Next Article in Journal
Effects of Family-Based Interventions Using Mobile Apps on Youth’s Physical Activity: A Systematic Review
Previous Article in Journal
Association between Metformin Use and Risk of Total Knee Arthroplasty and Degree of Knee Pain in Knee Osteoarthritis Patients with Diabetes and/or Obesity: A Retrospective Study
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:

Is Alcohol Consumption Associated with a Lower Risk of Cardiovascular Events in Patients Treated with Statins? An Observational Real-World Experience

The Intermountain Medical Center Heart Institute, Salt Lake City, UT 84107, USA
The Cardiology Division, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT 84108, USA
Rocky Mountain University of Health Professions, Provo, UT 84606, USA
Division of Cardiovascular Medicine, Department of Medicine, Stanford University, Stanford, CA 94305, USA
Author to whom correspondence should be addressed.
J. Clin. Med. 2022, 11(16), 4797;
Submission received: 20 July 2022 / Revised: 13 August 2022 / Accepted: 15 August 2022 / Published: 17 August 2022
(This article belongs to the Section Cardiovascular Medicine)


Alcohol consumption has long been associated with cardiovascular (CV) benefit, but it also has adverse potential. Statins are currently widely used for CV prevention. We evaluated whether alcohol use is associated with lower CV risk in patients on statins. We searched Intermountain Medical Center cardiac catheterization laboratory medical records for patients with a prescription history of statin use or non-use and a self-report of alcohol use or non-use. Alcohol and statin prescription data were available together with long-term (mean [SD], 4.4 [2.4] years) major adverse CV events (MACE, including death, myocardial infarction, stroke, and heart failure hospitalizations) in 1701 patients at primary and 3266 patients at secondary CV risk. MACE rates were lower for primary prevention alcohol users than non-users not on statins (adjusted hazard ratio [adj-HR] 0.50 (95% CI 0.33, 0.78, p = 0.002), but not for those on statins (adj-HR 0.84, CI 0.54, 1.32, p = 0.45). MACE rates for secondary prevention were not reduced by alcohol consumption either in statin non-users or users (adj HR 1.18, CI 0.85, 1.64, p = 0.33; adj HR 1.08, CI 0.87, 1.35, p = 0.45, respectively). These findings, together with other recent supportive studies, can help inform personal choices in alcohol consumption and professional society recommendations for CV prevention.

1. Introduction

Cardiovascular (CV) disease remains the leading global cause of mortality [1,2]. Consequently, CV disease represents a key target for preventive measures through lifestyle and medical interventions [3,4]. Alcohol consumption was long associated with cardiovascular preventive benefits in observational epidemiological studies [5,6], but it also has well-known adverse potential, and no randomized controlled trials assessed its benefit/risk ratio [7].
As preventive and treatment therapies evolve and advance, older therapies often showed diminished benefit, and indications for their use are more limited. In CV medicine, examples of this phenomenon include a diminished or more restricted role for aspirin for primary prevention [8], beta-blocker therapy for patients with stable coronary artery disease (CAD) [9], and digitalis glycosides for treatment of heart failure (HF) [10]. In the current prevention era, statins are widely used as safe and effective CV preventive therapies [11,12,13]. We asked the question whether alcohol use would still be associated with a lower risk of adverse CV events in patients taking statins for primary or secondary prevention.

2. Materials and Methods

Study aim: The primary aim of the study was to assess whether alcohol consumption is associated with CV benefit in patients prescribed or not prescribed statins for primary CV prevention in Intermountain Medical Center. The secondary aim was to evaluate this question in patients at secondary CV risk.
Study design and IRB approval: The study hypothesis was prespecified prior to study analyses and was applied to a prospectively collected observational registry (the INSPIRE registry: NCT02450006) using patient-reported alcohol consumption data that were merged with electronic medical records of Intermountain Healthcare. Subjects consented to participation in the registry to provide survey information, biobanked plasma and DNA samples, and linked medical records, and this study was approved by the Intermountain Healthcare Institutional Review Board.
Study population and data source: Intermountain Healthcare is a nonprofit, integrated healthcare system that, at the time of this study, included 24 hospitals and 215 clinics in Utah, Idaho, and Nevada. Intermountain Healthcare has a long-standing integrated electronic medical records system and a complementary, detailed catheterization laboratory records database. Intermountain Medical Center is the flagship tertiary referral hospital of Intermountain Healthcare.
Patients undergoing cardiac catheterization and coronary angiography at Intermountain Medical Center were approached to enroll in the Intermountain INSPIRE Registry, which involves gaining written permission to obtain a blood sample for DNA and plasma banking-related medical research, and for linking to clinical outcomes through the Intermountain Healthcare electronic data warehouse (EDW). Patients undergoing angiography were also invited to complete a customized questionnaire focusing on key measures of lifestyle potentially related to CV health and outcomes [14]. Specific to the question of alcohol consumption, the questionnaire asked, “In the past year, how many drinks of alcoholic beverages have you had per week?” The possible responses were the following: None, <1 drink per week,1–7 drinks per week, >7 drinks per week, or decline to answer. “None” was defined as non-use and any of the <1 drink, 1–7 drinks, or >7 drinks per week responses was considered to represent alcohol consumption. Those who declined to answer were excluded from the analysis.
Those providing written consent and completing and returning the demographic- and lifestyle-related questionnaire formed the current study population. The dates of enrollment were 2013 to 2020.
The study population was then stratified into those at primary risk (no clinical history of myocardial infarction [MI], coronary revascularization procedure, or significant coronary artery stenosis at current or prior angiography [defined as ≥70% coronary artery stenosis]), and those at secondary risk (i.e., having had at least one of these criteria).
Study outcomes and hypothesis testing: Major adverse cardiovascular events (MACE) were defined as the occurrence after study enrollment (defined as the date of questionnaire completion) of an EDW documented MI, ischemic stroke, heart failure (HF) hospitalization, or all-cause mortality. (Our records did not consistently contain a specific cause of death.) Hypothesis testing included a comparison of patients on statins with those off statins who were alcohol users or non-users in the primary prevention cohort (primary comparisons) and the secondary prevention cohort (secondary comparisons). MACE was determined and compared by alcohol and statin use.
We prospectively hypothesized that alcohol would not reduce the MACE risk in statin users. We also tested whether an alcohol-related benefit would be observed in non-statin users, especially in the primary prevention cohort.
Statistics: Chi-square tests and t-tests were used to examine differences in baseline characteristics and medications for patients on/off statins and on/off alcohol. Cox proportional hazards regression was used to examine outcomes, adjusted for baseline differences, comparing on/off alcohol use and on/off statin use for primary and secondary prevention. Hazard ratios were adjusted for age, sex, race, ethnicity, marital status, education, income, employment status, general physical activity, walking, cycling, body mass index, smoking status, medical history (i.e., hypertension, hyperlipidemia, diabetes, atrial fibrillation, MI, HF, stroke, cancer, COPD, renal failure, peripheral vascular disease, dementia, and depression), family history of early CAD, hospital presentation (stable, unstable angina, or acute MI), and baseline medications (including aspirin, statins, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, antiplatelets, anticoagulants, calcium channel blockers, anti-diabetic medications, digoxin, and diuretics). Patients with CAD also had associations adjusted for prior CAD diagnosis, number of diseased coronaries (left main involvement was considered 2 vessel disease), and treatment type (medical only, percutaneous coronary intervention, or coronary bypass surgery).

3. Results

Characteristics of the study population: Alcohol and statin prescription data were available together with long-term (mean [SD], 4.4 [2.4] years) MACE outcomes in 1701 patients at primary CV risk (4.0 [2.3] years of follow-up) and 3266 patients at secondary CV risk (4.6 [2.4] years of follow-up) (total N = 4967). Age, sex, and frequency distributions by alcohol status and statin prescription are shown in Table 1 for patients at primary CV risk and in Table 2 for patients at secondary CV risk. In the primary prevention group (average age, 57.9 years; 52.4% male), 28% of study patients were prescribed a statin. In the secondary prevention group (average age, 66.2 years; 67.8% male), 64.5% had a documented statin prescription.
Major coronary risk factors (hyperlipidemia, hypertension, diabetes, smoking) were present in 19.8%, 25.9%, 21.8%, and 2.3% at primary risk, respectively, and 54.4%, 56.8%, 45.0%, and 8.6% at secondary risk (Table 3). At coronary angiography, no/negligible, mild, and obstructive (≥70% stenosis) CAD was found in n = 1701 (100%), 0 (0%), and 0 (0%) of the study population at primary risk, and n = 963 (29.5%), 438 (13.4%), and 1865 (57.1%) at secondary risk (Table 3). Past h/o stroke and MI were present in 4.5% and 0%, respectively, of the primary risk population and 7.1% and 12.4% of the secondary risk population (Table 3).
Long-term outcomes by statin and alcohol status in the primary prevention cohort: MACE rates during follow-up were 6.5% and 14.2% for primary prevention alcohol users and non-users, respectively (Figure 1), with an adjusted hazard ratio (adj-HR) of 0.50 (95% CI 0.33, 0.78), p = 0.002, for those not on statins. In contrast, rates were 19.5% and 22.7%, adj-HR 0.84 (CI 0.54, 1.32), p = 0.45, for those on statins (Figure 1). Individual components of MACE are shown in Table 3.
Long-term outcomes by statin and alcohol status in the secondary prevention cohort: For secondary prevention, MACE rates for alcohol users and non-users were, respectively, 18.2% and 19.9% for patients not on a statin, adj HR 1.18 (CI 0.85, 1.64), p = 0.33, and 19.9% and 22.7%, adj HR 1.08 (CI 0.87, 1.35), p = 0.45, for those on statins (Figure 2). Individual components of MACE are shown in Table 3.
Tertiary and exploratory analyses: An analysis also was performed by dose of alcohol (0 drinks/day, <2 drinks/day, or ≥2 drinks/day) in the primary prevention population where n = 56 patients not taking statins reported ≥2 drinks/day and n = 22 taking statins had ≥2 drinks/day. In patients on no statins, those consuming alcohol but <2 drinks/day had lower MACE risk compared with non-drinkers, with 5.8% vs. 14.2% MACE (adj HR 0.47 [CI 0.29, 0.75], p = 0.002), while ≥2 drinks/day was not different to none with 10.7% vs. 14.2% MACE (adj HR 0.82 [CI 0.36, 1.90], p = 0.65). For patients taking statins, MACE was 22.7%, 21.1%, and 9.1%, respectively, for no alcohol, <2 drinks/day (adj HR 0.998 vs. non-drinkers [CI 0.65, 1.54], p = 0.99). Too few in this subgroup consumed ≥2 drinks/day for valid statistical comparison.

4. Discussion

Summary of Study Findings: In a prespecified analysis of this prospectively collected database, we asked the question whether alcohol in statin-treated patients further lowers cardiovascular risk either for primary or secondary CV prevention. The results of our analysis show no significant incremental benefit in either risk cohort. We did find evidence of a benefit of alcohol consumption in the primary prevention cohort not taking a statin. This latter result could be viewed as a ‘positive control’, consistent with long-standing epidemiological evidence of benefit dating to the pre-statin era. However, we did not find a benefit of alcohol in untreated patients in the secondary risk population, perhaps because of other aggressive preventive measures.
Literature Insights: Epidemiological studies dating back several decades have repeatedly reported light to moderate consumption of alcohol to be associated with a lower risk of CV disease compared with abstinence or heavy intake, which has suggested a ‘U-shaped’ dose–response curve [5,6,15,16,17,18]. However, controversy arises because of reports that light–moderate alcohol intake is also associated with favorable lifestyle, behavioral, and socioeconomic factors, which could explain the apparent beneficial alcohol-related association [19]. Mendelian randomization methodology, based on genetic variants predictive of alcohol consumption, represents a promising approach for the testing of causality apart from environmental factors [20,21,22]. Recently, Biddinger et al., studied 371,463 participants enrolled in the UK Biobank to test for confounding associations between alcohol intake and CV diseases and risk factors, including by nonlinear mendelian randomization [23]. They found that coincident favorable lifestyle factors attenuated or nullified the benefits of modest alcohol intake and suggested that any and all amounts of alcohol consumption were associated with increased CV risk, with risk exponentially increasing from minor (with modest intake) to several fold greater, with intake of 21 or more drinks per week. Nonlinear risk increases were noted not only for CAD but also for blood pressure, lipids, and atrial fibrillation. Consistent with their conclusion of lack of benefit with even modest amounts of alcohol, the World Heart Federation recently advocated against any consumption of alcohol for health benefits [24], citing the extensive 2018 Lancet report of ‘Alcohol use and burden for 195 countries and territories’ [25].
These recent reports both support our findings and go beyond, raising the possibility that the apparent benefit of alcohol in our primary prevention, non-statin cohort might be explained by uncorrected confounding of other associated beneficial factors.
Mechanistic Considerations: Several potential mechanisms were proposed for the reported CV preventive benefits of alcoholic beverages, including antioxidant (e.g., in red wine), anticoagulant, and psychosocial factors (stress reducing). In the current era of CV prevention, statins represent a highly beneficial, cost-effective preventive strategy.
Medical history is replete with examples of therapeutics that, over time, offer only attenuated benefits and, consequently, more restricted indications. Digitalis, beta-blockers, and aspirin (for primary prevention) represent just a few examples. With controversy surrounding the role of alcohol in CV risk reduction, we asked the question whether alcohol has a benefit incremental to statins in primary and/or secondary prevention of cardiovascular (CV) disease, and we found a negative answer.
Clinical Implications: Given controversies associated with the modest evidence for the benefits of alcohol and the known harmful potential of excessive alcohol intake, how to advise patients with questions about alcohol consumption is challenging and does not have a current consensus answer. The 2021 ESC Guidelines on Cardiovascular Disease Prevention in Clinical Practice advise limiting alcohol intake to less than 100 g per week, while not advocating it as a preventive measure (4). The 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease recommends limiting alcohol intake to ≤2 drinks/day in men and ≤1 drink/day in women with hypertension, again while neither advocating nor proscribing it for coronary heart prevention (3). US general dietary guidelines recommend similar upper dose thresholds, albeit with limited evidence for overall safety of those thresholds [26].
Our study findings, indicating no benefit in statin users, and the UK Biobank-related [23] and World Health Federation publications [24], suggest that an even stronger message may be appropriate to patients against the use of alcohol specifically for CV prevention. While modest alcohol consumption appears to adversely impact CV risk only modestly, alcohol does not appear to provide incremental benefit over associated healthy lifestyle habits and evidence-based medical therapies, such as statins.
Strengths and Limitations: The study has the strength of using a prospectively acquired database focused on lifestyle measures relevant to CV prevention and a moderately long follow-up period. Another strength is angiographic determination of baseline coronary status, allowing for precise assignment of primary versus secondary prevention cohorts. However, it does have the limitations of all observational studies, including the possibility of residual confounding influencing study results despite adjusted analyses. Another potential limitation is dependence on the accuracy of patient assessment of alcohol consumption. However, it is likely that any discrepancies would tend to be toward underestimates rather than overestimates of intake and tend to nudge results toward the null rather than inflating them. The study is of moderate size, which is adequate for the primary analyses, but it lacks high power for some secondary and tertiary analyses (e.g., alcohol dose–response relationships). Moreover, it cannot exclude small advantages (e.g., of the order of 10%) in MACE reduction by alcohol in the setting of statin use. Its restriction to a single healthcare system increases internal consistency, but it may limit applicability to other systems with differing racial/ethnic make-up and prevention approaches.

5. Conclusions

In this single-center healthcare population, alcohol consumption was associated with lower risk of MACE in statin untreated primary prevention patients, but it showed no incremental benefit when added to statins for primary prevention and no benefit with or without statin use for secondary prevention. In keeping with other recent and supportive reports, these findings can help to inform personal choices in alcohol consumption and professional society recommendations for cardiovascular prevention.

Author Contributions

Conceptualization, J.L.A., V.T.L. and B.D.H.; methodology, J.L.A. and B.D.H.; formal analysis, B.D.H.; investigation, J.L.A., T.L.B. and B.D.H.; resources, J.L.A.; data curation, V.T.L. and B.D.H.; writing—original draft preparation, J.L.A. and B.D.H.; writing review and editing, J.L.A., V.T.L., T.L.B., J.B.M., K.U.K. and B.D.H.; visualization, B.D.H.; supervision, J.L.A.; project administration, J.L.A. and K.U.K.; funding acquisition, J.L.A. All authors have read and agreed to the published version of the manuscript.


This research received no external funding.

Institutional Review Board Statement

This study utilized data collected through the INSPIRE registry (Intermountain Healthcare Biological Samples Collection Project and Investigational Registry) and details of INSPIRE are available at (NCT02450006). The study was conducted according to the guidelines of the Declaration of Helsinki and was initially approved by the Intermountain Healthcare Institutional Review Board (IRB number 1024811) in 1994 with subjects providing informed consent to participate. The protocol was amended in 2013 to add the collection of data through a routine 3-page survey for subjects enrolling in the INSPIRE registry.

Informed Consent Statement

Informed consent was obtained for entry into the INSPIRE registry from all subjects involved in the study.

Data Availability Statement

The data underlying this article cannot be shared publicly due to US privacy laws. Data are available upon reasonable request to the corresponding author.

Conflicts of Interest

B.D.H. is a member of the scientific advisory boards of Lab Me Analytics and Opsis Health. The authors declare no other conflicts of interest.


  1. Roth, G.A.; Abate, D.; Abate, K.H.; Abay, S.M.; Abbafati, C.; Abbasi, N.; Borschmann, R. GBD 2017 Causes of Death CO\ollaborators. Global, regional, and national age sex specific mortality for 282 causes of death in 195 countries and territories, 1980–2017: A systematic analysis for the Global Burden of Disease Study 2017. Lancet 2018, 392, 1736–1788. [Google Scholar] [CrossRef]
  2. Tsao, C.W.; Aday, A.W.; Almarzooq, Z.I.; Alonso, A.; Beaton, A.Z.; Bittencourt, M.S.; Boehme, A.K.; Buxton, A.E.; Carson, A.P.; Commodore-Mensah, Y.; et al. Heart Disease and Stroke Statistics—2022 Update: A Report From the American Heart Association. Circulation 2022, 145, e153–e639. [Google Scholar] [CrossRef] [PubMed]
  3. Arnett, D.K.; Blumenthal, R.S.; Albert, M.A.; Buroker, A.B.; Goldberger, Z.D.; Hahn, E.J.; Himmelfarb, C.D.; Khera, A.; Lloyd-Jones, D.; McEvoy, J.W.; et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary. J. Am. Coll. Cardiol. 2019, 74, 1376–1414. [Google Scholar] [CrossRef]
  4. Visseren, F.L.J.; Mach, F.; Smulders, Y.M.; Carballo, D.; Koskinas, K.; Bäck, M.; Benetos, A.; Biffi, A.; Boavida, J.-M.; Capodanno, D.; et al. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. Eur. Heart J. 2021, 42, 3227–3337. [Google Scholar] [CrossRef] [PubMed]
  5. Pearson, T. Alcohol and heart disease. Circulation 1996, 94, 3023–3025. [Google Scholar] [CrossRef] [PubMed]
  6. O’Keefe, J.H.; Bybee, K.A.; Lavie, C. Alcohol and cardiovascular health: The razor-sharp double-edged sword. J. Am. Coll. Cardol. 2007, 50, 1009–1014. [Google Scholar] [CrossRef] [PubMed]
  7. National Institutes of Health Advisory Committee to the Director. ACD Working Group for Review of the Moderate Alcohol and Cardiovascular Health Trial. Available online:>documents>presentations>PDF (accessed on 14 June 2018).
  8. Raber, I.; McCarthy, C.P.; Vaduganathan, M.; Bhatt, D.L.; A Wood, D.; Cleland, J.G.F.; Blumenthal, R.S.; McEvoy, J.W. The rise and fall of aspirin in the primary prevention of cardiovascular disease. Lancet 2019, 393, 2155–2167. [Google Scholar] [CrossRef]
  9. Bangalore, S.; Steg, G.; Deedwania, P.; Crowley, K.; Eagle, K.A.; Goto, S. Beta-blocker use and clinical outcomes in stable outpatients with and without coronary artery disease. JAMA 2012, 308, 1340–1349. [Google Scholar] [CrossRef]
  10. Heidenreich, P.A.; Bozkurt, B.; Aguilar, D.; Allen, L.A.; Byun, J.J.; Colvin, M.M.; Deswal, A.; Drazner, M.H.; Dunlay, S.M.; Evers, L.R.; et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2022, 145, e895–e1032. [Google Scholar] [CrossRef]
  11. Baigent, C.; Keech, A.; Kearney, P.M.; Blackwell, L. Cholesterol Treatment Trialists’ (CTT) Collaborators. Efficacy and safety of cholesterol-lowering treatment: Prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005, 366, 1267–1278. [Google Scholar]
  12. Ridker, P.M.; Danielson, E.; Fonseca, F.A.; Genest, J.; Gotto, A.M., Jr.; Kastelein, J.J.; Glynn, R.J. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. N. Engl. J. Med. 2008, 359, 2195–2207. [Google Scholar] [CrossRef]
  13. Grundy, S.M.; Stone, N.J.; Bailey, A.L.; Beam, C.; Birtcher, K.K.; Blumenthal, R.S.; Yeboah, J. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation 2019, 139, e1082–e1143. [Google Scholar]
  14. Bartholomew, C.L.; Muhlestein, J.B.; Anderson, J.L.; May, H.T.; Knowlton, K.U.; Bair, T.L.; Horne, B.D. Association of periodic fasting lifestyles with survival and incident major adverse cardiovascular events in patients undergoing cardiac catheterization. Eur. J. Prev. Cardiol. 2022, 28, 1774–1781. [Google Scholar] [CrossRef]
  15. Thompson, P. J-curve revisited: Cardiovascular benefits of moderate alcohol use cannot be dismissed. Med. J. Aust. 2013, 198, 419–422. [Google Scholar] [CrossRef]
  16. Bell, S.; Daskalopoulou, M.; Rapsomaniki, E.; George, J.; Britton, A.; Bobak, M.; Hemingway, H. Association between clinically recorded alcohol consumption and clinical presentation of 12 cardiovascular diseases: Population based study using linked health records. BMJ 2017, 356, j909. [Google Scholar] [CrossRef]
  17. Wood, A.M.; Kaptoge, S.; Butterworth, A.S.; Willeit, P.; Warnakula, S.; Bolton, T.; Thompson, S. Emerging risk factors collaboration/EPIC-CVD/UK Biobank Alcohol Study Group. Risk thresholds for alcohol consumption: Combined analysis of individual participant data for 599,912 current drinkers in 83 prospective studies. Lancet 2018, 391, 1513–1523. [Google Scholar] [CrossRef]
  18. Viscontay, R.; Sunderland, M.; Slade, T.; Wilson, J.L. Are there non-linear relationships between alcohol consumption and long-term health? BMJ Open 2021, 11, e043985. [Google Scholar] [CrossRef]
  19. Naimi, T.S.; Brown, D.W.; Brewer, R.D.; Giles, W.H.; Mensah, G.; Serdula, M.K.; Mokdad, A.H.; Hungerford, D.W.; Lando, J.; Naimi, S.; et al. Cardiovascular risk factors and confounders among nondrinking and moderate-drinking US adults. Am. J. Prev. Med. 2005, 28, 369–373. [Google Scholar] [CrossRef]
  20. Davey Smith, G.; Ebrahim, S. ‘Mendelian randomization’: Can genetic epidemiology contribute to understanding environmental determinants of disease? Int. J. Epidemiol. 2003, 32, 1–22. [Google Scholar] [CrossRef]
  21. Millwood, I.Y.; Walters, R.G.; Mei, X.W.; Guo, Y.; Yang, L.; Bian, Z.; A Bennett, D.; Chen, Y.; Dong, C.; Hu, R.; et al. Conventional and genetic evidence on alcohol and vascular disease aetiology: A prospective study of 500,000 men and women in China. Lancet 2019, 393, 1831–1842. [Google Scholar] [CrossRef]
  22. Larsson, S.C.; Burgess, S.; Mason, A.M.; Michaëlsson, K. Alcohol consumption and cardiovascular disease: A mendelian randomization study. Circ. Genomic Precis. Med. 2020, 13, e002814. [Google Scholar] [CrossRef] [PubMed]
  23. Biddinger, K.J.; Emdin, C.A.; Haas, M.E.; Wang, M.; Hindy, G.; Ellinor, P.T.; Aragam, K.G. Association of habitual alcohol intake with risk of cardiovascular disease. JAMA Netw. Open 2021, 5, e223849. [Google Scholar] [CrossRef]
  24. Arora, M.; ElSayed, A.; Beger, B.; Naidoo, P.; Shilton, T.; Jain, N.; Champagne, B.M. The Impact of Alcohol Consumption on Cardio. The impact of alcohol consumption on cardiovascular health: Myths and measures. Glob. Heart 2022, 17, 1. [Google Scholar] [CrossRef]
  25. Griswold, M.G.; Fullman, N.; Hawley, C.; Arian, N.; Zimsen, S.R.; Tymeson, H.D.; Farioli, A. Alcohol use and burden for 195 countries and territories, 1990–2016: A systematic analysis for the Blobal Burden of Disease Study 2016. Lancet 2018, 392, 1015–1035. [Google Scholar] [CrossRef]
  26. USDA. Dietary Guidelines for Americans. Scientific Report of the 2020 Dietary Guidelines Advisory Committee; USDA: Washington, DC, USA, 2020.
Figure 1. MACE Outcomes in Primary Prevention Patients by Alcohol and Statin Status. Alcohol+ = alcohol user. Alcohol− = Alcohol non-user.
Figure 1. MACE Outcomes in Primary Prevention Patients by Alcohol and Statin Status. Alcohol+ = alcohol user. Alcohol− = Alcohol non-user.
Jcm 11 04797 g001
Figure 2. MACE Outcomes in Secondary Prevention Patients by Alcohol and Statin Status. Alcohol+ = alcohol user. Alcohol− = Alcohol non-user.
Figure 2. MACE Outcomes in Secondary Prevention Patients by Alcohol and Statin Status. Alcohol+ = alcohol user. Alcohol− = Alcohol non-user.
Jcm 11 04797 g002
Table 1. Frequencies by Alcohol and Statin Category, together with Age and Sex in Patients at Primary Cardiovascular Risk.
Table 1. Frequencies by Alcohol and Statin Category, together with Age and Sex in Patients at Primary Cardiovascular Risk.
N patients164416
Age, mean y (SD)62 (11)54 (16)
Sex, % male67.7%57.2%
N patients313808
Age, mean y (SD)64 (13)57 (17)
Sex, % male53.7%46.4%
Table 2. Frequencies by Alcohol and Statin Category, together with Age and Sex in Patients at Secondary Cardiovascular Risk.
Table 2. Frequencies by Alcohol and Statin Category, together with Age and Sex in Patients at Secondary Cardiovascular Risk.
N patients599292
Age, mean y (SD)64 (12)63 (14)
Sex, % male75.9%67.8%
N patients1509866
Age, mean y (SD)67 (11)67 (13)
Sex, % male69.6%58.9%
Table 3. Major coronary risk factors and baseline history of MACE by primary or secondary prevention status.
Table 3. Major coronary risk factors and baseline history of MACE by primary or secondary prevention status.
Characteristic orPrimary PreventionSecondary Prevention
Baseline Characteristics
Hyperlipidemia19.8%16.7%21.3% *54.4%55.0%54.2%
Diabetes21.8%14.1%25.8% †45.0%35.6%48.5% †
Smoking2.3%3.8%1.5% *8.6%14.4%6.4% †
Family History4.5%5.2%4.1%19.4%19.1%19.5%
Prior CAD0%0%0%76.2%70.3%78.4% †
Prior MI0%0%0%12.4%10.0%13.3% *
Prior Stroke4.5%4.3%4.6%7.1%4.7%8.0% †
HF History9.8%9.5%9.9%13.8%11.0%14.9% *
Atrial Fibrillation43.7%44.8%43.2%40.8%35.7%42.7% †
Renal Failure0.5%0.0%0.7% *2.2%2.1%2.3%
PVD19.9%16.9%21.5% *39.2%34.0%41.1% †
Angiography: Obstructive CAD
Hospital Treatment Modality
Medical Only100%100%100%71.4%70.3%71.9%
Longitudinal MACE Outcomes
HF Hospitalization3.4%2.3%4.0%5.7%4.8%6.1%
All-Cause Mortality5.3%3.4%6.3% *9.7%8.2%10.2%
Alcohol+ = alcholol user. Alcohol− = Alcohol non-user. * p ≤ 0.05 (and p ≥ 0.001) for alcohol− vs. alcohol+; † p < 0.001 for alcohol− vs. alcohol+.
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Anderson, J.L.; Le, V.T.; Bair, T.L.; Muhlestein, J.B.; Knowlton, K.U.; Horne, B.D. Is Alcohol Consumption Associated with a Lower Risk of Cardiovascular Events in Patients Treated with Statins? An Observational Real-World Experience. J. Clin. Med. 2022, 11, 4797.

AMA Style

Anderson JL, Le VT, Bair TL, Muhlestein JB, Knowlton KU, Horne BD. Is Alcohol Consumption Associated with a Lower Risk of Cardiovascular Events in Patients Treated with Statins? An Observational Real-World Experience. Journal of Clinical Medicine. 2022; 11(16):4797.

Chicago/Turabian Style

Anderson, Jeffrey L., Viet T. Le, Tami L. Bair, Joseph B. Muhlestein, Kirk U. Knowlton, and Benjamin D. Horne. 2022. "Is Alcohol Consumption Associated with a Lower Risk of Cardiovascular Events in Patients Treated with Statins? An Observational Real-World Experience" Journal of Clinical Medicine 11, no. 16: 4797.

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop