Search Results (487)

Background/Objectives: Nowadays, intravascular lithotripsy (IVL) has emerged as a novel technique for treatment of vascular calcifications, first in coronary and then in peripheral arteries. In the current literature there is little evidence that describes IVL as an effective and safe solution in treating severe aortic and aorto-iliac calcifications. The aim of this study is to report current available data about the use of IVL in treating aortic and aorto-iliac calcified lesions and its application in facilitating other endovascular procedures. Methods: the present review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) Guidelines. Preliminary searches were conducted on MEDLINE and Pubmed from January 2015 to February 2025. Studies were divided into 3 main categories depending on the location of calcifications and the type of treatment: IVL in visceral and infrarenal obstructive disease (group 1), IVL in aorto-iliac obstructive disease (group 2), IVL used to facilitate other endovascular procedures. Main primary outcomes in the perioperative period were technical and clinical successes and perioperative complications. Primary outcomes at 30 days and mid-term (2 years) were overall survival, limb salvage rate, primary patency, primary assisted patency, secondary patency, and residual stenosis. Results: Sixteen studies were identified for a total of 1674 patients. Technical and clinical successes were 100%, with low rates of perioperative complications. Dissection rate reaches up to 16.1% in some studies, without any differences compared to plain old balloon angioplasty (POBA) alone (22.8%; p = 0.47). At 30 days, limb salvage and survival rates were 100%. At 2 years, primary patency, assisted primary patency, and secondary patency were 95%, 98%, and 100%, respectively, with no difference compared to IVL + stenting. Conclusions: IVL has emerged as a novel approach to treat severe calcified lesions in visceral and aorto-iliac atherosclerotic disease and to facilitate other endovascular procedures. This technique seems to offer satisfactory early and mid-term outcomes in terms of primary, primary assisted patency, and secondary patency with low complication rates. Full article

Coronary artery disease (CAD) is the main cause of morbidity and death worldwide, and atherosclerosis represents the leading pathophysiological pathway responsible for CAD. Atherosclerotic process is a complex interplay of mechanisms and mediators resulting in plaque formation, progression and destabilization, the latter being the most frequent cause of acute cardiovascular events. Considering the systemic nature of atherosclerosis, polyvascular disease involvement is possible and has been described since 1960s. Accordingly, epidemiologic studies reported that concomitant CAD and atherosclerosis in other arterial beds like carotid arteries, lower limb arteries, mesenteric and renal circulation, and aorta, is frequent and related to increased chance of future cardiovascular events. Although risk factors, atherosclerotic plaque features and mechanisms of plaque destabilization are largely shared across different sites, many studies have reported some disparities among districts. Moreover, simultaneous polyvascular disease has been associated with increased likelihood of having particular plaque characteristics depending on the affected arterial level. In this comprehensive narrative review, we aim to discuss about epidemiology of concomitant CAD and atherosclerosis in other arterial beds, and to examine differences in risk factors, plaque features and mechanisms of plaque instability between CAD and other atherosclerotic locations. Finally, we review the studies observing differences on plaque features according to involved atherosclerotic sites, focusing on CAD. Full article

Background and Objectives: Galectin-3 (Gal-3), a pro-inflammatory cytokine, has been implicated in atherosclerosis and adverse cardiovascular outcomes. While its role in coronary artery disease (CAD) is increasingly recognized, its association with systemic atherosclerosis remains underexplored. Objective: To investigate serum Gal-3 levels in patients with CAD and evaluate correlations between CAD severity and extra-coronary atherosclerotic involvement (carotid, femoral, and radial territories). Materials and Methods: We prospectively enrolled 56 patients with CAD undergoing coronary angiography (42.8% with acute-ACS; 57.2% with chronic coronary syndromes-CCS). Gal-3 levels were measured within 24 h of admission. Atherosclerosis severity was assessed angiographically and through vascular ultrasound of the carotid, femoral, and radial arteries. Patients were stratified by median Gal-3 levels, and clinical follow-up was performed at 1 and 3 months. Results: Gal-3 levels were significantly higher in CAD vs. controls (20.7 vs. 10.1 ng/mL; p < 0.00001) and in ACS vs. CCS (22.18. vs. 17.93 ng/mL; p = 0.019). Gal-3 correlated positively with culprit lesion diameter stenosis (DS) (R = 0.30; p = 0.023) and maximum severity of additional treated lesions (R = 0.62; p = 0.006). Gal-3 also correlated positively with carotid plaque thickness (R = 0.32; p = 0.016), while patients with Gal-3 levels above the median showed increased median values for femoral plaque thickness (32.4 vs. 26.45 mm, p = 0.046). No correlation was found with radial artery calcification. Gal-3 showed moderate discrimination for ACS (AUC = 0.685; cut-off 20.18 ng/mL). On multivariate analysis age, DS, and ACS presentation were independent predictors of Gal-3 above 19.07 ng/mL. Conclusions: Gal-3 levels are elevated in ACS and correlate with atherosclerotic burden, particularly in coronary, carotid, and femoral territories. These findings support Gal-3 as a potential marker of lesion severity and systemic vascular involvement, highlighting its possible role in risk stratification and the monitoring of atherosclerotic disease progression. This study provides integrated insights into the impact of Gal-3 across multiple vascular beds by assessing them concurrently within the same patient cohort. Full article

Advances in plaque imaging have transformed cardiovascular diagnostics through detailed characterization of atherosclerotic plaques beyond traditional stenosis assessment. This review outlines the clinical applications of varying modalities, including dual-layer spectral CT, photon-counting CT, dual-energy CT, and CT-derived fractional flow reserve (CT-FFR). These technologies offer improved spatial resolution, tissue differentiation, and functional assessment of coronary lesions. Additionally, artificial intelligence has emerged as a powerful tool to automate plaque detection, quantify burden, and refine risk prediction. Collectively, these innovations provide a more comprehensive approach to coronary artery disease evaluation and support personalized management strategies. Full article

Acute myocardial infarction (AMI) in young adults, though less common than in older populations, is an emerging clinical concern with increasing incidence and diverse etiologies. Unlike classic atherosclerotic presentations, a significant proportion of AMI cases in individuals under 45 years are due to nonatherothrombotic mechanisms such as coronary vasospasm, spontaneous coronary artery dissection (SCAD), vasculitis, hypercoagulable states, and drug-induced coronary injury. This manuscript aims to explore the multifactorial nature of AMI in young adults through a focused review of current evidence and a series of illustrative clinical cases. We present and analyze four distinct cases of young patients with AMI, each demonstrating different pathophysiological mechanisms and risk profiles—including premature atherosclerosis, substance use, human immunodeficiency virus (HIV)-related coronary disease, and SCAD. Despite the heterogeneity of underlying causes, early diagnosis, individualized management, and aggressive secondary prevention were key to favorable outcomes. Advanced imaging, lipid profiling, and risk factor modification played a central role in guiding therapy. AMI in young adults requires heightened clinical suspicion and a comprehensive, multidisciplinary approach. Early intervention and recognition of nontraditional risk factors are essential to improving outcomes and preventing recurrent events in this vulnerable population. Full article

Aim: The frontal QRS-T (fQRS-T) angle serves as an electrocardiography indicator that visually represents the disparity between the frontal QRS axis and the T axis. The heterogeneity between cardiac depolarization and repolarization rises with an increase in the fQRS-T angle. Prior research has demonstrated a relationship between the fQRS-T angle and the extent of atherosclerosis, along with the risk of cardiovascular mortality. The non-alcoholic fatty liver disease fibrosis score (NFS) is a non-invasive scoring tool used to quantify the degree of liver fibrosis in individuals with non-alcoholic fatty liver disease (NAFLD). Non-alcoholic fatty liver disease increases the risk of atherosclerotic cardiovascular disease, which can be predicted using the NFS. The objective of this study is to examine the potential correlation between the fQRS-T angle and NFS in patients with stable angina pectoris. Materials and Methods: This cross-sectional study included 177 (48 women) non-alcoholic patients who underwent coronary angiography due to stable angina pectoris. Individual NFS values were calculated using clinical and laboratory data. Patients were categorized into two groups based on a NFS threshold value of 0.67. Following a minimum fasting period of 12 h, biochemical laboratory parameters were acquired using a peripheral venous sample, and electrocardiographic data were recorded. Results: The univariate logistic regression analysis revealed significant associations between hypertension (p = 0.018), coronary artery disease (p = 0.014), neutrophil (p = 0.024), hemoglobin (p = 0.038), and low-density lipoprotein (LDL, p = 0.007) with the NFS. The electrocardiographic variables related to the score included the QRS duration (p = 0.015), Pmax (p = 0.026), QTC interval (p = 0.02), and fQRS-T angle (p < 0.001). In the multivariate logistic regression analysis, NFS was independently associated with LDL (OR: 0.984, 95% CI: 0.970–0.998, p = 0.024) and fQRS-T angle (OR: 3.472, 95% CI: 1.886–6.395, p < 0.001). Conclusions: The FQRS-T angle may exhibit a distinct correlation with NAFLD. Extensive investigations should validate this link, since the fibrosis score can serve as an effective tool for monitoring patients prior to the onset of clinical symptoms associated with liver fibrosis. Full article

HMG-CoA reductase inhibitors, statins, are extensively used to treat hyperlipidemia, coronary artery disease, and other atherosclerotic disorders. However, one of the common side effects of statin therapy is a mild elevation in liver aminotransferases, observed in less than 3% of patients. Atorvastatin and simvastatin, in particular, are most frequently associated with statin-induced liver injury, leading to treatment discontinuation. Recent research has highlighted the antioxidant and anti-inflammatory properties of glucagon-like peptide-1 receptor (GLP-1R) activation in protecting against liver injury. Nonetheless, the potential protective effects of liraglutide (LIRA), a GLP-1R agonist, against atorvastatin (ATO)-induced liver dysfunction have not been fully elucidated. In this context, the present study aimed to investigate the protective role of LIRA in mitigating ATO-induced liver injury in rats, offering new insights into managing statin-associated hepatotoxicity. Indeed, LIRA treatment improved liver function enzymes and attenuated histopathological alterations. LIRA treatment enhanced antioxidant defenses by increasing Nrf2 content and superoxide dismutase (SOD) activity, while reducing NADPH oxidase. Additionally, LIRA suppressed inflammation by downregulating the HMGB1/TLR-4/RAGE axis and inhibiting the protein expression of pY323-MAPK p38 and pS635-NFκB p65 content resulting in decreased proinflammatory cytokines (TNF-α and IL-1β). Furthermore, LIRA upregulated GLP-1R gene expression and promoted autophagic influx via the activation of the pS473-Akt/pS486-AMPK/pS758-ULK1/Beclin-1 signaling cascade, along with inhibiting apoptosis by reducing caspase-3 content. In conclusion, LIRA attenuated ATO-induced oxidative stress and inflammation via activation of the Nrf-2/SOD cascade and inhibition of the HMGB1/TLR-4/RAGE /MAPK p38/NFκB p65 axis. In parallel, LIRA stimulated autophagy via the AMPK/ULK1/Beclin-1 axis and suppressed apoptosis, thus restoring the balance between autophagy and apoptosis. Full article

Atherosclerosis, a chronic inflammatory disease, remains a leading cause of cardiovascular mortality worldwide. Despite standard treatments like statins and percutaneous coronary intervention (PCI), significant residual risk and therapeutic limitations underscore the need for innovative strategies. This review summarizes recent advances in nanoparticle-based therapies for atherosclerosis, focusing on key developments from the last five years. We discuss various nanoplatforms designed to selectively target key cellular players in plaque pathogenesis, including macrophages, endothelial cells, and vascular smooth muscle cells (VSMCs), to inhibit inflammation, modulate cellular phenotypes, and stabilize plaques. A significant focus is placed on the emerging field of biomimetic nanoparticles, where therapeutic cores are camouflaged with cell membranes derived from macrophages, platelets, neutrophils, or erythrocytes. This approach leverages the natural biological functions of the source cells to achieve enhanced immune evasion, prolonged circulation, and precise targeting of atherosclerotic lesions. Furthermore, the review covers nanoparticles engineered for specific functional interventions, such as lowering LDL levels and exerting direct anti-inflammatory and anti-oxidative effects. Finally, we address the critical challenges hindering clinical translation, including nanotoxicity, biodistribution, and manufacturing scalability. In conclusion, nanotechnology offers a versatile and powerful platform for atherosclerosis therapy, with targeted and biomimetic strategies holding immense promise to revolutionize future cardiovascular medicine. Full article

Despite significant advances in understanding and management, cardiovascular diseases remain the leading cause of mortality worldwide. Historically, diagnostic and therapeutic strategies have typically targeted obstructive coronary arteries. However, growing evidence supports the pivotal role of non-obstructive mechanisms in myocardial ischemia, prompting a new classification that distinguishes Acute Myocardial Ischemic Syndromes from Non-Acute Myocardial Ischemic Syndromes. In this evolving context, Optical Coherence Tomography (OCT) plays an important diagnostic role in the assessment of both obstructive and non-obstructive ischemic mechanisms. In Acute Myocardial Ischemic Syndromes, OCT enables the identification of major plaque destabilization mechanisms and contributes to the diagnosis of Myocardial Infarction with Non-Obstructive Coronary Arteries, helping to differentiate between atherosclerotic and non-atherosclerotic causes. In Non-Acute Myocardial Ischemic Syndromes, OCT assists in evaluating stenosis severity, plaque morphology, vulnerability, and healing, and may contribute to the diagnosis of Ischemia with Non-Obstructive Coronary Arteries, identifying myocardial bridge and epicardial spasm alongside conventional functional assessment of intermediate stenoses. This narrative review outlines the expanding clinical applications of OCT across the full spectrum of ischemic syndromes, emphasizing its role in bridging obstructive and non-obstructive pathophysiology and supporting a more comprehensive diagnostic approach to ischemic heart disease. Full article

Background: Coronary artery disease (CAD) is a leading global cause of mortality. The role of calcium (Ca), a key metabolic and structural element, in atherosclerosis and inflammation remains unclear. Ca influences immune cell function and is a component of atherosclerotic plaques. Hair analysis reflects long-term mineral exposure and may serve as a non-invasive biomarker. Objectives: This pilot study aimed to investigate the association between hair Ca levels and acute coronary syndrome (ACS), and to evaluate correlations with the Systemic Inflammatory Index (SII), Systemic Inflammatory Response Index (SIRI), and selected CAD risk factors. Methods: Ca levels were measured in hair samples from patients undergoing coronary angiography for suspected myocardial infarction. Associations with ACS diagnosis, Syntax score, SII, SIRI, and CVD risk factors were analyzed. Results: Serum calcium levels were not significantly associated with the presence of acute coronary syndrome (ACS) (p = 0.392) or with its clinical subtypes, including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA) (p = 0.225). Diagnosis of ACS was linked to higher SII (p = 0.028) but not SIRI (p = 0.779). Ca levels correlated negatively with Syntax score (R = −0.19, p = 0.035) and SII (R = −0.22, p = 0.021) and positively with HDL-C (R = 0.18, p = 0.046). Conclusions: Hair calcium content may reflect subclinical inflammation and CAD severity. Although no direct link to ACS was observed, the associations with SII, HDL-C, and Syntax score suggest a potential diagnostic role which should be further explored in larger, well-controlled studies. Full article

Background/Objectives: The hemoglobin-to-red blood cell distribution width (RDW) ratio (HRR) reflects the status of inflammation and oxidative stress size. Previously, it has been suggested that HRR is associated with cardiovascular diseases (CVD). However, evidence has been limited for examining the association between HRR and the incidence of specific cardiovascular events (e.g., cardiovascular disease, stroke, congestive heart failure) and all-cause cardiovascular death and non-cardiovascular death, adjusting for known confounders. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) in the year cycle of 1999–2018 were collected. HRR was calculated as the ratio of hemoglobin divided by the RDW. The outcomes were CVD, including stroke, congestive heart failure, atherosclerotic cardiovascular diseases (ASCVD), coronary artery disease as well as all-cause death including cardiovascular death and non-cardiovascular death. Univariate and multivariate analyses were performed to explore the association between HRR and outcomes. Restricted cubic spline curves were delineated. Results: In total, 47,719 participants were eligible for further analysis. In multivariate analysis adjusting for all confounding factors, higher HRR levels were significantly associated with a decreased risk of CVD. Compared to Q1 (<9.86), the odds ratio (OR) and 95% confidence intervals (95% CI) in Q2 (9.86–10.96), Q3 (10.96–11.97), and Q4 (≥11.97) were 0.79 (0.66, 0.94), 0.59 (0.48, 0.73), and 0.53, (0.42, 0.67), respectively, for predicting CVD. Similar results were observed for different subtypes of CVD, including stroke, congestive heart failure, and ASCVD. Notably, for predicting coronary heart disease, only Q3 was significant compared to Q1 (0.70, [0.54, 0.92], p = 0.010). HRR was significant for predicting all-cause death, cardiovascular death, and non-cardiovascular death. Additionally, HRR had the highest discriminative ability for predicting all-cause death compared with that of hemoglobin and RDW. Conclusions: A higher HRR was associated with a lower risk of CVD and death. Moderate levels of HRR were associated with the lowest risk for coronary heart disease. HRR had better discriminative ability than hemoglobin and RDW. Full article

Mitral annular calcification (MAC) is usually considered an incidental, benign, age-related finding without serious complications in patients evaluated for cardiovascular or pulmonary disease with imaging studies that may result in mitral regurgitation or stenosis when severe. Therefore, it is usually not considered a significant alteration. However, there is accumulating evidence that it is associated with a higher risk of cardiovascular events, such as atherosclerotic coronary artery disease, aortic artery disease, carotid artery disease, peripheral artery disease, stroke, atrial fibrillation, atrioventricular and/or intraventricular conduction disturbance, systemic embolization, infective endocarditis, heart failure and mortality. The presence of MAC also significantly influences the outcome of mitral valve transcatheter and surgical interventions. Several conditions may predispose to MAC. MAC is strongly related to cardiovascular risk factors, such as hypertension, diabetes, smoking and cardiovascular atherosclerosis, and inflammation may also play a role in the pathogenesis of MAC. Also, conditions that increase mitral valve stress, such as hypertension, aortic stenosis and hypertrophic cardiomyopathy, predispose to accelerated degenerative calcification of the mitral annulus area. Congenital disorders, e.g., Marfan syndrome and Hurler syndrome, are also associated with MAC, due to an intrinsic abnormality of the connective tissue composing the annulus. Full article

Calcium (Ca²⁺) signaling is a fundamental regulatory mechanism controlling essential processes in the endothelium, vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM), including maintaining the endothelial barrier, modulation of vascular tone, and vascular remodeling. Cytosolic free Ca²⁺ concentration is tightly regulated by a balance between Ca²⁺ mobilization mechanisms, including Ca²⁺ release from the intracellular stores in the sarcoplasmic/endoplasmic reticulum and Ca²⁺ entry via voltage-dependent, transient-receptor potential, and store-operated Ca²⁺ channels, and Ca²⁺ elimination pathways including Ca²⁺ extrusion by the plasma membrane Ca²⁺-ATPase and Na⁺/Ca²⁺ exchanger and Ca²⁺ re-uptake by the sarco(endo)plasmic reticulum Ca²⁺-ATPase and the mitochondria. Some cell membranes/organelles are multifunctional and have both Ca²⁺ mobilization and Ca²⁺ removal pathways. Also, the individual Ca²⁺ handling pathways could be integrated to function in a regenerative, capacitative, cooperative, bidirectional, or reciprocal feed-forward or feed-back manner. Disruption of these pathways causes dysregulation of the Ca²⁺ signaling dynamics and leads to pathological cardiovascular conditions such as hypertension, coronary artery disease, atherosclerosis, and vascular calcification. In the endothelium, dysregulated Ca²⁺ signaling impairs nitric oxide production, reduces vasodilatory capacity, and increases vascular permeability. In VSMCs, Ca²⁺-dependent phosphorylation of the myosin light chain and Ca²⁺ sensitization by protein kinase-C (PKC) and Rho-kinase (ROCK) increase vascular tone and could lead to increased blood pressure and hypertension. Ca²⁺ activation of matrix metalloproteinases causes collagen/elastin imbalance and promotes vascular remodeling. Ca²⁺-dependent immune cell activation, leukocyte infiltration, and cholesterol accumulation by macrophages promote foam cell formation and atherosclerotic plaque progression. Chronic increases in VSMCs Ca²⁺ promote phenotypic switching to mesenchymal cells and osteogenic transformation and thereby accelerate vascular calcification and plaque instability. Emerging therapeutic strategies targeting these Ca²⁺-dependent mechanisms, including Ca²⁺ channel blockers and PKC and ROCK inhibitors, hold promise for restoring Ca²⁺ homeostasis and mitigating vascular disease progression. Full article

Background: Atherosclerotic disease is the leading global cause of death, driven by progressive plaque accumulation in the arteries. Ultrasound (US) imaging, both conventional (CUS) and intravascular (IVUS), is crucial for the non-invasive assessment of atherosclerotic plaques. Deep learning (DL) techniques have recently gained attention as tools to improve the accuracy and efficiency of image analysis in this domain. This paper reviews recent advancements in DL-based methods for the segmentation, classification, and quantification of atherosclerotic plaques in US imaging, focusing on their performance, clinical relevance, and translational challenges. Methods: A systematic literature search was conducted in the PubMed, Scopus, and Web of Science databases, following PRISMA guidelines. The review included peer-reviewed original articles published up to 31 January 2025 that applied DL models for plaque segmentation, characterization, and/or quantification in US images. Results: A total of 53 studies were included, with 72% focusing on carotid CUS and 28% on coronary IVUS. DL architectures, such as UNet and attention-based networks, were commonly used, achieving high segmentation accuracy with average Dice similarity coefficients of around 84%. Many models provided reliable quantitative outputs (such as total plaque area, plaque burden, and stenosis severity index) with correlation coefficients often exceeding R = 0.9 compared to manual annotations. Limitations included the scarcity of large, annotated, and publicly available datasets; the lack of external validation; and the limited availability of open-source code. Conclusions: DL-based approaches show considerable promise for advancing atherosclerotic plaque analysis in US imaging. To facilitate broader clinical adoption, future research should prioritize methodological standardization, external validation, data and code sharing, and integrating 3D US technologies. Full article

Background/Objectives: Cardiovascular disease remains the leading global cause of death, with atherosclerotic plaque vulnerability, rather than stenosis severity, playing a central role in acute coronary events. Epicardial adipose tissue (EAT) has emerged as a key contributor to coronary atherosclerosis and myocardial ischemia. This study aimed to investigate the relationship between EAT thickness and the development and severity of atherosclerotic plaques in these coronary arteries, and to evaluate the influence of demographic factors on EAT thickness and plaque vulnerability. Methods: A retrospective analysis was conducted on autopsy data from 245 sudden cardiac death (SCD) cases (2021–2023). EAT thickness was measured at the left anterior descending artery (LAD) and left circumflex coronary artery (LCx) levels. From each artery, one segment that showed evidence of an atherosclerotic plaque was collected and sent for histological examination. Additionally, we documented demographic data, including age, sex, and body mass index (BMI) for each case. Results: In the present study, we enrolled 245 subjects with SCD, among whom 175 (71.42%) were male, and 70 (28.58%) were female. The mean age was 62.31 ± 12.69 years, and the mean BMI was 26.12 ± 4.16. We observed a mean EAT thickness value of 0.74 ± 0.26 cm at the LAD artery level and 0.71 ± 0.27 cm at the LCx artery level. We observed a positive correlation between BMI and EAT thickness at the LAD level (r = 0.260, p < 0.001) and similarly at the LCx level (r = 0.260, p < 0.001). Additionally, advancing age is associated with an increase in EAT thickness at both the LAD level (r = 0.188, p = 0.003) and the LCx level (r = 0.242, p < 0.001). Furthermore, we observed a higher EAT thickness at the LAD level (p = 0.0019) and the LCx level (p = 0.0225) among subjects with unstable atherosclerotic plaques. In the logistic regression analysis, the elevated value of EAT thickness was associated with unstable atherosclerotic plaque at LAD (OR: 1.88, p = 0.002) and LCx (OR: 1.51, p = 0.010) for the entire study cohort. Conclusions: Our data revealed that higher baseline values of EAT LCx and EAT LAD are associated with unstable plaque at the level of the left coronary arteries. Furthermore, our findings indicate that male individuals are more susceptible to developing unstable plaques in the coronary arteries. Full article