Aortic stenosis (AS) and atherosclerosis are progressive cardiovascular conditions that frequently coexist and share multiple clinical and molecular features. Medical therapies have shown effectiveness in preventing and treating atherosclerosis and its consequences. For AS, effective pharmacological therapies remain limited. Understanding the shared risk factors and mechanisms between the two conditions may provide opportunities for therapeutic repositioning in AS. We performed a narrative review focusing on studies published from 2005 to 2025. Inclusion criteria encompassed clinical trials, experimental models, and molecular studies addressing overlapping risk factors, pathological pathways, and treatment approaches for AS and atherosclerosis. AS and atherosclerosis share key risk factors, including age, hypertension, hyperlipidemia, and diabetes. Molecular mechanisms, such as chronic inflammation, endothelial dysfunction, oxidative stress, lipid accumulation, and calcific remodeling, are common to both. Pathways involving the renin-angiotensin system, Notch signaling, and osteogenic mediators contribute to disease progression. Several drug classes, notably proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, lipoprotein(a) (Lp(a)) lowering therapies, anti-inflammatory agents, and immunomodulators, show potential for repositioning in AS management. The substantial overlap in risk factors and molecular mechanisms between AS and atherosclerosis supports a rationale for therapeutic repositioning. Targeting shared pathways could lead to innovative strategies for slowing AS progression and improving patient outcomes.

Background and Objectives: Coronary atherosclerosis remains a leading cause of global morbidity and mortality. Chronic systemic inflammation has emerged as a key factor in atherosclerosis development. Tooth loss—often the final consequence of periodontitis—has been proposed as a potential clinical marker of systemic inflammation and cardiovascular risk. Objective: This narrative review synthesizes the available literature on the relationship between tooth loss and coronary artery disease (CAD) severity, exploring biological mechanisms, key epidemiological findings, and clinical implications. Materials and Methods: We reviewed observational studies, meta-analyses, and clinical reports assessing whether tooth loss is predictive of CAD severity and adverse outcomes. Results: A consistent association is reported between tooth loss and increased coronary involvement. Proposed mechanisms include periodontal inflammation, dysbiosis, systemic inflammatory responses, and translocation of oral bacteria. However, confounders such as smoking, diabetes, and socioeconomic status complicate causality. Conclusions: Tooth loss may serve as a simple, non-invasive clinical indicator of systemic inflammation and CAD severity. Incorporating oral health evaluation into cardiovascular risk assessment could enhance early detection and prevention strategies. Further longitudinal and interventional studies are required to establish causality and inform clinical guidelines.

Background: Pulmonary embolism (PE) is a major cause of cardiovascular mortality, with heterogeneous presentation. Syncope, reported in 10–20% of cases, may indicate severe hemodynamic compromise, but its independent prognostic role remains uncertain. Methods: We retrospectively analyzed 300 patients admitted with acute PE confirmed by computed tomography pulmonary angiography between January 2022 and December 2024. Patients were stratified according to the presence of syncope at admission. Clinical, laboratory, and echocardiographic findings and outcomes were compared. Logistic regression was used to identify independent predictors of in-hospital mortality. The present study is a single-center, retrospective analysis. Results: Syncope occurred in 48 patients (16%). Compared with those without syncope, these patients had higher rates of right ventricular dysfunction (68.7% vs. 32.5%, p = 0.002), elevated troponin (75% vs. 44%, p = 0.01), hypotension (29% vs. 8%, p < 0.001), Intensive Care Unit (ICU) admission (56% vs. 22%, p < 0.001), and thrombolysis (19% vs. 8%, p = 0.03). In-hospital mortality was markedly higher in the syncope group (37.5% vs. 7.1%, p < 0.001). Multivariate analysis confirmed syncope as an independent predictor of mortality (OR 4.2, 95% CI 2.1–8.4, p < 0.001), alongside right ventricular dysfunction and elevated troponin. Conclusions: Syncope at presentation is a simple but powerful clinical marker of high-risk PE and should prompt intensive monitoring and consideration of early reperfusion therapy.

Here, we report an unusual case of a nonsmoker and hypertensive 72-year-old male who was admitted with a transient ischemic attack to the Neurology Department of Clinical County Emergency Hospital Bihor. He presented a first transient ischemic attack and paroxysmal atrial fibrilation 2 years before, when anticoagulation was started on top of his antihypertensive medication. At that time, carotid Doppler ultrasound revealed nonobstructive atherosclerosis and statin therapy was started, according to current guidelines, in order to lower the initial 70 mg/dL LDL-cholesterol level to under 55 mg/dL. Cardio-embolism was considered the mechanism of stroke at that time. Despite all the medication and the maintenance of LDL below 50 mg/dL, carotid atherosclerosis evolved to an important left internal carotid artery stenosis and transient ischemic attacks reappeared two years later. Carotid stenosis was then considered the most probable cause, although elucidating the exact mechanism was difficult. After medical treatment and subsequent endarterectomy, the patient had a good outcome. The progressive course of atheromatosis, despite maximal medication, urged us to look for further proper measures of prevention. No chronic disease was detected during the postoperative phase, except for early-stage periodontal disease, for which adequate preventive measures were applied. Considering that subclinical inflammation induced by periodontal disease can induce the progression of atherosclerosis, chronic treatment with colchicine was added, with a favorable outcome.

Background/Objectives: Inflammation plays a central role in the pathophysiology of ST-elevation myocardial infarction (STEMI) and may influence myocardial injury, ventricular dysfunction and clinical outcomes. Simple inflammatory biomarkers derived from routine laboratory tests have been proposed as potential prognostic indicators in patients undergoing primary percutaneous coronary intervention (PCI). Objective: This study aimed to evaluate the association between admission inflammatory biomarkers, echocardiographic markers of ventricular dysfunction and in-hospital mortality in patients with STEMI treated with primary PCI. Methods: We conducted a retrospective observational study including 600 consecutive patients admitted with STEMI and treated with primary PCI between January 2021 and August 2025. Inflammatory biomarkers measured at admission included C-reactive protein (CRP); neutrophil-to-lymphocyte ratio (NLR); platelet-to-lymphocyte ratio (PLR); systemic immune-inflammation index (SII) and C-reactive protein-to-lymphocyte ratio (CLR). Echocardiographic parameters and clinical outcomes were recorded. Multivariable logistic regression analysis was performed to identify independent predictors of in-hospital mortality. Results: In-hospital mortality occurred in 54 patients (9.0%). Patients with reduced left ventricular ejection fraction (LVEF ≤ 40%) had significantly higher CRP and CLR levels (p < 0.01). Inflammatory biomarkers were associated with markers of ventricular dysfunction but were not independent predictors of mortality. Age, LVEF < 40% and the number of residual coronary lesions independently predicted in-hospital death. Conclusions: In STEMI patients undergoing primary PCI, early mortality is mainly determined by age; ventricular dysfunction and residual coronary disease burden, while inflammatory biomarkers primarily reflect the severity of myocardial injury rather than independently predicting short-term mortality.

Background: Aortic stenosis (AS) has long been considered a degenerative disease and is typically diagnosed in older men at an advanced stage. However, accumulating evidence has highlighted the similarities between AS and atherosclerosis, particularly regarding shared risk factors and overlapping pathophysiological mechanisms. This connection has led to a paradigm shift, suggesting that AS may be preventable in its early stages. Methods: This narrative review synthesizes the existing literature exploring the parallels between AS and atherosclerosis, focusing on common risk factors, pathogenic pathways, and evolving therapeutic strategies. Clinical trials and translational studies were examined to assess the effectiveness of atherosclerosis-based treatments for AS. Results: Multiple studies have confirmed the shared inflammatory, lipid-mediated, and calcific mechanisms of AS and atherosclerosis. Despite these similarities, therapeutic strategies effective in atherosclerosis, such as statin therapy, have not consistently shown benefits in AS. New medical approaches aim to delay aortic valve replacement and reduce the associated morbidity. The partially overlapping pathogenesis continues to guide future research. Conclusions: While AS and atherosclerosis share several pathogenic features, their clinical courses and treatment responses diverge. Understanding the limits and potential of their overlap may inform future preventive and therapeutic strategies. Earlier detection and targeted intervention in AS remain key goals, drawing on insights from cardiovascular disease management.