Abstract 10: Cigarette Smoking and the Risk of Adverse Events in Patients With Heart Failure With Preserved Ejection Fraction

2018 ◽  
Vol 11 (suppl_1) ◽  
Author(s):  
Pratik Sandesara ◽  
Wesley O’Neal ◽  
Sanjay Venkatesh ◽  
Laurence Sperling
Keyword(s):  
Heart Failure ◽  
Cigarette Smoking ◽  
Cox Regression ◽  
Smoking Status ◽  
Vascular Dysfunction ◽  
Cardiovascular Death ◽  
Adverse Outcomes ◽  
Current Smoking ◽  
Increased Risk ◽  
Never Smokers

Background: Cigarette smoking predisposes individuals to the development of cardiovascular disease by promoting inflammation, vascular dysfunction, and accelerated atherosclerosis. However, the association between smoking and outcomes in HFpEF remains unclear. Objectives: To examine the relationship between smoking and outcomes in patients with HFpEF. Methods: This analysis included 1,717 (mean age=71±10 years; 50% male; 78% white) patients with HFpEF enrolled in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) Trial from the Americas. Smoking was ascertained by self-reported history and was categorized as never, former, or current. Multivariable cox regression was used to examine the risk of hospitalization, hospitalization for heart failure, death, and cardiovascular death across smoking categories. Results: There were 116 (7%), 871 (51%), and 729 (42%) patients whose smoking status was classified as current, former, or never. Current smoking was associated with an increased risk for hospitalization (never: HR=1.0; former: HR=1.14, 95%CI=0.99, 1.31; current: HR=1.38, 95%CI=1.05, 1.80), hospitalization for heart failure (never: HR=1.0; former: HR=1.25, 95%CI=0.99, 1.57; current: HR=1.68, 95%CI=1.08, 2.61), death (never: HR=1.0; former: HR=1.02, 95%CI=0.81, 1.29; current: HR=1.82, 95%CI=1.19, 2.78), and cardiovascular death (never: HR=1.0; former: HR=1.00, 95%CI=0.74, 1.35; current: HR=1.85, 95%CI=1.09, 3.24) compared with former or never smokers in a multivariable model adjusted for cardiovascular risk factors. The cumulative incidence estimates for hospitalization for heart failure across smoking categories are shown in Figure 1 (log-rank p=0.0029). Similar effect estimates were observed for smoking categories and the outcomes examined when further adjusted for quantity of cigarette use. Conclusion: Current smoking is associated an increased risk for adverse outcomes in HFpEF, including hospitalization for heart failure. Smoking cessation possibly has role to reduce the risk for hospital admission and death in these high-risk patients.

Abstract 14922: Prognostic Value of Baseline BNP and NT-ProBNP and its Interaction With Spironolactone in Patients With Heart Failure and Preserved Ejection Fraction in the TOPCAT Trial

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Inder S Anand ◽  
Scott D Solomon ◽  
Brian Claggett ◽  
Sanjiv J Shah ◽  
Eileen O’Meara ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Primary Outcome ◽  
Cox Regression ◽  
Selection Criterion ◽  
Adverse Outcomes ◽  
Preserved Ejection Fraction ◽  
Patient Selection Criterion ◽  
Increased Risk ◽  
Patients With Heart Failure

Background: Plasma natriuretic peptides (NP) are helpful in the diagnosis of heart failure (HF) with preserved ejection fraction (HFpEF) and predict adverse outcomes. Levels of NP beyond a certain cut-off level are often used as inclusion criteria in clinical trials to ensure that the patients have HF, and to select patients at higher risk. Whether treatments have a differential effect on outcomes across the spectrum of NP levels is unclear. In the I-Preserve trial a benefit of irbesartan on all outcomes was only seen in HFpEF patients with low but not high NP levels. We hypothesized that in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial, spironolactone might have a greater benefit in patients with lower NP levels. Methods and Results: BNP (n=468) or NT-proBNP (n=400) levels were available at baseline in 868 patients with HFpEF enrolled in the natriuretic peptide stratum (BNP ≥100 pg/mL or an NT- proBNP ≥360 pg/mL) of the TOPCAT trial. In a multi-variable Cox regression model, that included age, gender, region (Americas vs. Russia/Georgia), atrial fibrillation, diabetes, eGFR, BMI and heart rate, higher BNP or NT-proBNP as a continuous, standardized log-transformed variable or grouped by terciles (see Figure for BNP & NT-proBNP tercile values) was independently associated with an increased risk of the primary endpoint of cardiovascular mortality, aborted cardiac arrest, or hospitalization for heart failure (Figure-1). There was a significant interaction between the effect of spironolactone and baseline BNP or NT-proBNP terciles for the primary outcome (P=0.02, Figure-2), with greater benefit of the drug in the lower compared to higher NP terciles. Conclusions: The benefit of spironolactone in lower risk HFpEF patients may indicate effects of the drug on early, but not late higher-risk stage of the disease. These findings question the strategy of using elevated NP as a patient selection criterion in HFpEF trials.

Myocardial reperfusion reverses the J-curve association of cardiovascular risk and diastolic blood pressure in patients with left ventricular dysfunction and heart failure after myocardial infarction: insights from the EPHESUS trial

2020 ◽  
Vol 41 (17) ◽  
pp. 1673-1683 ◽  
Author(s):  
Michael Böhm ◽  
João Pedro Ferreira ◽  
Felix Mahfoud ◽  
Kevin Duarte ◽  
Bertram Pitt ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Cox Regression ◽  
Cardiovascular Death ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Increased Risk ◽  
The Impact

Abstract Aims The described association of low diastolic blood pressure (DBP) with increased cardiovascular outcomes could be due to reduced coronary perfusion or is simply due to reverse causation. If DBP is physiologically relevant, coronary reperfusion after myocardial infarction (MI) might influence DBP–risk association. Methods and results The relation of achieved DBP with cardiovascular death or cardiovascular hospitalization, cardiovascular death, and all-cause death was explored in 5929 patients after acute myocardial infarction (AMI) with impaired left ventricular function, signs and symptoms of heart failure, or diabetes in the EPHESUS trial according to their reperfusion status. Cox regression models were used to assess the impact of reperfusion status on the association of DBP and systolic blood pressure (SBP) with outcomes in an adjusted fashion. In patients without reperfusion, lower DBP <70 mmHg was associated with increased risk for all-cause death [adjusted hazard ratios (HRs) 1.80, 95% confidence interval (CI) 1.41–2.30; P < 0.001], cardiovascular death (HR 1.70, 95% CI 1.3–3.22; P < 0.001), cardiovascular death or cardiovascular hospitalization (HR 1.54, 95% CI 1.26–1.87; P < 0.001). In patients with reperfusion, the risk increase at low DBP was not observed. At low SBP, risk increased independently of reperfusion. A sensitivity analysis in the subgroup of patients with optimal SBP of 120–130 mmHg showed again risk reduction of reperfusion at low DBP. Adding the treatment allocation to eplerenone or placebo into the models had no effects on the results. Conclusion Patients after AMIs with a low DBP had an increased risk, which was sensitive to reperfusion therapy. Low blood pressure after MI identifies in patients with particular higher risk. These data support the hypothesis that low DBP in patients with stenotic coronary lesions is associated with risk, potentially involving coronary perfusion pressure and the recommendations provided by guidelines suggesting lower DBP boundaries for these high-risk patients.

Abstract 15224: Importance of Beta Blocker Subtype for the Risk of Perioperative Adverse Events in Patients Without Heart Failure and Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Mads E Jørgensen ◽  
Gunnar H Gislason ◽  
Christian Torp-Pedersen ◽  
Mark Hlatky ◽  
C harlotte Andersson
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Beta Blocker ◽  
Beta Blockers ◽  
Cardiovascular Death ◽  
Adverse Outcomes ◽  
Major Adverse Cardiovascular Events ◽  
Blocker Therapy ◽  
Beta Blocker Therapy ◽  
Increased Risk

Objective: Beta blocker therapy in patients undergoing surgery is being revisited. Previous studies have demonstrated increased risks of perioperative adverse outcomes associated with beta blocker therapy, but whether some beta blocker subtypes may be superior to others remains unknown. Methods: Using nationwide Danish registries we included all non-cardiac surgeries in patients without heart failure or myocardial infarction in 2005-2011. Patients were grouped according to beta blocker use prior to surgery. Risks of 30-day MACE (major adverse cardiovascular events; non-fatal myocardial infarction, non-fatal stroke or cardiovascular death) were estimated using logistic regression models adjusted for gender, age, body mass index, pharmacotherapy, comorbidities, type of surgery and surgery risk. Results: We included 607,338 patients in the study. Patients on beta blockers (n=50,480) were older with similar gender distribution (mean age 66 years [sd=12.9], 45%male) compared with patients not on beta blockers (n=556,858) (mean age 52 years [sd=17.6], 44%male). Patients on beta blockers had more comorbidities and received more pharmacotherapy (all p<0.001). Unadjusted absolute risks of MACE were increased with all beta blocker subtypes (range 1.7% for propranolol to 4.2% for sotalol) compared with untreated patients (0.8%). Odds ratios for the risk of 30-day MACE are shown in the Figure Conclusion: Patients without chronic heart failure and prior myocardial infarction were at increased risk of 30-day perioperative MACE when treated with beta blockers, with the exception of bisoprolol. Patients treated with carvedilol seemed to be at especially high risk.

Association Between Cigarette Smoking and Systemic Lupus Erythematosus: An Updated Multivariate Bayesian Metaanalysis

2019 ◽  
Vol 47 (10) ◽  
pp. 1514-1521 ◽  
Author(s):  
Monica Hui Yan Chua ◽  
Irene Ai Ting Ng ◽  
Mike W.L.-Cheung ◽  
Anselm Mak
Keyword(s):  
Cigarette Smoking ◽  
Lupus Erythematosus ◽  
Smoking Status ◽  
Effect Sizes ◽  
Systemic Lupus ◽  
Current Smoking Status ◽  
Current Smoking ◽  
Publication Time ◽  
Never Smokers ◽  
Over Time

ObjectiveThe association between cigarette smoking and the risk of systemic lupus erythematosus (SLE) remains a matter for debate. Additionally, the effect of the change of smokers’ demographics on the risk of development of SLE over time has not been formally addressed. We aimed to examine the association between cigarette smoking and the risk of SLE by performing an updated metaanalysis.MethodsA literature search using keywords including “lupus,” “smoking,” “cigarette,” “environmental,” “autoimmune,” and “connective tissue disease” was performed in computerized databases to identify studies addressing the relationship between cigarette smoking and SLE occurrence. A Bayesian metaanalysis was conducted by computing the log-OR between current and never smokers, and between former and never smokers. The average log-OR (subsequently converted to OR) and their corresponding 95% credible intervals (CrI) were calculated. The effect of publication time, sex, and age of patients with SLE on the effect sizes was examined by multivariate metaregression.ResultsData aggregation of 12 eligible studies comprising 3234 individuals who developed SLE and 288,336 control subjects revealed a significant association between SLE occurrence and current smoking status (OR 1.54, 95% CrI 1.06–2.25), while only a non-significant trend was demonstrated between SLE occurrence and former smoking status (OR 1.39, 95% CrI 0.95–2.08). Publication time, sex, and the mean age of patients with SLE did not explain the heterogeneity of the effect sizes.ConclusionCurrent smoking status is associated with risk of SLE. Sex and age of patients with SLE had no significant effect on the risk of SLE over time.

scholarly journals Cigarette Smoking Status, Cigarette Exposure, and Duration of Abstinence Predicting Incident Dementia and Death: A Multistate Model Approach

2021 ◽  
Vol 80 (3) ◽  
pp. 1013-1023
Author(s):  
Adrienne L. Johnson ◽  
Naomi C. Nystrom ◽  
Megan E. Piper ◽  
Jessica Cook ◽  
Derek L. Norton ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Competing Risks ◽  
Smoking Status ◽  
Risk Of Death ◽  
Incident Dementia ◽  
Smoking Exposure ◽  
Increased Risk ◽  
State Models ◽  
Never Smokers ◽  
The Impact

Background: To fully characterize the risk for dementia associated with cigarette smoking, studies must consider competing risks that hinder the observation of dementia or modify the chance that dementia occurs (i.e., death). Extant research examining the competing risks fails to account for the occurrence of death following dementia, limiting our understanding of the relation between smoking and dementia. Objective: Examine the impact of smoking status, lifetime smoking exposure, and duration of abstinence on incident dementia, death following dementia, and death without dementia. Methods: Multi-state models estimated hazard ratios (HR) for 95% confidence interval (CI) of 10,681 cognitively healthy adults for transition from baseline to dementia, baseline to death, and dementia to death based on smoking status, lifetime cigarette exposure, and abstinence duration. Results: Compared to never smokers, current smokers had increased risk of dementia (HR = 1.66; 95% CI 1.18– 2.32; p = 0.004), and death from baseline (HR = 2.98; 95% CI 2.24– 3.98; p < 0.001) and incident dementia (HR = 1.88; 95% CI 1.08– 3.27; p = 0.03). Pack years increased risk of death from baseline (HR = 1.01; 95% CI 1.00– 1.01; p < 0.001), but not dementia risk (HR = 1.00; 95% CI 1.00– 1.00; p = 0.78) or death following dementia (HR = 1.01; 95% CI 1.00– 1.01; p = 0.05). Recent quitters (quit < 10 years), compared to never smokers, had increased risk of death after baseline (HR = 2.31; 95% CI 1.55– 3.43; p < 0.001), but not dementia (HR = 1.17; 95% CI 0.73– 1.88; p = 0.52) or death following dementia (HR = 1.01; 95% CI 0.42– 2.41; p = 0.99). Conclusion: Current smoking increases the risk for dementia and death, but dementia is better attributed to smoking recency than lifetime exposure. Smoking cessation at any age might reduce these risks for cognitively healthy individuals.

Cigarette smoking and risk of infection-related mortality: A cohort study

2021 ◽  
Author(s):  
Hae Suk Cheong ◽  
Yoosoo Chang ◽  
Eun-Jeong Joo ◽  
Seungho Ryu
Keyword(s):  
Cohort Study ◽  
Cigarette Smoking ◽  
Smoking Status ◽  
Risk Of Infection ◽  
Current Smoking ◽  
South Korean ◽  
Korean Adults ◽  
Increased Risk ◽  
Related Mortality

Abstract Background Cigarette smoking is a leading cause of death worldwide and is associated with various diseases. However, studies addressing its impact on infection-related deaths are limited. This study examined the relationship between smoking and infection-related mortality. Methods A cohort of 583,034 South Korean adults who underwent annual or biennial health examinations were followed-up for infection-related deaths using national records. Cox proportional hazards regression assessed hazard ratios (HRs) and 95% confidence intervals (CIs) for infection-related mortality. Results The median follow-up was 9.1 years (maximum 18 years), and 335 infection-related deaths were identified. Current smoking, but not former smoking, was positively associated with an increased risk of infection-related mortality. After adjusting for possible confounders, the multivariable-adjusted HRs ( 95% CIs) for infection-related mortality comparing former and current smokers with never smokers were 0.94 (0.68–1.30) and 1.45 (1.05–2.02), respectively; and those for infection-related mortality by number of pack-years comparing 10–19.9 and ≥20 pack-years to &lt;10 pack-years were 1.26 (0.81–1.96) and 1.47 (1.03–2.09), respectively, while those comparing 10–19 and ≥20 cigarettes/day to &lt;10 cigarettes/day were 1.35 (0.86–2.11) and 1.54 (1.13–2.11), respectively (p for trend &lt;0.05). Individuals with ≥20 pack-years had a 2.06 times greater risk of infection-related mortality when changes in smoking status and confounders during follow-up were updated in the analysis as time-varying covariates. Conclusion Current smoking status, intensity and pack-years were associated with an increased risk of infection-related death, with the highest risk of infection-related mortality found consistently in individuals with ≥20 pack-years. Implications In this large-scale cohort study of relatively young and middle-aged South Korean adults, current smoking, smoking intensity, and pack-years were associated with an increased risk of death due to infections; in particular, a significantly increased risk of infection-related mortality was consistently found in individuals with ≥20 pack-years. When appropriate, infection-related mortality should be included in smoking-attributable mortality burdens, and effective smoking control measures should be considered to improve infection-related mortality.

scholarly journals Cigarette Smoking and Incident Stroke in Blacks of the Jackson Heart Study

2020 ◽  
Vol 9 (12) ◽  
Author(s):  
Adebamike A. Oshunbade ◽  
Wondwosen K. Yimer ◽  
Karen A. Valle ◽  
Donald Clark ◽  
Daisuke Kamimura ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Smoking Status ◽  
Jackson Heart Study ◽  
Smoking Intensity ◽  
Heart Study ◽  
Increased Risk ◽  
Significant Difference ◽  
Never Smokers ◽  
The Relationship ◽  
Dose Dependent

Background Blacks are disproportionately affected by stroke compared with whites; however, less is known about the relationship between stroke and cigarette smoking in blacks. Therefore, we evaluated the relationship between cigarette smoking and all incident stroke in the JHS (Jackson Heart Study). Methods and Results JHS participants without a history of stroke (n=4410) were classified by self‐reported baseline smoking status into current, past (smoked at least 400 cigarettes/life), or never smokers at baseline (2000–2004). Current smokers were further classified by smoking intensity (number of cigarettes smoked per day [1–19 and ≥20]) and followed up for incident stroke (through 2015). Hazard ratios (HRs) for incident stroke for current and past smoking compared with never smoking were estimated with adjusted Cox proportional hazard regression models. After adjusting for cardiovascular risk factors, the risk for stroke in current smokers was significantly higher compared with never smokers (HR, 2.48; 95% CI, 1.60–3.83) but there was no significant difference between past smokers and never smokers (HR, 1.10; 95% CI, 0.74–1.64). There was a dose‐dependent increased risk of stroke with smoking intensity (HR, 2.28 [95% CI, 1.38–3.86] and HR, 2.78 [95% CI, 1.47–5.28] for current smokers smoking 1–19 and ≥20 cigarettes/day, respectively). Conclusions In a large cohort of blacks, current cigarette smoking was associated with a dose‐dependent higher risk of all stroke. In addition, past smokers did not have a significantly increased risk of all stroke compared with never smokers, which suggests that smoking cessation may have potential benefits in reducing the incidence of stroke in blacks.

scholarly journals Cigarette smoking and the risk of systemic lupus erythematosus, overall and by anti-double stranded DNA antibody subtype, in the Nurses’ Health Study cohorts

2017 ◽  
Vol 77 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Medha Barbhaiya ◽  
Sara K Tedeschi ◽  
Bing Lu ◽  
Susan Malspeis ◽  
David Kreps ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cigarette Smoking ◽  
Lupus Erythematosus ◽  
Cox Regression ◽  
Smoking Status ◽  
Clinical Manifestations ◽  
Health Study ◽  
Systemic Lupus ◽  
Double Stranded Dna ◽  
Never Smokers

ObjectivesSystemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease, subtyped according to clinical manifestations and autoantibodies. Evidence concerning cigarette smoking and SLE risk has been conflicting. We investigated smoking and SLE risk, overall and by anti-double stranded DNA (dsDNA) presence, in two prospective cohort studies.MethodsThe Nurses’ Health Study (NHS) enrolled 121 701 US female nurses in 1976; Nurses’ Health Study II (NHSII) enrolled 116 430 in 1989. Lifestyle, environmental and medical data were collected through biennial questionnaires. Incident SLE was confirmed by medical record review. Cox regression models estimated HRs of SLE, overall and by dsDNA subtype, in association with time-varying smoking status and cumulative smoking pack-years through the 2-year cycle prior to diagnosis, controlling for potential confounders.ResultsAmong 286 SLE cases identified (159 in NHS (1978–2012) and 127 in NHSII (1991–2013)), mean age was 49.2 (10.3) years and 42% were dsDNA+ at SLE diagnosis. At baseline, 45% of women had ever smoked, 51% of whom currently smoked. Compared with never smokers, current smokers had increased dsDNA+ SLE risk (HR 1.86 (1.14–3.04)), whereas past smokers did not (HR 1.31 (0.85–2.00)). Women who smoked >10 pack-years (vs never) had an elevated dsDNA+ SLE risk (HR 1.60(95% CI 1.04 to 2.45)) compared with never smokers. No associations were observed between smoking status or pack-years and overall SLE or dsDNA− SLE.ConclusionStrong and specific associations of current smoking and >10 pack-years of smoking with dsDNA+ SLE were observed. This novel finding suggests smoking is involved in dsDNA+ SLE pathogenesis.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

scholarly journals Associations between smoking and blood-group, and the risk of dyslipidaemia amongst French women

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. J. MacDonald ◽  
A. L. Madika ◽  
G. Severi ◽  
A. Fournier ◽  
M. C. Boutron-Ruault
Keyword(s):  
Blood Group ◽  
Smoking Status ◽  
Effect Modification ◽  
Blood Groups ◽  
Cross Sectional ◽  
Increased Risk ◽  
Cardio Vascular Disease ◽  
Never Smokers ◽  
Cardio Vascular ◽  
Incident Cases

AbstractDyslipidaemia is a major risk factor for cardio-vascular disease, as it promotes atherosclerosis. While cross-sectional studies have identified higher serum cholesterol amongst individuals with the A blood group, there is less evidence from prospective studies whether this translates into a higher risk of dyslipidaemia that requires treatment, nor if this genetic factor interacts with smoking status. This study aimed to prospectively determine potential associations between smoking, ABO blood groups, and risk of incident dyslipidaemia requiring treatment, and to assess associations over strata of blood ABO group. We assessed associations between blood ABO group, smoking and dyslipidaemia in 74,206 women participating in the E3N cohort. We included women who did not have cardiovascular disease at baseline. Logistic regression was used to determine associations between ABO group, smoking and prevalent dyslipidaemia at baseline. Cox proportional hazard models were then used to determine if blood ABO group and smoking were associated with the risk of incident dyslipidaemia, amongst women free of dyslipidaemia at baseline. At baseline 28,281 women with prevalent dyslipidaemia were identified. Compared to the O-blood group, the non-O blood group was associated higher odds of with prevalent dyslipidaemia (ORnon-O = 1.09 [1.06: 1.13]). Amongst the women free of dyslipidaemia at baseline, 6041 incident cases of treated dyslipidaemia were identified during 454,951 person-years of follow-up. The non-O blood groups were associated with an increased risk of dyslipidaemia when compared to the O-group (HRnon-O = 1.16 [1.11: 1.22]), specifically the A blood-group (HRA = 1.18 [1.12: 1.25]). Current smokers were associated with an increased risk of incident dyslipidaemia (HR smokers = 1.27 [1.16: 1.37]), compared to never-smokers. No evidence for effect modification between smoking and ABO blood group was observed (p-effect modification = 0.45), although the highest risk was observed among AB blood group women who smoked (HR = 1.76 [1.22: 2.55]). In conclusion, the non-O blood groups, specifically the A group were associated with an increased risk of dyslipidaemia. Current smokers were associated with a 30% increased risk of dyslipidaemia. These results could aid in personalised approaches to the prevention of cardiovascular risk-factors.

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