Stress echocardiography (SE) detects myocardial ischemia while coronary computed tomography angiography (CCTA) detects structural abnormalities associated with coronary artery disease (CAD). A pilot retrospective study of 270 consecutive patients who underwent both SE and CCTA to explore which test is more accurate in patients with CAD. Health records and risk factors, SE, and CCTA outcomes were reviewed. SE outcomes were positive (n = 36) and negative (n = 234); CCTA outcomes were based on CAD severity (absent, mild, moderate, and severe). 219 (81.1%) patients had a positive CCTA, indicating the presence of CAD with mild, moderate, or severe stenosis. Despite a positive CCTA (n = 191), 70.7% had a negative SE. This discrepancy was most prevalent in the moderate CCTA category, where 110 patients had a negative SE but positive CCTA. Additionally, 9 patients demonstrated a positive SE despite no significant CCTA findings, indicating that functional abnormalities could have remained undetected by anatomical imaging. It is suggested that significant CAD detected by CCTA does not necessarily suggest myocardial ischemia, while the presence of myocardial ischemia is not necessarily associated with significant CAD, suggesting other causes (e.g., microvascular angina). A positive CCTA but negative SE findings may suggest the presence of coronary collaterals.

The present review aimed to evaluate the prognostic value of inflammatory biomarkers in patients undergoing endovascular aortic aneurysm repair (EVAR). A systematic review of relevant studies was performed according to PRISMA guidelines. Articles assessing associations of inflammatory biomarkers with the post-EVAR outcomes were considered. After screening, 34 studies were included (7019 patients were reviewed; mean age: 73.6 years; 91.6% were men); 22 different inflammatory biomarkers were identified among the included studies. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and lymphocyte-to-monocyte ratio (LMR) were investigated in 11, 4, and 3 studies, respectively. Nine studies evaluated the post-implantation syndrome (PIS) and examined its role in post-EVAR outcomes. Increased preoperative NLR was associated with all-cause mortality and acute kidney injury after EVAR. NLR was also reported as an independent risk factor for aneurysm sac regression failure. High preoperative PLR and low preoperative LMR were correlated with acute kidney injury and overall mortality, respectively. PIS was associated with a lower type 2 endoleak rate but had no impact on mortality rates. NLR may be a useful predictor for mortality and poor prognosis in EVAR populations. This may have clinical implications in post-EVAR surveillance programs.

Arteriosclerosis is a systemic degenerative vascular disorder characterized by arterial wall thickening, reduced elasticity (arterial stiffness), and luminal narrowing, and is closely associated with aging and hypertension. Key pathological processes include lipid deposition, chronic inflammation, vascular calcification, and hemodynamic disturbances. These processes progressively injure high metabolic demand organs, including the heart, brain, and kidneys, through both direct vascular damage and indirect regulatory pathways. Conversely, injury to these target organs can activate compensatory and stress responses that further accelerate vascular remodeling, establishing a self-reinforcing cycle of "vascular-organ interactive injury." This review summarizes mechanisms by which arteriosclerosis drives multi-organ damage, highlights related clinical manifestations and outcomes, discusses how cardiac, cerebral, and renal dysfunction feeds back to worsening vascular disease, and outlines current strategies for clinical assessment and intervention.

Aneurysms are permanent, focal dilations of vessels that are ≥150% of normal diameter. While single aneurysms are relatively common, the presence of multiple aneurysms in different vascular territories is uncommon, and consolidated discussions of such cases remain limited. We report the case of a 96-year-old male cadaver with extensive but clinically silent aortic aneurysms identified during routine anatomical dissection. A large abdominal tumor was also noted compressing the right renal artery. Additionally, we review published reports of multi-territory aneurysms, which highlight the heterogeneity in patients and presentation types, including genetic disorders that lead to aneurysmal disease. Rupture risk is multifactorial, influenced by size, morphology, multiplicity, growth rate, and thrombus burden. Multi-territory aneurysmal disease, though rare, represents a clinically significant entity that may remain undetected until rupture or incidental discovery. Four domains emerge as central to management: screening, risk factor modification, genetic considerations, and counseling. This cadaveric case illustrates the breadth of aneurysm presentations and reinforces the importance of broad screening strategies in their surveillance. It also highlights the roles of risk reduction, genetic evaluation, and patient-centered counseling in reducing morbidity and mortality from this often silent vascular pathology.

Contrast-induced nephropathy (CIN) remains a frequent and clinically relevant complication in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). This study evaluated the predictive performance of inflammation-based indices for CIN development, with a focus on the inflammatory prognostic index (IPI). STEMI patients (n = 563) were retrospectively analyzed. CIN developed in 85 patients (15.1%). Admission IPI values were significantly higher in patients who developed CIN compared with those without CIN (10.9 [7.6-16.2] vs 4.8 [3.1-7.9], P < .001). In multivariate logistic regression analysis, IPI remained independently associated with CIN (odds ratio [OR] 1.31, 95% confidence interval [CI] 1.06-1.61, P = .013), together with advanced age, higher blood urea nitrogen levels, reduced left ventricular ejection fraction, history of stroke, and the occurrence of no-reflow. Receiver operating characteristic analysis demonstrated superior discriminative performance for IPI (area under the curve [AUC] 0.826, 95% CI 0.783-0.869) compared with neutrophil-to-lymphocyte ratio (NLR; AUC 0.691), C-reactive protein-to-albumin ratio (CAR; AUC 0.712), and systemic immune inflammation index (SII; AUC 0.704). An admission IPI cutoff value of 8.35 predicted CIN with 82.4% sensitivity and 65.9% specificity. IPI demonstrates superior discriminative performance compared with CAR, NLR, and SII for predicting CIN in STEMI patients undergoing pPCI.

Vascular cognitive impairment (VCI) affects 20% to 40% of cardiovascular patients, yet early identification remains challenging. This retrospective study evaluated the predictive value of carotid ultrasound parameters for VCI in 412 patients with cardiovascular risk factors who underwent carotid ultrasound and cognitive assessment between January 2019 and December 2023. Patients were categorized into normal cognition (n = 156), mild cognitive impairment (n = 184), and vascular dementia (n = 72) based on Montreal Cognitive Assessment scores. Carotid intima-media thickness (cIMT) progressively increased from normal cognition (0.89 ± 0.15 mm) to vascular dementia (1.18 ± 0.24 mm, P < .001). After multivariable adjustment, cIMT >1.0 mm (Odds Ratio [OR]: 2.84, 95% CI: 1.76-4.58), carotid stenosis ≥50% (OR: 4.92, 95% CI: 2.31-10.47), and resistive index >0.75 (OR: 3.15, 95% CI: 1.89-5.24) were independently associated with VCI. A combined model incorporating multiple carotid parameters achieved an area under the curve of 0.82 for VCI detection. These findings suggest that carotid ultrasound parameters may help identify cardiovascular patients at elevated risk for cognitive impairment, though external validation is needed before clinical implementation.

MicroRNAs (miRNAs) has emerged as a key regulatory factor in cardiovascular diseases, including acute myocardial infarction (AMI). We aim to explore the effects of miR-1306-5p on AMI. We enrolled 130 AMI patients and 85 healthy individuals. The levels of genes were measured by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, myocardial injury markers and inflammatory factor levels were assessed via cell counting kit-8 (CCK-8) and Enzyme-Linked Immunosorbent Assay (ELISA) assays. Target relationships were confirmed via dual-luciferase reporter assays and RNA immunoprecipitation (RIP) experiments. miR-1306-5p was remarkably diminished in AMI patients. It was an independent predictor of AMI, showing a positive correlation with the cardiac troponin I (cTnI) and a negative correlation with high-density lipoprotein cholesterol (HDL-C) and ejection fraction. Mechanistically, upregulated miR-1306-5p diminished the levels of cTnI, creatine kinase-MB (CK-MB), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) while promoting proliferation in hypoxia-reoxygenation (H/R)-treated AC16 cells. These effects could be reversed by overexpressing ten-eleven translocation 3 (TET3). Moreover, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was found to function as a microRNA sponge for miR-1306-5p. In conclusion, miR-1306-5p could bind to NEAT1 and subsequently mitigate cardiomyocyte damage by negatively regulating TET3.