Cardiovascular System

Cardiovascular System (11)

We tested whether teetotalism explains the upturn in cardiovascular risk for non-drinkers and whether wine is a more favorable alcohol type. We studied 115,592 men and women aged 40-44 years who participated in the age 40 program in Norway in 1994-1999 and were followed for an average of 16 years with 550 cardiovascular deaths. Self-reported number of glasses of beer, wine and spirits during 14 days was transformed to alcohol units/day. One unit is approximately 8 grams of pure alcohol. The mean and median number of alcohol units/day were 0.70 and 0.46. Teetotallers had higher risk of dying from cardiovascular disease than alcohol consumers, multivariate adjusted hazard ratio (95% CI) 1.97 (1.52-2.56). The use of alcohol-related deaths as endpoint substantiated a selection of previous alcohol users to the teetotal group. Without teetotallers there was no association between alcohol consumption and cardiovascular disease mortality. However, the multivariate adjusted hazard ratio per one unit/day of wine was 0.76 (0.58-0.99). The corresponding figures for beer and spirits were 1.04 (0.94-1.15) and 0.98 (0.75-1.29). The upturn in risk for non-drinkers could be explained by a higher risk for teetotallers who likely included previous alcohol users or teetotalers who started to drink during follow-up. Wine gave the most favorable risk estimates
OBJECTIVES: The aim of this study was to assess the hypothesis that alcohol consumption is associated with onset of atrial fibrillation (AF) and/or heart failure (HF). BACKGROUND: The connection between ethanol intake and AF or HF remains controversial. METHODS: The study population was 22,824 AF- or HF-free subjects (48% men, age >/=35 years) randomly recruited from the general population included in the Moli-sani study, for whom complete data on HF, AF, and alcohol consumption were available. The cohort was followed up to December 31, 2015, for a median of 8.2 years (183,912 person-years). Incident cases were identified through linkage to the Molise regional archive of hospital discharges. Hazard ratios were calculated using Cox proportional hazard models and cubic spline regression. RESULTS: A total of 943 incident cases of HF and 554 of AF were identified. In comparison with never drinkers, both former and occasional drinkers showed comparable risk for developing HF. Drinking alcohol in the range of 1 to 4 drinks/day was associated with a lower risk for HF, with a 22% maximum risk reduction at 20 g/day, independent of common confounders. In contrast, no association of alcohol consumption with onset of AF was observed. Very similar results were obtained after restriction of the analyses to regular or only wine drinkers or according to sex, age, social status, or adherence to the Mediterranean diet. CONCLUSIONS: Consumption of alcohol in moderation was associated with a lower incidence of HF but not with development of AF
BACKGROUND: Compelling evidence suggests that excessive alcohol consumption increases the risk of atrial fibrillation (AF), but the effect of light-moderate alcohol consumption is less certain. We investigated the association between alcohol consumption within recommended limits and AF risk in a light-drinking population. METHODS AND RESULTS: Among 47 002 participants with information on alcohol consumption in a population-based cohort study in Norway, conducted from October 2006 to June 2008, 1697 validated AF diagnoses were registered during the 8 years of follow-up. We used Cox proportional hazard models with fractional polynomials to analyze the association between alcohol intake and AF. Population attributable risk for drinking within the recommended limit (ie, at most 1 drink per day for women and 2 drinks per day for men without risky drinking) compared with nondrinking was also calculated. The average alcohol intake was 3.8+/-4.8 g/d. The adjusted hazard ratio for AF was 1.38 (95% confidence interval, 1.06-1.80) when we compared participants consuming >7 drinks per week with abstainers. When we modeled the quantity of alcohol intake as a continuous variable, the risk increased in a curvilinear manner. It was higher with heavier alcohol intake, but there was virtually no association at
AIMS: The aim of this study was to clarify the relationship between drinking and metabolically healthy status in men with normal weight, overweight and obesity. METHODS: The subjects were Japanese men aged from 35 to 60 years (n=31781) and they were divided by daily amount of drinking (g ethanol) into light (/=22 and /=44 and /=66) drinkers. Metabolically healthy subjects were defined as those without hypertension, dyslipidemia and diabetes. RESULTS: The percentage of metabolically healthy subjects was much lower in the overweight (BMI>/=25 and /=30) groups than in the normal weight group (BMI>/=18.5 and
Introduction The benefits of alcohol consumption for cardiovascular and metabolic health may have been overstated due to inappropriate comparisons with abstainers and inadequate control for confounding factors including physical activity and mental health. We examined alcohol consumption and cardio-metabolic health in a cohort of young Australian adults overcoming these limitations. Methods Cross-sectional data of a cohort of 2200 participants (age range 25-36 years) from the 2004-06 Childhood Determinants of Adult Health were used. Alcohol consumption was assessed from questionnaire and cardio-metabolic risk factors were measured in clinics. Linear and log binomial regression were used to examine total alcohol consumption (categories: none 0 g/day; light >0-10 g/day [reference]; moderate >10-20 g/day; heavy >20-30 g/day; very heavy >30 g/day) against dichotomous metabolic syndrome and its components: waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure and glucose. Covariates included socio-demographics, smoking, diet, physical activity, fitness, depression and anxiety. Results Of the 2220 participants (48% males, mean (standard deviation) age 29.5 (2.5) years), most were classified in the 'light drinking' group (54.2%), less were in the 'non-drinking' (13.2%), 'heavy' (5.2%) or 'very heavy' (5.5%) drinking groups. Only moderate drinking was associated with a significantly lower prevalence of metabolic syndrome (prevalence ratio = 0.64, p
BACKGROUND: Observational studies show moderate alcohol use negatively associated with ischemic heart disease (IHD) and cardiovascular disease (CVD). However, healthier attributes among moderate users compared to never users may confound the apparent association. A potentially less biased way to examine the association is Mendelian randomization, using alcohol metabolizing genes which influence alcohol use. METHODS: We used instrumental variable analysis with aldehyde dehydrogenase 2 (ALDH2) genotypes (AA/GA/GG) as instrumental variables for alcohol use to examine the association of alcohol use (10 g ethanol/day) with CVD risk factors (blood pressure, lipids and glucose) and morbidity (self-reported IHD and CVD) among men in the Guangzhou Biobank Cohort Study. RESULTS: ALDH2 genotypes were a credible instrument for alcohol use (F-statistic 74.6). Alcohol was positively associated with HDL-cholesterol (0.05 mmol/L per alcohol unit, 95% confidence interval (CI) 0.02 to 0.08) and diastolic blood pressure (1.15 mmHg, 95% CI 0.23 to 2.07) but not with systolic blood pressure (1.00 mmHg, 95% CI -0.74 to 2.74), LDL-cholesterol (0.03 mmol/L, 95% CI -0.03 to 0.08), log transformed triglycerides (0.03 mmol/L, 95% CI -0.01 to 0.08) or log transformed fasting glucose (0.01 mmol/L, 95% CI -0.006 to 0.03), self-reported CVD (odds ratio (OR) 0.98, 95% CI 0.76 to 1.27) or self-reported IHD (OR 1.10, 95% CI 0.83 to 1.45). CONCLUSION: Low to moderate alcohol use among men had the expected effects on most CVD risk factors but not fasting glucose. Larger studies are needed to confirm the null associations with IHD, CVD and fasting glucose
BACKGROUND: Alcohol is a possible risk factor for abdominal aortic aneurysm (AAA), but evidence from individual studies is weak and inconsistent. Existing narrative reviews suggest the possibility of non-linear associations. The aim here was to quantify any association using a systematic literature review, followed by dose-response meta-analysis of prospective studies. METHODS: MEDLINE, Embase and Web of Science were searched systematically to January 2017 for relevant prospective studies of alcohol consumption and AAA risk. Summary estimates of highest versus lowest levels of consumption, and linear and non-linear dose-response curves were quantified using random-effects models. RESULTS: Eleven relevant cohorts were identified describing results from 3580 individuals with among 473 092 participants. Data were extracted from ten cohorts for meta-analyses of high versus low levels of alcohol consumption (risk ratio for AAA 0.93, 95 per cent c.i. 0.78 to 1.11; P = 0.4, I2 = 47 per cent). The linear dose-response risk ratio for AAA, derived from 11 cohorts, was 1.00 (0.97 to 1.04) per 8 g alcohol per day (P = 0.9, I2 = 73 per cent). Non-linear dose-response results showed a tick-shaped curve with lower risk up to 2 units/day, but increasing risk beyond that (P = 0.05). The increase in risk beyond 2 units/day was stronger in men than in women. CONCLUSION: Although the linear dose-response analysis revealed little evidence of an association between alcohol consumption and AAA risk, a tick-shaped trend in the association was observed. This non-linear dose-response analysis revealed reduced risks for alcohol consumption below 2 units/day, masking increased risks for 2 or more units/day
BACKGROUND: Whilst high levels of alcohol consumption are known to be associated with atrial fibrillation (AF), it is unclear if any level of alcohol consumption can be recommended to prevent the onset of the condition. The aim of this review is to characterise the association between chronic alcohol intake and incident AF. METHODS AND RESULTS: Electronic literature searches were undertaken using PubMed and Embase databases up to 1 February 2016 to identify studies examining the impact of alcohol on the risk of incident AF. Prospective studies reporting on at least three levels of alcohol intake and published in English were eligible for inclusion. Studies of a retrospective or case control design were excluded. The primary study outcome was development of incident AF. Consistent with previous studies, high levels of alcohol intake were associated with an increased incident AF risk (HR 1.34, 95% CI 1.20-1.49, p
BACKGROUND AND AIMS: Several studies have reported a significant inverse association of light to moderate alcohol consumption with coronary heart disease (CHD). However, studies assessing the relationship between alcohol consumption and atherosclerosis have reported inconsistent results. The current study was conducted to determine the relationship between alcohol consumption and aortic calcification. METHODS: We addressed the research question using data from the population-based ERA-JUMP Study, comprising of 1006 healthy men aged 40-49 years, without clinical cardiovascular diseases, from four race/ethnicities: 301 Whites, 103 African American, 292 Japanese American, and 310 Japanese in Japan. Aortic calcification was assessed by electron-beam computed tomography and quantified using the Agatston method. Alcohol consumption was categorized into four groups: 0 (non-drinkers), =1 (light drinkers), >1 to =3 (moderate drinkers) and >3 drinks per day (heavy drinkers) (1 drink = 12.5 g of ethanol). Tobit conditional regression and ordinal logistic regression were used to investigate the association of alcohol consumption with aortic calcification after adjusting for cardiovascular risk factors and potential confounders. RESULTS: The study participants consisted of 25.6% nondrinkers, 35.3% light drinkers, 23.5% moderate drinkers, and 15.6% heavy drinkers. Heavy drinkers [Tobit ratio (95% CI) = 2.34 (1.10, 4.97); odds ratio (95% CI) = 1.67 (1.11, 2.52)] had significantly higher expected aortic calcification score compared to nondrinkers, after adjusting for socio-demographic and confounding variables. There was no significant interaction between alcohol consumption and race/ethnicity on aortic calcification. CONCLUSIONS: Our findings suggest that heavy alcohol consumption may be an independent risk factor for atherosclerosis


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