scholarly journals Binge drinking and risk of ischemic heart disease and stroke: a study of pooled Norwegian health surveys

2021 ◽  
Author(s):  
Eirik Degerud ◽  
Gudrun Høiseth ◽  
Jørg Mørland ◽  
Inger Ariansen ◽  
Sidsel Graff-Iversen ◽  
...  
Keyword(s):  
Heart Disease ◽  
Confidence Interval ◽  
Ischemic Heart Disease ◽  
Binge Drinking ◽  
Alcohol Intake ◽  
Hazard Ratio ◽  
Adjusted Hazard Ratio ◽  
Ischemic Heart ◽  
Average Alcohol ◽  
Binge Drinkers

Abstract Norwegian health survey data (1987 – 2003) were analysed to determine if binge drinking increases the risk of incident major events from ischemic heart disease (IHD) and stroke. Among current drinkers reporting average alcohol intakes between 2 to 60 g/day (n = 44,476), frequent binge drinking (5+ units ≥ once per month) was not associated with a greater risk of IHD (adjusted hazard ratio = 0.91, 95% confidence interval: 0.76, 1.09) nor stroke (adjusted hazard ratio = 0.98, 95% confidence interval: 0.81, 1.19), in comparison with participants who reported that they never or only infrequently (<once per month) had episodes of binge drinking. Participants with an average alcohol intake between 2 – 60 g/day had a lower risk of IHD in comparison with participants with very low intakes (<2 g/day) both among frequent binge drinkers (adjusted hazard ratio = 0.67, 95% confidence interval: 0.56, 0.80) and among never/infrequent binge drinkers (adjusted hazard ratio = 0.75, 95% confidence interval: 0.67, 0.84). The findings suggest that frequent binge drinking does not, independently of the average alcohol intake, increase the risk of incident IHD or stroke events. However, the findings should be interpreted in light of the limitations of the study design.

scholarly journals Increased Remnant Cholesterol Explains Part of Residual Risk of All-Cause Mortality in 5414 Patients with Ischemic Heart Disease

2016 ◽  
Vol 62 (4) ◽  
pp. 593-604 ◽  
Author(s):  
Anne-Marie K Jepsen ◽  
Anne Langsted ◽  
Anette Varbo ◽  
Lia E Bang ◽  
Pia R Kamstrup ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Ldl Cholesterol ◽  
Hdl Cholesterol ◽  
Hazard Ratio ◽  
Residual Risk ◽  
Ischemic Heart ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Remnant Cholesterol

Abstract BACKGROUND Increased concentrations of remnant cholesterol are causally associated with increased risk of ischemic heart disease. We tested the hypothesis that increased remnant cholesterol is a risk factor for all-cause mortality in patients with ischemic heart disease. METHODS We included 5414 Danish patients diagnosed with ischemic heart disease. Patients on statins were not excluded. Calculated remnant cholesterol was nonfasting total cholesterol minus LDL and HDL cholesterol. During 35836 person-years of follow-up, 1319 patients died. RESULTS We examined both calculated and directly measured remnant cholesterol; importantly, however, measured remnant cholesterol made up only 9% of calculated remnant cholesterol at nonfasting triglyceride concentrations <1 mmol/L (89 mg/dL) and only 43% at triglycerides >5 mmol/L (443 mg/dL). Multivariable-adjusted hazard ratios for all-cause mortality compared with patients with calculated remnant cholesterol concentrations in the 0 to 60th percentiles were 1.2 (95% CI, 1.1–1.4) for patients in the 61st to 80th percentiles, 1.3 (1.1–1.5) for the 81st to 90th percentiles, 1.5 (1.1–1.8) for the 91st to 95th percentiles, and 1.6 (1.2–2.0) for patients in the 96th to 100th percentiles (trend, P < 0.001). Corresponding values for measured remnant cholesterol were 1.0 (0.8–1.1), 1.2 (1.0–1.4), 1.1 (0.9–1.5), and 1.3 (1.1–1.7) (trend, P = 0.006), and for measured LDL cholesterol 1.0 (0.9–1.1), 1.0 (0.8–1.2), 1.0 (0.8–1.3), and 1.1 (0.8–1.4) (trend, P = 0.88). Cumulative survival was reduced in patients with calculated remnant cholesterol ≥1 mmol/L (39 mg/dL) vs <1 mmol/L [log-rank, P = 9 × 10−6; hazard ratio 1.3 (1.2–1.5)], but not in patients with measured LDL cholesterol ≥3 mmol/L (116 mg/dL) vs <3 mmol/L [P = 0.76; hazard ratio 1.0 (0.9–1.1)]. CONCLUSIONS Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.

scholarly journals High Cardiovascular Risk in Older Men With Severe Peripheral Artery Calcification on High-Resolution Peripheral QCT Scans

2021 ◽  
Vol 41 (5) ◽  
pp. 1818-1829
Author(s):  
Pawel Szulc ◽  
Catherine Planckaert ◽  
Dominique Foesser ◽  
Janina Patsch ◽  
Roland Chapurlat
Keyword(s):  
Heart Disease ◽  
Cardiovascular Risk ◽  
Ischemic Heart Disease ◽  
Cardiovascular Event ◽  
Major Adverse Cardiovascular Event ◽  
Older Men ◽  
Hazard Ratio ◽  
Ischemic Heart ◽  
High Cardiovascular Risk ◽  
Adverse Cardiovascular Event

Objective: Arterial calcification is associated with high cardiovascular risk. Our aim was to assess the utility of peripheral arterial calcification (PAC) in distal forearm and distal leg for the prediction of acute coronary syndrome (ACS) and major adverse cardiovascular event in older men. Approach and Results: In 815 home-dwelling older men, PAC was assessed on the scans of distal forearm and leg obtained by high-resolution peripheral quantitative computed tomography. PAC score (0–12) was calculated on the basis of the number and severity in small peripheral arteries. The information on ACS and major adverse cardiovascular event was collected prospectively for 8 years. PAC severity increased with age and body mass index ( P <0.001). Median PAC score was higher in men with ischemic heart disease or pharmacologically treated diabetes ( P <0.001). After adjustment for confounders, the risk of ACS was higher in men with severe PAC (6+) versus men with lower PAC (0–5; hazard ratio, 3.86 [95% CI, 1.65–9.02], P <0.005). After adjustment for confounders, the risk of major adverse cardiovascular event was higher in men with severe PAC (6+) versus men with lower PAC (hazard ratio, 2.58 [95% CI, 1.41–4.72], P <0.005). In men who did not have cardiovascular risk factors, severe PAC was associated with higher risk of ACS, for example, in men who did not self-report ischemic heart disease (hazard ratio, 6.62 [95% CI, 2.16–20.23], P <0.001). Conclusions: Severe PAC is associated with higher risk of ACS and major adverse cardiovascular event in older home-dwelling men, also in men without known ischemic heart disease. Incidentally found severe PAC can be a serious warning indicating high cardiovascular risk.

scholarly journals The Incidence of Ischemic Heart Disease and Mortality in People with Subclinical Hypothyroidism: Reanalysis of the Whickham Survey Cohort

2010 ◽  
Vol 95 (4) ◽  
pp. 1734-1740 ◽  
Author(s):  
Salman Razvi ◽  
Jola U. Weaver ◽  
Mark P. Vanderpump ◽  
Simon H. S. Pearce
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Subclinical Hypothyroidism ◽  
Subsequent Treatment ◽  
Hazard Ratio ◽  
Community Dwelling ◽  
Ischemic Heart ◽  
Vascular Events ◽  
Thyroid Autoantibody

Abstract Context: The Whickham Survey evaluated vascular events over 20 yr in community-dwelling subjects stratified by thyroid function and thyroid autoantibody status. No association between ischemic heart disease (IHD) and a composite autoimmune thyroid disease group, comprising individuals with subclinical hypothyroidism (SCH), with positive thyroid antibodies or those using levothyroxine, was found. This result appears to be at odds with the findings of other cohort studies. Objective: The objective of the study was to evaluate incident IHD and mortality in participants in relation to their thyroid status. Outcomes, Design, and Participants: Data were reanalyzed assessing incident IHD events and mortality during 20 yr of follow-up in individuals with endogenous SCH (n = 97; TSH 6.0–15 mIU/liter) vs. the euthyroid group (n = 2279), who were IHD free at baseline. Results: Incident IHD was significantly higher in the SCH group [adjusted hazard ratio 1.76 (95% confidence interval 1.15–2.71); P = 0.01]. IHD mortality was also increased in the SCH group [hazard ratio of 1.79 (1.02–3.56); P = 0.05]. These findings lost their significance when subsequent treatment with levothyroxine was excluded from the regression model. There was no difference in all-cause mortality between the groups. Conclusion: In the Whickham Survey, there is an association between incident IHD events and IHD-related mortality with SCH over the 20 yr of follow-up. Furthermore, subsequent treatment of SCH with levothyroxine appears to attenuate IHD-related morbidity and mortality, and this may explain why some other longitudinal studies of SCH have not shown such an association; properly designed controlled trials of treatment of SCH are required to answer this question definitively.

scholarly journals Coagulation Factors and the Risk of Ischemic Heart Disease

2018 ◽  
Vol 11 (1) ◽  
Author(s):  
Jie V. Zhao ◽  
C. Mary Schooling
Keyword(s):  
Heart Disease ◽  
Single Nucleotide Polymorphisms ◽  
Confidence Interval ◽  
Ischemic Heart Disease ◽  
Plasminogen Activator ◽  
Odds Ratio ◽  
Coagulation Factors ◽  
Ischemic Heart ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide

Background: Coagulation plays a role in ischemic heart disease (IHD). However, which coagulation factors are targets of intervention is unclear. We assessed how genetically predicted vWF (von Willebrand factor), ETP (endogenous thrombin potential), FVIII (factor VIII), d -dimer, tPA (tissue-type plasminogen activator), and PAI (plasminogen activator inhibitor)-1 affected IHD. We similarly estimated effects on lipids to determine whether any associations were independent of lipids. Methods and Results: Separate sample instrumental variable analysis with genetic instruments, that is, Mendelian randomization, was used to obtain unconfounded estimates of effects on IHD using extensively genotyped studies of coronary artery disease/myocardial infarction, CARDIoGRAMplusC4D Metabochip (64 374 cases, 130 681 controls) and CARDIoGRAMplusC4D 1000 Genomes (60 801 cases, 123 504 controls), and on lipids using the Global Lipids Genetics Consortium Results (n=196 475). Genetically predicted ETP was positively associated with IHD (odds ratio, 1.05 per log-transformed SD; 95% confidence interval, 1.03–1.07) based on 15 single-nucleotide polymorphisms, as were vWF (odds ratio, 1.05 per SD; 95% confidence interval, 1.02–1.08) and FVIII (odds ratio, 1.06 per SD; 95% confidence interval, 1.03–1.09) based on 16 and 6 single-nucleotide polymorphisms, respectively, but the latter associations were null after considering pleiotropy. vWF and FVIII were associated with higher LDL (low-density lipoprotein) cholesterol, but not after considering pleiotropy. Genetically predicted d -dimer, tPA, and PAI-1 were not clearly associated with IHD or lipids based on 3, 3, and 5 single-nucleotide polymorphisms, respectively. Conclusions: ETP may affect IHD. Assessing the role of its drivers in more precisely phenotyped studies of IHD could be worthwhile.

scholarly journals Association between short-term exposure to sulfur dioxide and carbon monoxide and ischemic heart disease and non-accidental death in Changsha city, China

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0251108
Author(s):  
Zenghui Xu ◽  
Lili Xiong ◽  
Donghui Jin ◽  
Jie Tan
Keyword(s):  
Carbon Monoxide ◽  
Heart Disease ◽  
Sulfur Dioxide ◽  
Confidence Interval ◽  
Ischemic Heart Disease ◽  
Additive Models ◽  
Ischemic Heart ◽  
Accidental Death ◽  
Short Term ◽  
Short Term Exposure

Background To investigate the effects of short-term exposure to sulfur dioxide (SO2) and carbon monoxide (CO) in the central and southern China areas on ischemic heart disease (IHD) and non-accidental deaths. Method We investigated the associations between short-term exposure to SO2 and CO in a city in south-central China and IHD and non-accidental death using a time-series design and generalized additive models with up to a 5-day lag adjusting for day of the week, temperature, air pressure, wind speed, and relative humidity. The relative risks of IHD and non-accidental death per 10-unit increase in SO2 and CO were derived from zero to five days in single-pollutant models. Results Between 2016 and 2018, a total of 10,507 IHD and 44,070 non-accidental deaths were identified. The largest significant relative risk for IHD death was lag 02 for both SO2 (1.080; 95% confidence interval: 1.075–1.084) and CO (5.297; 95% confidence interval: 5.177–5.418) in single-pollutants models. A significant association was shown at all lag multiple-day moving averages. Two-pollutant models identified an association between SO2 and mortality when adjusting for CO. In stratified analyses, SO2 exhibited a stronger association with death during the cold season, while CO exhibited a stronger association with mortality from IHD during the warm season. The risk of death was more robust in the elderly for both pollutants, but was greater in men for CO and in women for SO2. Conclusions Overall, we found an association between short-term exposure to low-level SO2 and CO and the risk of IHD and non-accidental death.

Effect of Glucagon on Ischemic Heart Disease and Its Risk Factors: A Mendelian Randomization Study

2020 ◽  
Vol 105 (8) ◽  
pp. e2778-e2788
Author(s):  
Jack C M Ng ◽  
C Mary Schooling
Keyword(s):  
Risk Factors ◽  
Heart Disease ◽  
Confidence Interval ◽  
Ischemic Heart Disease ◽  
Odds Ratio ◽  
Mendelian Randomization ◽  
Ischemic Heart ◽  
Fasting Insulin ◽  
Inverse Variance

Abstract Context Glucagon acts reciprocally with insulin to regular blood glucose. However, the effect of glucagon on cardiovascular disease has not been widely studied. It has been suggested that insulin may increase the risk of ischemic heart disease. Objective To investigate whether glucagon, the main counteracting hormone of insulin, plays a role in development of ischemic heart disease. Design, Setting, and Participants In this 2-sample Mendelian randomization study, we estimated the causal effect of glucagon on ischemic heart disease and its risk factors using the inverse-variance weighted method with multiplicative random effects and multiple sensitivity analyses. Genetic associations with glucagon and ischemic heart disease and its risk factors, including type 2 diabetes and fasting insulin, were obtained from publicly available genome-wide association studies. Main Outcome Measure Odds ratio for ischemic heart disease and its risk factors per 1 standard deviation change in genetically predicted glucagon. Results Twenty-four single-nucleotide polymorphisms strongly (P &lt; 5 × 10−6) and independently (r2 &lt; 0.05) predicting glucagon were obtained. Genetically predicted higher glucagon was associated with an increased risk of ischemic heart disease (inverse-variance weighted odds ratio, 1.03; 95% confidence interval, 1.0003-1.05) but not with type 2 diabetes (inverse-variance weighted odds ratio, 0.998, 95% confidence interval, 0.97-1.03), log-transformed fasting insulin (inverse-variance weighted beta, 0.002, 95% confidence interval, -0.01 to 0.01), other glycemic traits, blood pressure, reticulocyte, or lipids. Conclusion Glucagon might have an adverse impact on ischemic heart disease. Relevance of the underlying pathway to existing and potential interventions should be investigated.

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