4.32) increased, the risk of a first cardiovascular event. No effect of statins emerged. Conclusion Our study confirms an additive role of aspirin and hydroxychloroquine in the primary prophylaxis of cardiovascular events in Italian patients with systemic lupus erythematosus. The lack of any detected effect in previous reports may depend on the design of studies and their short follow-up period.

scholarly journals D-Dimer Levels and Risk of Recurrence Following Provoked Venous Thromboembolism: Findings from the Riete Registry

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3810-3810
Author(s):  
Martin Ellis ◽  
Martin Mar ◽  
Monreal Manuel ◽  
Orly Hamburger-Avnery ◽  
Alessandra Bura-Riviere ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Anticoagulant Therapy ◽  
Conflicts Of Interest ◽  
Hazard Ratio ◽  
Increased Risk ◽  
Risk Patients ◽  
Recurrent Vte ◽  
D Dimer

Abstract Background. Patients with venous thromboembolism (VTE) secondary to transient risk factors or cancer may develop VTE recurrences after discontinuing anticoagulant therapy. Identifying at-risk patients could help to guide the ideal duration of anticoagulant therapy in these patients. Methods. We used the RIETE database to assess the prognostic value of d-dimer testing after discontinuing anticoagulation to identify patients at increased risk for recurrences. The proportion of patients with raised d-dimer levels was determined and the hazard ratio (HR) for VTE recurrences compared to those with normal levels was calculated. Univariate and multivariate analyses of factors associated with VTE recurrence were performed. Results. 3 606 patients were identified in the database in April 2018: 2 590 had VTE after a transient risk factor and 1016 had a cancer. D-dimer levels were measured after discontinuing anticoagulation in 1 732 (67%) patients with transient risk factors and 732 (72%) patients with cancer-associated VTE and these patients formed the cohort in which recurrent VTE rate was calculated. D-dimers and were elevated in 551 (31.8%) of patients with a transient risk factor and were normal in 1181 (68.2%). In the cancer-associated group, d-dimers were elevated in 398 (54.3%) and normal in 334 (45.7%) patients. The adjusted hazard ratio for recurrent VTE was: 2.32 (95%CI: 1.55-3.49) in patients with transient risk factors and 2.23 (95%CI: 1.50-3.39) in those with cancer. Conclusions. Patients with raised d-dimer levels after discontinuing anticoagulant therapy for provoked or cancer-associated VTE are at increased risk for recurrent VTE and death. Future studies could target these patients for extended anticoagulation. Disclosures No relevant conflicts of interest to declare.

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