Background/Objectives: Nicotine-free electronic cigarettes (NFECs) are becoming increasingly popular, especially among youth and non-smokers, yet their effects on the gastrointestinal tract (GIT) remain poorly understood. This systematic review synthesizes available in vitro, in vivo, and limited human evidence on NFEC-associated changes in gastrointestinal health and function. Methods: Literature searches were conducted in Medline, Web of Science, Cochrane, and Scopus in July 2025, following PRISMA guidelines. Eligible studies examined NFEC effects on any GIT segment, including the oral cavity, liver, intestines, and microbiome. Data on study design, exposure characteristics, and main outcomes were extracted and narratively synthesized. Results: Of 111 identified records, 94 full-text articles were retrieved, and 21 studies met the inclusion criteria. Most were preclinical, with only one human pilot study. Evidence from oral cell and microbial models suggests that NFEC aerosols can induce pro-inflammatory cytokine production, impair cell viability, and disrupt microbial metabolism through their base constituents (propylene glycol, vegetable glycerine, and flavourings). Animal studies indicate possible hepatic oxidative stress, altered lipid metabolism, and gut barrier dysfunction, with some data suggesting more pronounced steatosis in nicotine-free exposures compared to nicotine-containing counterparts. Microbiome studies report reduced tight junction expression and altered neutrophil function. Conclusions: Current evidence is limited and predominantly preclinical but indicates that NFEC exposure can affect multiple aspects of gastrointestinal health. Robust longitudinal and interventional human studies are urgently needed to determine the clinical relevance of these findings and to inform regulation and public health policy.

Background: The cardiovascular effects of nicotine-containing e-cigarettes are well-established; however, far less is known about nicotine-free formulations, which are often perceived as safer alternatives. Yet, these products generate complex aerosols that may still pose toxicological risks. Methods: Following the PRISMA 2020 guidelines, we systematically searched PubMed, Scopus, Web of Science, and the Cochrane Library up to 27 August 2025. Eligible studies included human and animal research on nicotine-free e-cigarettes evaluating vascular, hemodynamic, arrhythmic, oxidative, or inflammatory outcomes. Owing to the heterogeneity of the studies, the findings were synthesized qualitatively. Results: Nine studies met the inclusion criteria. Human trials consistently demonstrated acute vascular impairments, including endothelial dysfunction, oxidative stress, increased arterial stiffness, and transient blood pressure elevations. Experimental models corroborated these findings and further revealed systemic inflammation, mitochondrial injury, and developmental cardiotoxicity. Conclusions: Nicotine-free e-cigarettes produce reproducible acute cardiovascular effects. Although the long-term outcomes remain uncertain, preclinical evidence highlights biologically plausible mechanisms, including mitochondrial dysfunction and proarrhythmogenic potential. Until large-scale longitudinal studies have been conducted to clarify their risk profile, nicotine-free products should not be regarded as risk-free.

Background and Objectives: Cardiometabolic disease, a term encompassing metabolic syndrome (MS) and cardiovascular disease (CVD), represents a major and growing global health burden driven by interconnected metabolic and cardiovascular dysfunction. Emerging evidence suggests that the gut microbiota plays a central role in modulating metabolic, inflammatory, and cardiovascular (CV) pathways, giving rise to the concept of the heart–gut axis. However, human evidence integrating microbiome-mediated mechanisms across the cardiometabolic spectrum remains incompletely synthesized. This focused systematic review aimed to synthesize the current human evidence on microbiome-mediated mechanisms linking metabolic syndrome (MS) and related metabolic phenotypes with cardiovascular risk (CVR) and subclinical cardiovascular (CV) outcomes within the conceptual framework of the heart–gut axis. Materials and Methods: A systematic literature search was conducted in PubMed, Scopus, Web of Science, and the Cochrane Library in accordance with PRISMA 2020 guidelines. Human observational and interventional studies evaluating gut microbiota composition, function, or microbiota-derived metabolites in relation to cardiometabolic, and CV outcomes were included. Risk of bias was assessed using the Cochrane RoB 2 and ROBINS-I tools, and findings were synthesized narratively. Results: Ten human studies published between 2016 and 2025 met the inclusion criteria. Across these studies, gut dysbiosis was consistently associated with adverse cardiometabolic risk profiles and subclinical CV outcomes, including insulin resistance, systemic inflammation, subclinical atherosclerosis, and CV prognosis in high-risk populations. Microbiota-derived metabolites, particularly trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), as well as emerging metabolites such as phenylacetylglutamine (PAGln) and imidazole propionate (ImP), were identified as key mediators linking metabolic syndrome and related metabolic disturbances with CVR and subclinical cardiovascular disease (CVD). Markers of intestinal barrier dysfunction and endotoxemia further supported the role of chronic low-grade inflammation within the heart–gut axis. Conclusions: Current human evidence supports the heart–gut axis as a biologically plausible and clinically relevant contributor to cardiometabolic disease. Gut microbiota-derived metabolites, intestinal barrier dysfunction, and systemic inflammation represent interconnected pathways linking MS with CVR. Advancing our understanding of these mechanisms may inform the development of microbiome-targeted strategies to complement established approaches for cardiometabolic and CV prevention.

Systemic sclerosis (SSc) is a complex autoimmune connective tissue disease characterized by microvascular dysfunction, immune activation, and progressive fibrosis affecting multiple organs, including the heart. Myocardial involvement represents an important but frequently underrecognized manifestation of SSc and may develop even in the absence of overt clinical symptoms. Cardiac manifestations include ventricular dysfunction, arrhythmias, conduction abnormalities, and heart failure, contributing substantially to morbidity and mortality. The underlying pathophysiology involves coronary microvascular dysfunction, immune-mediated myocardial inflammation, and progressive myocardial fibrosis, which often precede clinically apparent cardiac disease. This review aims to summarize the current understanding of myocardial involvement in SSc and to provide a comprehensive overview of contemporary multimodality cardiovascular imaging techniques for its detection, characterization, and risk stratification. A comprehensive overview of the current literature was conducted focusing on established and emerging cardiovascular imaging modalities for the evaluation of myocardial involvement in SSc. Particular attention was given to echocardiography, cardiac magnetic resonance (CMR), nuclear imaging techniques including positron emission tomography (PET) and single-photon emission computed tomography (SPECT), and cardiac computed tomography (CT). Recent advances in imaging biomarkers, parametric mapping, myocardial strain analysis, and emerging technologies such as artificial intelligence (AI), radiomics, and molecular imaging were also considered. Multimodality cardiovascular imaging plays a central role in the early detection and comprehensive assessment of myocardial involvement in SSc. Advanced imaging techniques enable improved identification of subclinical myocardial dysfunction, microvascular impairment, inflammation, and fibrosis. An integrated imaging approach combining echocardiography, CMR, nuclear imaging, and CT may facilitate earlier diagnosis, enhance risk stratification, and ultimately improve cardiovascular outcomes in patients with SSc.

Background: Echocardiographic imaging has become central to planning and guiding percutaneous left atrial appendage occlusion (LAAO), particularly in patient populations in whom long-term anticoagulation is unsuitable. This systematic review synthesizes current evidence on transesophageal (TEE) and intracardiac echocardiography (ICE) guidance during LAAO, with special emphasis on outcomes in high-risk cohorts, including chronic liver disease (CLD) and prior gastrointestinal (GI) bleeding. Methods: Following PRISMA 2020 guidelines, four databases (PubMed, Scopus, Web of Science, and Cochrane CENTRAL) were searched up to 5 December 2025. Eligible studies included adult patients with atrial fibrillation (AF) undergoing percutaneous LAAO with intraprocedural echocardiographic guidance. Eight studies (n = 1739 patients) met the inclusion criteria. Data were synthesized qualitatively due to heterogeneity across devices, imaging protocols, and outcomes. Results: TEE was the predominant imaging modality (62.5%), providing high spatial resolution for transseptal puncture, device positioning, and peri-device leak (PDL) assessment. ICE-guided LAAO (25.0%) was associated with high procedural success and favorable safety profiles in selected observational cohorts, while reducing anesthesia requirements and fluoroscopy time. Across all studies, procedural success ranged from 93 to 100%, with low rates of major complications. Reported follow-up durations varied substantially across studies and were predominantly short- to mid-term, limiting assessment of long-term device-related outcomes. Evidence specific to patients with chronic liver disease and prior gastrointestinal bleeding was limited, with only two included studies directly evaluating these populations, while remaining insights were extrapolated from broader LAAO cohorts. In high-risk groups, LAAO remained feasible: cirrhotic patients demonstrated high implantation success with acceptable bleeding profiles, while patients with prior GI bleeding showed low recurrence after closure. Conclusions: Both TEE and ICE provide reliable intraprocedural imaging for LAAO, with ICE offering workflow and safety advantages in patients unsuitable for general anesthesia. The available evidence suggests that LAAO is a feasible and potentially safe therapeutic option in selected patients with CLD and prior GI bleeding, although direct data remain limited. Future studies should compare imaging modalities prospectively in high-risk cohorts and evaluate emerging 3D/4D ICE technologies.

Background: Cigarette smoking exposes the human body to a complex mixture of toxic and carcinogenic compounds that can exert widespread biological effects across different organ systems. From addictive responses and consequence maladaptive neuroendocrine responses, cigarette smoke delivers a variety of reactive oxygen species, polycyclic aromatic hydrocarbons, nitrosamines, and heavy metals that collectively contribute to oxidative stress, inflammation, endothelial dysfunction, and metabolic disruption. The liver, as the primary organ responsible for xenobiotic metabolism, plays a central role in processing these harmful substances and is therefore uniquely susceptible to their effects. This narrative review will aim to provide an overview of the current evidence of cigarette smoking effects on hepatic structure and function and discuss clinical implications. Methods: This narrative review synthesizes evidence from in vitro studies, animal models, and human clinical research examining the effects of cigarette smoking on liver biology. Mechanistic pathways of injury, metabolic and vascular alterations, and clinical consequences for liver disease were considered. Results: Smoking influences hepatic function both directly—through biotransformation pathways generating reactive intermediates—and indirectly via vascular impairment, immune modulation, hormonal alterations, and changes in lipid and glucose metabolism. Emerging evidence indicates that cigarette smoking contributes to hepatic steatosis, accelerates fibrosis progression, worsens outcomes in viral and alcohol-related liver disease, and increases the risk of hepatocellular carcinoma. Conclusions: Cigarette smoking exerts multifaceted deleterious effects on the liver. Recognition of smoking as a modifiable risk factor for liver-related morbidity underscores the importance of smoking cessation in patients with or at risk for liver disease and highlights implications for research and clinical practice.