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.

Acute coronary syndrome (ACS) remains a leading cause of cardiovascular morbidity and mortality worldwide. Although traditional cardiovascular risk factors remain central to ACS development, recreational drug use is increasingly recognized as a clinically relevant trigger, particularly in younger patients with fewer conventional risk factors. This narrative review synthesized evidence identified through searches of PubMed/MEDLINE and Scopus up to June 2026, including clinical guidelines, systematic reviews, observational studies, mechanistic investigations, and clinically informative case-based evidence. Cannabis, cocaine, amphetamines, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), opioids, lysergic acid diethylamide (LSD), synthetic cannabinoids, and polysubstance use may promote myocardial ischemia and infarction through overlapping mechanisms, including sympathetic activation, coronary vasospasm, endothelial dysfunction, oxidative stress, inflammation, platelet activation, thrombosis, arrhythmogenesis, and myocardial oxygen supply–demand mismatch. Clinical presentation may be typical or atypical and may overlap with intoxication, withdrawal, anxiety, neurological symptoms, or non-cardiac chest pain, making diagnosis challenging. Underreporting of recreational drug use is common, and targeted toxicology screening may improve diagnostic accuracy and risk stratification, particularly in patients younger than 50 years, those with few traditional cardiovascular risk factors, or those presenting with otherwise unexplained ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), coronary vasospasm, arrhythmias, or cardiac arrest. Acute management should generally follow standard ACS guidelines, while considering drug-specific issues such as stimulant-induced vasospasm, sympathetic excess, cautious use of beta-blockers during acute intoxication, and preference for primary percutaneous coronary intervention when fibrinolysis carries increased risk. Long-term care should combine evidence-based secondary prevention with substance-use counseling, addiction medicine referral, cardiac rehabilitation, and behavioural interventions. This review summarizes the pathophysiology, clinical manifestations, epidemiology, treatment considerations, preventive strategies, and knowledge gaps related to recreational drug-associated ACS.

Heart failure with preserved ejection fraction (HFpEF) represents a heterogeneous clinical syndrome characterized by complex pathophysiological mechanisms and substantial diagnostic and prognostic challenges. Recently, circulating biomarkers have emerged as potential tools for improving risk stratification and disease characterization in this population. Among these biomarkers, soluble suppression of tumorigenicity-2 (sST2) and galectin-3 (Gal-3) have gained particular attention due to their association with myocardial fibrosis, inflammation, and adverse cardiac remodeling. This scoping review aimed to evaluate the current evidence on the diagnostic and prognostic roles of sST2 and Gal-3 in patients with HFpEF. A literature search was conducted in PubMed and ScienceDirect to identify studies investigating the clinical significance of these biomarkers in HFpEF. Titles and abstracts were screened, and eligible studies were assessed through full-text review according to predefined inclusion criteria. Ultimately, 11 studies were included in the qualitative synthesis. Evidence from the available literature suggests that both sST2 and Gal-3 are associated with markers of myocardial fibrosis, inflammation, and disease severity in HFpEF. Elevated circulating levels of these biomarkers have been linked to poorer clinical outcomes, including an increased risk of hospitalization and mortality. However, variability across studies in study populations, biomarker thresholds, and methodological approaches limits the direct translation of these findings into routine clinical practice. Overall, sST2 and Gal-3 appear to hold promise as complementary biomarkers for risk stratification in HFpEF. Nonetheless, further large-scale prospective studies are needed to clarify the clinical utility of these biomarkers and determine the subsequent integration into multimarker strategies for the management of patients with HFpEF.