In recent years, gut microbiota has emerged as a central modulator of cardiovascular health and disease. This has led to a transition from the old understanding of cardiovascular pathology as a largely cardiac-centric problem to a systemic, multi-organ process. A growing body of evidence demonstrates that changes in the makeup of gut microbes, generally called dysbiosis, are significant in the development and progression of cardiovascular illnesses, including heart failure. Moreover, there are bidirectional interactions between the failing heart and the gut. In heart failure, impaired hemodynamics and venous congestion further worsen intestinal hypoperfusion and barrier dysfunction in a self-perpetuating cycle that exacerbates dysbiosis and systemic inflammation. The gut–heart axis offers a fresh paradigm for illness progression beyond classical neurohormonal and hemodynamic processes. The gut microbiota acts as an endocrine organ by producing bioactive metabolites such as TMAO (trimethylamine N-oxide), SCFA (short-chain fatty acids) and bile acids, which, via several routes, have a serious impact on host health and disease. This narrative review aims to summarize the current evidence for the gut microbiota as a new cardiovascular risk factor, focusing on biological mechanisms and clinical and epidemiological evidence.

Background: The literature shows that anterior communicating artery (AcoA) aneurysms are the most common intracranial aneurysms. To date, there has only been one postmortem study focused on the correlations between autopsy findings and imaging results in cases of intracranial aneurysms associated with anatomical variants of the circle of Willis (CW). Methods: We investigated the anatomical variants of the CW associated with the occurrence and rupture of AcoA aneurysms by performing comparative analyses, in the same patients, of postmortem autopsy data with antemortem computed tomography–angiography (CTA) results obtained in the first 48 h after the onset of subarachnoid hemorrhage. Our retrospective observational study identified the anatomical variants of the CW at autopsy in 16 deceased adult Romanian patients with AcoA aneurysms over a 12-year period (2010–2022). Results: The autopsy findings revealed that the AcoA ruptured aneurysms had a mean external diameter of 9.50 mm, and 71.4% of them presented three or four anatomical variants inside the same CW. The initial antemortem CTA examination correctly located the AcoA aneurysms in all cases (100%), and an anatomical variant of the CW was only noted in 18.75% of patients. The final postmortem re-analyzed the same CTA images identified in all cases (100%), focusing on both the AcoA aneurysm and all anatomical variants of the CW found during the autopsies. Conclusions: Although it was previously thought that the occurrence of AcoA aneurysms is related only to the hemodynamic changes induced by the nearby arterial anatomical variants, we identified the simultaneous involvement of at least one hypoplastic artery and one or two PCA fetal-type anatomical variants that were located in both the anterior and posterior parts of the CW. Furthermore, if sufficient time is devoted to the CT–angiography analysis and interpretation of the images, anatomical variants of the circle of Willis associated with AcoA aneurysms can be identified as accurately as they are in invasive postmortem autopsy examinations.

The gut microbiota is increasingly recognized as an important modulator of cardiovascular health, demonstrating complicated interactions among diet, metabolism, immunology and host physiology. Evidence is accumulating that changes in the composition and function of the gut microbiome may contribute to the pathogenesis of atherosclerosis, hypertension, heart failure, thrombosis and other cardiovascular phenotypes through mechanisms involving microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation. In this context, the key question of this narrative review is: how far can modulation of the gut microbiome and its metabolic functions be a clinically meaningful approach in the prevention and treatment of cardiovascular disease, and which of the currently available microbiome-targeted approaches have sufficient mechanistic and clinical evidence to justify translation into cardiovascular practice? To answer this question, we review the evidence linking the gut microbiome to major cardiovascular phenotypes, such as atherosclerosis, hypertension, heart failure, thrombosis and atrial fibrillation, with particular focus on the mechanisms through which microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation may affect cardiovascular risk. We then review current and emerging strategies for microbiome modulation, including dietary interventions, prebiotics, probiotics, synbiotics, postbiotics, fecal microbiota transplantation and targeted inhibition of microbial metabolic pathways such as trimethylamine (TMA)/trimethylamine N-oxide (TMAO) production. We also examine bidirectional interactions between cardiovascular drugs and gut microbiome and the role of these interactions in the development of precision methods to cardiovascular prevention and treatment. Finally, we outline the major limitations of the current evidence and highlight goals for future mechanistic, translational and clinical research.