Differential culprit plaque morphology in acute coronary syndrome: a comparison between very young patients (≤35 years) and older counterparts using optical coherence tomography.

Aims: Underlying mechanisms responsible for acute coronary syndrome (ACS) in young patients compared with older counterparts are yet to be explored with optical coherence tomography (OCT). This study aims to explore underlying mechanisms of ACS in ≤35- (very young) and >35-year-old (older counterparts) ACS patients using OCT. Methods and results: This was a prospective, single-centre, investigational study. Patients were divided into groups according to age (≤35 and >35 years) and further subdivided according to the underlying mechanism i.e. plaque rupture (PR) and plaque erosion (PE). A total of 93 patients were analysed. Thin-cap fibroatheroma (TCFA) was significantly higher among older counterparts than very young patients for both PR (80.0% vs. 31.8%, P = 0.002) and PE (66.7% vs. 6.3%, P < 0.001) groups. Microchannels were also significantly more prevalent among older than very young patients for both PR (65.0% vs. 18.2%, P = 0.004) and PE groups (55.6% vs.12.5%, P = 0.013). Macrophages were significantly higher in older than very young patients for both PR (25.0% vs. 0%, P = 0.018) and PE (44.4% vs. 0%, P = 0.003) groups. In contrast, fibrous cap thickness was greater in very young than older patients for both PR (105.71 ± 48.02 vs. 58.00 ± 15.76 µm, P < 0.001) and PE (126.67 ± 48.22 vs. 54.38 ± 24.21 µm, P < 0.001) groups. Intimal thickness was greater in older than very young patients for both PR (728.00 ± 313.92 vs. 342.27 ± 142.02 µm, P < 0.001) and PE (672.78 ± 334.57 vs. 295.00 ± 99.60 µm, P < 0.001) groups. Conclusion: Frequency of TCFA, microchannels, macrophages, and intimal thickness was significantly higher in older ACS patients compared with very young patients. However, fibrous cap thickness was significantly greater in very young ACS patients compared with older patients.

Fluorescence and photoacoustic (FL/PA) dual-modal probe: Responsive to reactive oxygen species (ROS) for atherosclerotic plaque imaging.

Accurate and early detection of atherosclerosis (AS) is imperative for their effective treatment. However, fluorescence probes for efficient diagnosis of AS often encounter insufficient deep tissue penetration, which hinders the reliable assessment of plaque vulnerability. In this work, a reactive oxygen species (ROS) activated near-infrared (NIR) fluorescence and photoacoustic (FL/PA) dual model probe TPA-QO-B is developed by conjugating two chromophores (TPA-QI and O-OH) and ROS-specific group phenylboronic acid ester. The incorporation of ROS-specific group not only induces blue shift in absorbance, but also inhibits the ICT process of TPA-QO-OH, resulting an ignorable initial FL/PA signal. ROS triggers the convertion of TPA-QO-B to TPA-QO-OH, resulting in the concurrent amplification of FL/PA signal. The exceptional selectivity of TPA-QO-B towards ROS makes it effectively distinguish AS mice from the healthy. The NIR emission can achieve a tissue penetration imaging depth of 0.3 cm. Moreover, its PA775 signal possesses the capability to penetrate tissues up to a thickness of 0.8 cm, ensuring deep in vivo imaging of AS model mice in early stage. The ROS-triggered FL/PA dual signal amplification strategy improves the accuracy and addresses the deep tissue penetration problem simultaneously, providing a promising tool for in vivo tracking biomarkers in life science and preclinical applications.

Association Between Lipoprotein(a) and Obstructive Coronary Artery Disease and High-Risk Plaque: Insights From the PROMISE Trial.

BACKGROUND: The role of lipoprotein (a), or Lp(a), in the development of obstructive coronary artery disease (CAD) and high-risk plaque (HRP) among primary prevention patients with stable chest pain is unknown. We sought to evaluate the relationship of Lp(a), independent of low-density lipoprotein cholesterol (LDL-C), with the presence of obstructive CAD and HRP in an attempt to improve understanding of the residual risk imparted by Lp(a) on CAD. METHODS: We performed a secondary analysis among PROMISE (Prospective Multicenter Imaging Study for Evaluation of Chest Pain) Trial participants who had coronary computed tomographic angiography (CTA) performed and Lp(a) data available. Lp(a) concentration was analyzed as a binary variable with elevated Lp(a) defined as ≥50 mg/dL. "Stenosis ≥ 50%" was defined as ≥50% coronary artery stenosis in any epicardial vessel, and "Stenosis ≥ 70%" was defined as ≥70% coronary artery stenosis in any epicardial vessel and/or ≥50% left main coronary artery stenosis. HRP was defined as presence of plaque on CTA imaging with evidence of positive remodeling, low CT attenuation, or napkin ring sign. Multivariate logistic regression models were constructed to evaluate the association between Lp(a) and the outcomes of obstructive CAD and HRP stratified by LDL-C ≥100 mg/dL vs. <100 mg/dL. RESULTS: Of the 1,815 patients who underwent CTA and had Lp(a) data available, those with elevated Lp(a) were more commonly female and Black than those with lower Lp(a). Elevated Lp(a) was associated with both Stenosis ≥ 50% (OR 1.57, 95% CI 1.14-2.15, p=0.005) and Stenosis ≥ 70% (OR 2.05, 95% CI 1.34-3.11, p=0.0008) in multivariate models, and this relationship was not modified by LDL-C ≥100 mg/dL vs. <100 mg/dL (interaction p>0.4). Elevated Lp(a) was not associated with HRP when adjusted for obstructive CAD. CONCLUSIONS: This study of patients without known CAD found that elevated Lp(a) ≥50 mg/dL was independently associated with the presence of obstructive CAD regardless of controlled vs. uncontrolled LDL-C, but was not independently associated with HRP when Stenosis ≥ 50% or ≥ 70% was accounted for. Further research is warranted to delineate the role of Lp(a) in the residual risk for ASCVD that patients may have despite optimal LDL-C lowering.

NIRS-IVUS Assessment of OCT-Derived Healed Coronary Plaques.

AIMS: Healed plaque (HP) is associated with rapid plaque growth and luminal narrowing. Thin-cap fibroatheroma (TCFA) is recognized as a precursor lesion to plaque rupture. The aim of the present study was to compare the lipid size among optical coherence tomography (OCT)-derived HP, TCFA, and thick-cap fibroatheroma (ThCFA) using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS). METHODS: The present study included 173 patients with acute myocardial infarction (AMI) who underwent percutaneous coronary intervention. Non-culprit lesions with angiographically intermediate stenosis were assessed by both OCT and NIRS-IVUS. RESULTS: The frequency of TCFA, HP, and ThCFA was 35 (20%), 53 (30%), and 85 (49%), respectively. Minimum lumen area was not significantly different between TCFA and HP, but was smaller in TCFA and HP than in ThCFA (4.6 [interquartile range {IQR}: 3.5-6.4] mm2 vs. 4.3 [3.4-5.3] mm2 vs. 6.5 [4.8-8.6] mm2, P＜0.001). Plaque burden was not significantly different between TCFA and HP, but was larger in TCFA and HP than in ThCFA (72 [IQR: 66-80] % vs. 75 [67-80] % vs. 62 [54-69] %, P＜0.001). Maximum lipid core burden index in 4mm (maxLCBI4mm) was largest in TCFA, followed by HP and ThCFA (493 [IQR: 443-606] vs. 446 [347-520] vs. 231 [161-302], P＜0.001). The frequency of lipid rich plaque with maxLCBI4mm ＞400 was highest in TCFA, followed by HP and ThCFA (89% vs. 60% vs. 7%, P＜0.001). CONCLUSIONS: Based on NIRS-IVUS findings, non-culprit coronary HP in AMI was associated with vulnerable plaque characteristics, but not as much as TCFA.

Outcomes of surgical correction of Peyronie's disease with plaque excision and grafting: Comparison of testicular tunica vaginalis graft versus bovine pericardium graft.

Objective: Peyronie's disease (PD) is an abnormal wound healing in the penile tunica albuginea. After fibrotic plaque excision, different graft materials have been used to repair the defects, but the optimal graft remains unknown. This study aimed to compare the functional outcomes of testicular tunica vaginalis grafts and bovine pericardium grafts in patients with severe PD. Methods: A retrospective comparative study was conducted on 33 PD patients undergoing partial plaque excision and grafting from September 2015 to May 2021. The patients were divided into two groups depending on the type of graft used. For 15 patients in Group B, testicular tunica vaginalis grafts were used to repair the defect, while for 18 patients in Group A, bovine pericardium grafts were used. Data of the patient's age, comorbidities, sexual function, penile curvature, postoperative complications, need for further treatment, change in penile length, and satisfaction were gathered and compared between the groups. Sexual function was evaluated using the 5-item version of the International Index of Erectile Function (IIEF-5), and a functional less than 20-degree penile curvature after surgery was considered a successful intervention. Results: There was no difference in age, comorbidities, degree of curvature, perioperative IIEF-5, operative time, plaque size, or complication rates. After surgery, a statistically significant improvement in curvature degree (p<0.05) and satisfactory penile appearance (p<0.05) were seen in both groups without any superiority between the two groups (p=0.423 and p=0.840, respectively). With a 30-month follow-up, the IIEF-5 was consistent in both groups, with no statistical significance between the groups (p=0.492). The main change in penile length during the operation was increased and still positive in the last follow-up in both groups without statistical significance (p=0.255 and p=0.101, respectively). Conclusion: Partial plaque excision and corporoplasty with both testicular tunica vaginalis or bovine pericardium grafts are equally effective in treating males with clinically significant PD.

Methotrexate Toxicity-Induced Pancytopenia and Mucocutaneous Ulcerations in Psoriasis.

Methotrexate (MTX) is a commonly used immunosuppressant and chemotherapeutic agent, widely prescribed for autoimmune diseases such as psoriasis, rheumatoid arthritis, and certain malignancies. It functions by inhibiting dihydrofolate reductase, leading to impaired DNA synthesis and cell proliferation. While generally well-tolerated, MTX has a narrow therapeutic index, and its adverse effects can be severe, including hepatotoxicity, pulmonary toxicity, and hematological complications such as pancytopenia. Pancytopenia involves the reduction of all three blood cell lines and can result in significant morbidity and mortality. The risk of MTX toxicity is notably higher in patients with renal impairment, as the kidneys are the primary route of drug excretion. Renal dysfunction can lead to the accumulation of MTX, enhancing its toxicity. Numerous studies and case reports have highlighted the risks of MTX toxicity, especially in patients with renal impairment. Pancytopenia can present insidiously, with symptoms such as mucosal ulcers, fever, and generalized weakness, making early detection crucial. We report a case of a male patient in his late 40s with a complex medical history, including psoriasis, insulin-dependent type 2 diabetes mellitus, chronic kidney disease (CKD) stage 3b, and coronary artery disease (CAD). The patient presented to the emergency department with a one-week history of fever, generalized weakness, mouth sores, and a five-day history of bilateral lower limb swelling and pain. Vital signs were stable, but physical examination revealed pallor, large ulcerative lesions in the buccal mucosa, and erythematous, scaly lesions on the lower limbs. The patient's medication history included methotrexate, which he had stopped two months prior but was inadvertently resumed at an increased dose two weeks prior to presentation. Laboratory findings revealed pancytopenia with worsening trends, prompting a bone marrow biopsy that showed hypocellular marrow. The patient's CKD likely exacerbated the MTX toxicity due to impaired drug clearance, leading to pancytopenia. Treatment included intravenous leucovorin, blood and platelet transfusions, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Despite initial critical presentation, the patient showed significant improvement, with recovery of blood counts and resolution of symptoms. He was discharged with stable hemoglobin, platelet, and white blood cell counts.

Elastin-specific MR probe for visualization and evaluation of an interleukin-1ß targeted therapy for atherosclerosis.

Atherosclerosis is a chronic inflammatory condition of the arteries and represents the primary cause of various cardiovascular diseases. Despite ongoing progress, finding effective anti-inflammatory therapeutic strategies for atherosclerosis remains a challenge. Here, we assessed the potential of molecular magnetic resonance imaging (MRI) to visualize the effects of 01BSUR, an anti-interleukin-1ß monoclonal antibody, for treating atherosclerosis in a murine model. Male apolipoprotein E-deficient mice were divided into a therapy group (01BSUR, 2 × 0.3 mg/kg subcutaneously, n = 10) and control group (no treatment, n = 10) and received a high-fat diet for eight weeks. The plaque burden was assessed using an elastin-targeted gadolinium-based contrast probe (0.2 mmol/kg intravenously) on a 3 T MRI scanner. T1-weighted imaging showed a significantly lower contrast-to-noise (CNR) ratio in the 01BSUR group (pre: 3.93042664; post: 8.4007067) compared to the control group (pre: 3.70679168; post: 13.2982156) following administration of the elastin-specific MRI probe (p < 0.05). Histological examinations demonstrated a significant reduction in plaque size (p < 0.05) and a significant decrease in plaque elastin content (p < 0.05) in the treatment group compared to control animals. This study demonstrated that 01BSUR hinders the progression of atherosclerosis in a mouse model. Using an elastin-targeted MRI probe, we could quantify these therapeutic effects in MRI.

Prevalence and Severity of Periodontal Disease in Diabetic Patients in South Jordan: A Cross-Sectional Study.

INTRODUCTION: Poorly managed diabetes mellitus can elevate oral glucose levels, fostering gum disease. Conversely, untreated periodontal disease may worsen diabetes control. This study aims to assess the prevalence of periodontal disease and its association with diabetes characteristics in South Jordan. METHODS: This cross-sectional study enrolled 249 type 2 diabetic patients from Prince Hashim Bin Abdullah II Clinic in Aqaba, Jordan. Demographics, clinical history, and periodontal indices were recorded, with glycemic control measured via HbA1c. Statistical analyses utilized SPSS. RESULTS: Predominantly female (58%) and married (90%) participants had a mean age of 49.0 years, with uncontrolled diabetes prevalent in 86% (mean HbA1c: 9.16). Dyslipidemia (73%), hypertension (49%), and diabetic neuropathy (21%) were common. Periodontal indices indicated moderate to high scores, reflecting significant plaque accumulation (plaque index score (PIS) = 3: 20%), severe gingival inflammation (gingival index score (GIS) = 3: 22%), and notable bleeding upon probing (papillary bleeding index score (PBIS) = 3-4: 22%). Moreover, a considerable percentage exhibited advanced periodontal disease (community periodontal index score (CPIS) = 3-4: 19%). CONCLUSION: A high prevalence of periodontal disease among diabetic patients in South Jordan underscores the need for integrated diabetes and periodontal care strategies. These findings emphasize the interplay between diabetes control and periodontal health, warranting further investigation into effective intervention strategies.

Association between overweight/obesity and dental outcomes in early childhood: Findings from an Australian cohort study.

OBJECTIVES: Oral health is an important part of general health and well-being and shares risk factors, such as poor diet, with obesity. The published literature assessing the association between obesity and oral health in early childhood is sparse and inconsistent. The objective of this study was to investigate associations between overweight/obesity (measured by body mass index) and dental outcomes (caries, plaque index and gingival index) both cross-sectionally and longitudinally, taking account of potential confounding factors, based on data collected at age 2 and age 5 within the Australian Study of Mothers' and Infants' Life Events Affecting Oral Health (SMILE) birth cohort study. METHODS: This study used data from 1174 SMILE participants. Associations between overweight/obesity and dental outcomes were assessed using generalized linear regression models for the modified Poisson family with log link to estimate prevalence ratios. Cross-sectional and longitudinal models were fitted, after minimal and full adjustment for potential confounders. RESULTS: Approximately 12% of the participants were overweight/obese at 2 years and 9% at 5 years. Between 2 and 5 years, the prevalence of caries increased from approximately 4% to 24%, at least mild plaque accumulation increased from 37% to 90% and at least mild inflammation from 27% to 68%. There were no associations between overweight/obesity and the prevalence of dental caries; prevalence ratios (PR) [95% confidence interval (CI)] after adjustment for age and sex were 0.9 (0.3, 2.4) cross-sectionally at 2 years, 1.0 (0.6, 1.5) cross-sectionally at 5 years, and 1.0 (0.6, 1.5) for overweight/obesity at 2 years and caries at 5 years. Prevalence ratios were all around the value of 1 for the other dental outcomes and also after adjustment for additional confounders. CONCLUSIONS: There were no associations between overweight/obesity and dental caries, plaque index or gingival index in this cohort of preschool children. However, associations may emerge as the children become older, and it will be possible to extend analyses to include data collected at age 7 in the near future.

Spatial Transcriptomic Approach to Understanding Coronary Atherosclerotic Plaque Stability.

BACKGROUND: Coronary atherosclerotic plaques susceptible to acute coronary syndrome have traditionally been characterized by their surrounding cellular architecture. However, with the advent of intravascular imaging, novel mechanisms of coronary thrombosis have emerged, challenging our contemporary understanding of acute coronary syndrome. These intriguing findings underscore the necessity for a precise molecular definition of plaque stability. Considering this, our study aimed to investigate the vascular microenvironment in patients with stable and unstable plaques using spatial transcriptomics. METHODS: Autopsy-derived coronary arteries were preserved and categorized by plaque stability (n=5 patients per group). We utilized the GeoMx spatial profiling platform and Whole Transcriptome Atlas to link crucial histological morphology markers in coronary lesions with differential gene expression in specific regions of interest, thereby mapping the vascular transcriptome. This innovative approach allowed us to conduct cell morphological and spatially resolved transcriptional profiling of atherosclerotic plaques while preserving crucial intercellular signaling. RESULTS: We observed intriguing spatial and cell-specific transcriptional patterns in stable and unstable atherosclerotic plaques, showcasing regional variations within the intima and media. These regions exhibited differential expression of proinflammatory molecules (eg, IFN-γ [interferon-γ], MHC class II, proinflammatory cytokines) and prothrombotic signaling pathways. By using lineage tracing through spatial deconvolution of intimal CD68+ (cluster of differentiation 68) cells, we characterized unique, intraplaque subpopulations originating from endothelial, smooth muscle, and myeloid lineages with distinct regional locations associated with plaque instability. In addition, unique transcriptional signatures were observed in vascular smooth muscle and CD68+ cells among plaques exhibiting coronary calcification. CONCLUSIONS: Our study illuminates distinct cell-specific and regional transcriptional alterations present in unstable plaques. Furthermore, we characterize the first spatially resolved, in situ evidence supporting cellular transdifferentiation and intraplaque plasticity as significant contributors to plaque instability in human coronary atherosclerosis. Our results provide a powerful resource for the identification of novel mediators of acute coronary syndrome, opening new avenues for preventative and therapeutic treatments.

EPAS1 Attenuates Atherosclerosis Initiation at Disturbed Flow Sites Through Endothelial Fatty Acid Uptake.

BACKGROUND: Atherosclerotic plaques form unevenly due to disturbed blood flow, causing localized endothelial cell (EC) dysfunction. Obesity exacerbates this process, but the underlying molecular mechanisms are unclear. The transcription factor EPAS1 (HIF2A) has regulatory roles in endothelium, but its involvement in atherosclerosis remains unexplored. This study investigates the potential interplay between EPAS1, obesity, and atherosclerosis. METHODS: Responses to shear stress were analyzed using cultured porcine aortic EC exposed to flow in vitro coupled with metabolic and molecular analyses and by en face immunostaining of murine aortic EC exposed to disturbed flow in vivo. Obesity and dyslipidemia were induced in mice via exposure to a high-fat diet or through Leptin gene deletion. The role of Epas1 in atherosclerosis was evaluated by inducible endothelial Epas1 deletion, followed by hypercholesterolemia induction (adeno-associated virus-PCSK9 [proprotein convertase subtilisin/kexin type 9]; high-fat diet). RESULTS: En face staining revealed EPAS1 enrichment at sites of disturbed blood flow that are prone to atherosclerosis initiation. Obese mice exhibited substantial reduction in endothelial EPAS1 expression. Sulforaphane, a compound with known atheroprotective effects, restored EPAS1 expression and concurrently reduced plasma triglyceride levels in obese mice. Consistently, triglyceride derivatives (free fatty acids) suppressed EPAS1 in cultured EC by upregulating the negative regulator PHD2. Clinical observations revealed that reduced serum EPAS1 correlated with increased endothelial PHD2 and PHD3 in obese individuals. Functionally, endothelial EPAS1 deletion increased lesion formation in hypercholesterolemic mice, indicating an atheroprotective function. Mechanistic insights revealed that EPAS1 protects arteries by maintaining endothelial proliferation by positively regulating the expression of the fatty acid-handling molecules CD36 and LIPG to increase fatty acid beta-oxidation. CONCLUSIONS: Endothelial EPAS1 attenuates atherosclerosis at sites of disturbed flow by maintaining EC proliferation via fatty acid uptake and metabolism. This endothelial repair pathway is inhibited in obesity, suggesting a novel triglyceride-PHD2 modulation pathway suppressing EPAS1 expression. These findings have implications for therapeutic strategies addressing vascular dysfunction in obesity.

A Case Report With Dual Diagnosis of Candidiasis in a Patient With Uncontrolled Diabetes Mellitus.

Chronic hyperglycemia is a hallmark of diabetes mellitus (DM), one of the most common endocrine illnesses affecting millions of people globally. A key issue for diabetes patients is a compromised immune system, which impairs their capacity to fight off invading microbes and increases their susceptibility to infections. Compared to the healthy population, those with DM experience noticeably longer recovery from illnesses or injuries. Individuals suffering from DM are more susceptible to Candida albicans colonizing their oral and/or vaginal mucosa and urinary system. The present article presented a case of a 52-year-old female patient who reported recurrent multiple plaque-like lesions with the underlying condition of hyperglycemia. The oral lesions were treated using the local application of clotrimazole gel and the discomfort subsided with Aceclofenac. The underlying condition was treated by a general physician who prescribed the tablet metformin 500mg. The patient was educated about the predisposing condition, and motivated to make some lifestyle changes and to maintain a proper diet.

Treatment with APAC, a dual antiplatelet anticoagulant heparin proteoglycan mimetic, limits early collar-induced carotid atherosclerotic plaque development in Apoe-/- mice.

BACKGROUND AND AIMS: Mast cell-derived heparin proteoglycans (HEP-PG) can be mimicked by bioconjugates carrying antithrombotic and anti-inflammatory properties. The dual antiplatelet and anticoagulant (APAC) construct administered, either locally or intravenously (i.v.), targets activated endothelium, its adhesion molecules, and subendothelial matrix proteins, all relevant to atherogenesis. We hypothesized that APAC influences cellular interactions in atherosclerotic lesion development and studied APAC treatment during the initiation and progression of experimental atherosclerosis. METHODS: Male western-type diet-fed Apoe-/- mice were equipped with perivascular carotid artery collars to induce local atherosclerosis. In this model, mRNA expression of adhesion molecules including ICAM-1, VCAM-1, P-Selectin, and Platelet Factor 4 (PF4) are upregulated upon lesion development. From day 1 (prevention) or from 2.5 weeks after lesion initiation (treatment), mice were administered 0.2 mg/kg APAC i.v. or control vehicle three times weekly for 2.5 weeks. At week 5 after collar placement, mice were sacrificed, and lesion morphology was microscopically assessed. RESULTS: APAC treatment did not affect body weight or plasma total cholesterol levels during the experiments. In the prevention setting, APAC reduced carotid artery plaque size and volume by over 50 %, aligning with decreased plaque macrophage area and collagen content. During the treatment setting, APAC reduced macrophage accumulation and necrotic core content, and improved markers of plaque stability. CONCLUSIONS: APAC effectively reduced early atherosclerotic lesion development and improved markers of plaque inflammation in advanced atherosclerosis. Thus, APAC may have potential to alleviate the progression of atherosclerosis.

Sex differences in plaque characteristics of fractional flow reserve-negative non-culprit lesions after myocardial infarction.

BACKGROUND AND AIMS: Recurrent events after myocardial infarction (MI) are common and often originate from native non-culprit (NC) lesions that are non-flow limiting. These lesions consequently pose as targets to improve long-term outcome. It is, however, largely unknown whether these lesions differ between sexes. The aim of this study was to assess such potential differences. METHODS: From the PECTUS-obs study, we assessed sex-related differences in plaque characteristics of fractional flow reserve (FFR)-negative intermediate NC lesions in 420 MI-patients. RESULTS: Among the included patients, 80 (19.1 %) were female and 340 (80.9 %) male. Women were older and more frequently had hypertension and diabetes. In total, 494 NC lesions were analyzed. After adjustment for clinical characteristics and accounting for within-patients clustering, lesion length was longer in female patients (20.8 ± 10.0 vs 18.3 ± 8.5 mm, p = 0.048) and minimum lumen area (2.30 ± 1.42 vs 2.78 ± 1.54 mm2, p < 0.001) and minimum lumen diameter (1.39 ± 0.45 vs 1.54 ± 0.44 mm, p < 0.001) were smaller. The minimum fibrous cap thickness was smaller among females (96 ± 53 vs 112 ± 72 µm, p = 0.025), with more lesions harboring a thin cap fibroatheroma (39.3 % vs 24.9 %, p < 0.001). Major adverse cardiovascular events at two years occurred in 6.3 % of female patients and 11.8 % of male patients (p = 0.15). CONCLUSIONS: FFR-negative NC lesions after MI harbored more high-risk plaque features in female patients. Although this did not translate into an excess of recurrent events in female patients in this modestly sized cohort, it remains to be investigated whether this difference affects clinical outcome.

Activatable Photoacoustic/Near-Infrared Probes for the Detection of Copper Ions of Cardiovascular Disease In Vivo and in Urine.

Copper ions, implicated in processes such as oxidative stress and inflammation, are believed to play a crucial role in cardiovascular disease, a prevalent and deadly disease. Despite this, current diagnostic methods fail to detect early stage cardiovascular disease or track copper ion accumulation, limiting our understanding of the disease's progression. Therefore, the development of noninvasive techniques to image copper ions in cardiovascular disease is urgently needed to enhance diagnostic precision and therapeutic strategies. In this study, we report the successful synthesis and application of a copper ion-activated photoacoustic probe, CS-Cu, which exhibits high sensitivity and selectivity toward copper ions both in vitro and in vivo. CS-Cu was able to noninvasively monitor the changes in copper ion levels and differentiate between different mice based on copper ions in urine. Furthermore, the probe demonstrated good photoacoustic stability and exhibited no significant toxicity in the mice. These findings suggest that CS-Cu could be a promising tool for early detection and monitoring of Cu2+ levels in vivo and urine, providing a new perspective on the role of copper ions in cardiovascular disease.

Ultrasonographic changes of carotid vessels in patients in the early recovery period of atherothrombotic stroke.

OBJECTIVE: Aim: To study the state of extracranial carotid vessels in patients with atherothrombotic stroke in the early recovery period (ASERP) according to duplex scanning data. PATIENTS AND METHODS: Materials and Methods: 130 patients in ASERP, were studied. 69 men and 61 women. aged (60.42}7.4) years. Duplex scanning of the vessels of the neck was performed on a Siemens Acuson X 300 device with a linear multi-frequency sensor of 4-10 MHz. The classification of stenozoocclusive lesions of vessels was carried out according to the classification of B.V. Gaidar. Atherosclerotic plaques (AP) are divided into 5 types according to the Nicolaides and Gerulaka classification. RESULTS: Results: Atherosclerotic stenoses were found in all patients of ASERP: ( 90%),- in 3.4%. AP type 1 was found in 15% of cases; 2 types - in 33.8%; 3 types - in 26%; type 4 accounted for 12.3% and type 5 accounted for 12.3% of cases. APwhich causing moderate stenosis had a high degree of embologenicity due to the hypoechogenicity and heterogeneity of atherosclerotic plaques of types I, II and III. When the level of stenosis increased, tendency to increase the density and hyperechogenicity of the AP was noted. CONCLUSION: Conclusions: 89% patients with ASERP had non-critical, hemodynamically insignificant stenoses of the carotid arteries. Types II and III AP, mostly of an eccentric structure, dominated. Moderate stenoses were more often caused by echo-negative atherosclerotic layers, which is a source of increased embologenicity, and stenoses of a greater degree, for the most part, were echo-positive.

Alzheimer disease-like neuropathologic changes in a geriatric baboon (Papio hamadryas).

IMPORTANCE: Alzheimer's disease (AD) is the most common cause of dementia in the elderly with the incidence rising exponentially after the age of 65 years. Unfortunately, effective treatments are extremely limited and definite diagnosis can only be made at autopsy. This is in part due to our limited understanding of the complex pathophysiology, including the various genetic, environmental, and metabolic contributing factors. In an effort to better understand this complex disease, researchers have employed nonhuman primates as translational models. CASE PRESENTATION: This report aims to describe the AD-like neuropathology in the brain of a 37-year-old female baboon (Papio hamadryas), which at the time of her death made her the oldest hamadryas baboon at any member institution of the Association of Zoos and Aquariums. A diagnostic necropsy was performed, and the brain was evaluated for neurodegenerative disease. Frequent amyloid-ß deposits were identified, consistent with what has been described in other geriatric nonhuman primates. Phospho-tau pathology, including neurofibrillary tangles, a feature not well-described in other primate models, was also abundant. CONCLUSIONS AND RELEVANCE: Our results suggest that more detailed, prospective, longitudinal studies are warranted utilizing this particular species to see if they represent a viable model for human brain aging.