ReviewJournal of clinical medicine2025
Alcohol Consumption and Acute Coronary Syndrome: Epidemiology, Pathophysiology, and Clinical Perspectives.
Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Metabolic Signatures of Atrial Functional Impairment in Paroxysmal Atrial Fibrillation Patients: A CMR Strain-metabolomics Study.Journal of cardiovascular translational research · 2026Article
- Acute Coronary Syndrome and Recreational Drug Use: A Comprehensive Review.Medicina (Kaunas, Lithuania) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alcohol consumption is a globally prevalent lifestyle factor with complex and sometimes paradoxical effects on cardiovascular health, particularly regarding acute coronary syndrome (ACS). Earlier epidemiological studies described a J-shaped relationship between alcohol consumption and ACS risk; however, emerging evidence has increasingly challenged the validity of this concept. Mendelian randomization studies, genetic data, and recent pooled analyses suggest that the apparent cardioprotective effects of light-to-moderate drinking are largely attributable to residual confounding, including abstainer bias and socioeconomic factors, rather than true causal mechanisms. In contrast, excessive alcohol intake is linked to increased oxidative stress, inflammation, hypertension, and prothrombotic states, all of which contribute to plaque instability and the precipitation of ACS. Additionally, acute heavy drinking episodes may induce coronary vasospasm and arrhythmias, further elevating ACS risk. Genetic factors, drinking patterns, and beverage types may also modulate the relationship between alcohol and ACS, indicating the need for personalized risk assessment. Understanding these complex interactions is essential for clinicians when counseling patients on alcohol consumption within the context of cardiovascular prevention. This review aims to delve into current evidence on the epidemiology and pathophysiology linking alcohol consumption with ACS, providing a nuanced perspective that balances potential protective effects with the significant risks associated with excessive alcohol use, as well as summarizing all medical societies' recommendations regarding alcohol consumption and cardiovascular health.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.