29 October 2018 In Cardiovascular System

BACKGROUND: Alcohol-induced cardiotoxicity is incompletely understood. Specifically, the long-term impact of alcohol use on ventricular remodeling or dysfunction, its modulators, and effect thresholds among young adults remain controversial.

OBJECTIVES: The authors sought to evaluate a potential relationship between alcohol intake and cardiac remodeling, assessed by echocardiography, over 20 years of follow-up.

METHODS: Among the CARDIA (Coronary Artery Risk Development in Young Adults) study cohort, the authors studied all subjects without baseline heart disorders who provided adequate information on their drinking habits and underwent echocardiographic evaluation at years 5 and 25 of the study. The echocardiographic outcomes were left ventricular (LV) ejection fraction, indexed LV end-diastolic volume and LV mass, and left atrial diameter. Participants were grouped according to their weighted-average weekly drinking habits. An additional analysis used the estimated cumulative alcohol consumption. Regression models and multivariable fractional polynomials were used to evaluate the association between alcohol consumption and the outcomes.

RESULTS: Among the 2,368 participants, alcohol consumption was an independent predictor of higher indexed LV mass (p = 0.014) and indexed LV end-diastolic volume (p = 0.037), regardless of sex. No significant relationship between alcohol intake and LV ejection fraction was found. Drinking predominantly wine was associated with less cardiac remodeling and there was a nonsignificant trend for a harmful effect of binge drinking.

CONCLUSIONS: After 20 years of follow-up, alcohol intake was associated with adverse cardiac remodeling, although it was not related with LV systolic dysfunction in this initially healthy young cohort. Our results also suggest that drinking predominantly wine associates with less deleterious findings in cardiac structure.

27 September 2018 In Cardiovascular System

BACKGROUND/OBJECTIVES: Low/moderate alcohol consumption seems to be protective against cardiovascular disease (CVD). This study aimed to investigate the association of wine/beer consumption with the 10-year CVD incidence.

SUBJECTS/METHODS: During 2001-2002, 3042 CVD-free adults consented to participate in the ATTICA study; of them 2583 completed the 10-year follow-up (85% participation rate), but precise information about fatal/nonfatal CVD incidence (myocardial infarction, angina pectoris, cardiac ischemia, heart failure, chronic arrhythmias, and stroke) was available in 2020 participants (overall retention rate 66%). Alcohol/ethanol intake and the alcoholic beverages consumed were assessed; participants were categorized into three groups (no use; 1 glass/week).

RESULTS: Alcohol drinking was reported by 56% of the participants who did not develop a CVD event and 49% of those who had (p = 0.04); whereas ethanol intake was 14 +/- 16 g among those who did not had an event vs. 21 +/- 18 g among those who had a CVD event (p < 0.001). A strong inverse and similar association between low wine/beer intake (20 g/day had CVD-risk HRs (95% CI) of 0.60 (0.40-0.98), 1.22 (0.60-1.14), and 1.81 (0.70-4.61), respectively.

CONCLUSIONS: This study revealed similar results of low wine/beer consumption against CVD incidence, mainly due to its implication on low-grade chronic inflammation.

06 September 2018 In Cardiovascular System

BACKGROUND: Studies have shown that alcohol intake trajectories differ in their associations with biomarkers of cardiovascular functioning, but it remains unclear if they also differ in their relationship to actual coronary heart disease (CHD) incidence. Using multiple longitudinal cohort studies, we evaluated the association between long-term alcohol consumption trajectories and CHD.

METHODS: Data were drawn from six cohorts (five British and one French). The combined analytic sample comprised 35,132 individuals (62.1% male; individual cohorts ranging from 869 to 14,247 participants) of whom 4.9% experienced an incident (fatal or non-fatal) CHD event. Alcohol intake across three assessment periods of each cohort was used to determine participants' intake trajectories over approximately 10 years. Time to onset for (i) incident CHD and (ii) fatal CHD was established using surveys and linked medical record data. A meta-analysis of individual participant data was employed to estimate the intake trajectories' association with CHD onset, adjusting for demographic and clinical characteristics.

RESULTS: Compared to consistently moderate drinkers (males: 1-168 g ethanol/week; females: 1-112 g ethanol/week), inconsistently moderate drinkers had a significantly greater risk of incident CHD [hazard ratio (HR) = 1.18, 95% confidence interval (CI) = 1.02-1.37]. An elevated risk of incident CHD was also found for former drinkers (HR = 1.31, 95% CI = 1.13-1.52) and consistent non-drinkers (HR = 1.47, 95% CI = 1.21-1.78), although, after sex stratification, the latter effect was only evident for females. When examining fatal CHD outcomes alone, only former drinkers had a significantly elevated risk, though hazard ratios for consistent non-drinkers were near identical. No evidence of elevated CHD risk was found for consistently heavy drinkers, and a weak association with fatal CHD for inconsistently heavy drinkers was attenuated following adjustment for confounding factors.

CONCLUSIONS: Using prospectively recorded alcohol data, this study has shown how instability in drinking behaviours over time is associated with risk of CHD. As well as individuals who abstain from drinking (long term or more recently), those who are inconsistently moderate in their alcohol intake have a higher risk of experiencing CHD. This finding suggests that policies and interventions specifically encouraging consistency in adherence to lower-risk drinking guidelines could have public health benefits in reducing the population burden of CHD. The absence of an effect amongst heavy drinkers should be interpreted with caution given the known wider health risks associated with such intake.

TRIAL REGISTRATION: ClinicalTrials.gov, NCT03133689

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