Case Report: Transcatheter treatment of aortic coarctation in a 58-year-old patient with LACHT syndrome and left lung agenesis.

LACHT (Lung Agenesis, Congenital Heart, and Thumb anomalies) syndrome is an extremely rare congenital anomaly and presents significant challenges in adults due to its poor survival rates. Herein, we report a case of late diagnosis and successful transcatheter treatment of aortic coarctation in a 58-year-old male patient with LACHT syndrome, medically resistant arterial hypertension, and left lung agenesis. Baseline CT angiography showed isthmic aortic coarctation and left lung agenesis, with compensatory right pulmonary artery and vein thickenings. The patient underwent balloon dilation and subsequent implantation of a covered NuMED 45 mm 8-ZIG CP stent with satisfactory outcomes. The pressure gradient decreased from 43 to 23 mmHg. The arterial pressures normalized during the follow-up with fewer medications. Genetic testing identified a heterozygous mutation (c.6583C > T) in the FBN2, supporting the diagnosis of variant Marfan syndrome.

Gut microbiota and hypertension: a bibliometric analysis of recent research (2014-2023).

Background: Cardiovascular diseases persist as the primary cause of mortality in the global population. Hypertension (HTN) is widely recognized as one of the most crucial risk factors contributing to severe cardiovascular conditions. In recent years, a growing body of research has highlighted the therapeutic potential of gut microbiota (GM) in addressing cardiovascular diseases, particularly HTN. Consequently, unraveling and synthesizing the connections between GM and HTN, key research domains, and the underlying interaction mechanisms have grown increasingly vital. Methods: We retrieved articles related to GM and HTN from 2014 to 2023 using Web of Science. Bibliometric tools employed in this analysis include CiteSpace and VOSviewer. Result: From 2014 to 2023, we identified 1,730 related articles. These articles involved 88 countries (regions) and 9,573 authors. The articles were published in 593 journals, with 1000 references exhibiting co-occurrence more than 10 times. The number of studies in this field has been increasing, indicating that it remains a research hotspot. We expect this field to continue gaining attention in the future. China leads in the number of published articles, while the United States boasts the most extensive international collaborations, signifying its continued prominence as a research hub in this domain. Tain You-Lin, Hsu Chien-Ning, Raizada Mohan K, and Yang Tao are among the authors with the highest publication volume. Publications in this field are frequently found in nutrition, cardiovascular, and molecular biology journals. The most frequently occurring keywords include metabolic syndrome, cardiovascular disease, inflammation, short-chain fatty acids, trimethylamine N-oxide, chronic kidney disease, heart failure, and high-salt diet. Conclusion: The relationship between GM and HTN is presently one of the most active research areas. By employing bibliometric tools, we analyzed critical and innovative articles in this field to provide an objective summary of the primary research directions, such as the relationship between GM and HTN, GM metabolites, high-salt diet, the developmental origins of health and disease, obstructive sleep apnea-Induced hypertension and antihypertensive peptide. Our analysis aims to offer researchers insights into hotspots and emerging trends in the field of GM and HTN for future research reference.

Butyrate alleviates renal fibrosis in CKD by regulating NLRP3-mediated pyroptosis via the STING/NF-κB/p65 pathway.

Chronic kidney disease (CKD) is a serious and irreversible disease primarily characterized by chronic inflammation and renal fibrosis. Recent studies have suggested that gut microbiota-related metabolites, particularly short-chain fatty acids (SCFAs) are significantly associated with kidney diseases. Notably, butyrate, a type of SCFAs, plays a crucial role in this correlation. However, the effect of butyrate on renal fibrosis in patients with CKD and its potential mechanisms remain unclear. In this study, we demonstrated that butyrate levels are reduced as CKD progresses using a CKD C57BL/6 mouse model established by a 0.2% adenine diet. Exogenous supplementation of butyrate effectively alleviated renal fibrosis and repressed the levels of proteins associated with NLRP3-mediated pyroptosis (NLRP3, IL-1ß, caspase-1, and GSDMD). Additionally, we conducted an in vitro experiment using HK-2 cells, which also confirmed that the elevated levels of NLRP3-mediated pyroptosis proteins in TGF-ß1-stimulated HK-2 cells are reversed by butyrate intervention. Further, butyrate mitigated the activity of the STING/NF-κB/p65 pathway, and STING overexpression impaired the protective function of butyrate in CKD. Hence, we suggest that butyrate may have a renoprotective role in CKD, alleviating renal fibrosis possibly by regulating NLRP3-mediated pyroptosis via the STING/NF-κB/p65 pathway.

Hourly Ultrafine Particle Exposure and Acute Myocardial Infarction Onset: An Individual-Level Case-Crossover Study in Shanghai, China, 2015-2020.

Associations between ultrafine particles (UFPs) and hourly onset of acute myocardial infarction (AMI) have rarely been investigated. We aimed to evaluate the impacts of UFPs on AMI onset and the lag patterns. A time-stratified case-crossover study was performed among 20,867 AMI patients from 46 hospitals in Shanghai, China, between January 2015 and December 2020. Hourly data of AMI onset and number concentrations of nanoparticles of multiple size ranges below 0.10 µm (0.01-0.10, UFP/PNC0.01-0.10; 0.01-0.03, PNC0.01-0.03; 0.03-0.05, PNC0.03-0.05; and 0.05-0.10 µm, PNC0.05-0.10) were collected. Conditional logistic regressions were applied. Transient exposures to these nanoparticles were significantly associated with AMI onset, with almost linear exposure-response curves. These associations occurred immediately after exposure, lasted for approximately 6 h, and attenuated to be null thereafter. Each interquartile range increase in concentrations of total UFPs, PNC0.01-0.03, PNC0.03-0.05, and PNC0.05-0.10 during the preceding 0-6 h was associated with increments of 3.29, 2.08, 2.47, and 2.93% in AMI onset risk, respectively. The associations were stronger during warm season and at high temperatures and were robust after adjusting for criteria air pollutants. Our findings provide novel evidence that hourly UFP exposure is associated with immediate increase in AMI onset risk.

Ventricular septal defect complicating myocardial infarction: A case of delayed percutaneous transcatheter closure.

A 57-year-old man suffered chest pain during the COVID-19 pandemic, but he delayed medical treatment due to fear of infection. After 4 months, symptoms of chest tightness and shortness of breath appeared. Electrocardiogram (ECG) revealed old myocardial infarction; color sonography and myocardial computed tomography revealed apical myocardial defect. He refused surgery and percutaneous transcatheter closure, and follow-up observation. After 22 months, the symptoms of chest tightness and shortness of breath aggravated. He recovered after percutaneous transcatheter closure, and was discharged. This case shows delayed closure is one of the possible options for patients without severe organ dysfunction or hemodynamic disturbance.

EGCG decreases myocardial infarction in both I/R and MIRI rats through reducing intracellular Ca2+ and increasing TnT levels in cardiomyocytes.

BACKGROUND: Myocardial ischemia/reperfusion injury (MIRI) usually induces serious health problems. OBJECTIVES: This study attempted to explore protective effects of (-)-epigallocatechin-3-gallate (EGCG) on MIRI and the associated mechanism. MATERIAL AND METHODS: Ischemia/reperfusion of an isolated rat heart (I/R model) and the MIRI model were used in this study. Myocardial infarction was measured with staining with 2,3,5-triphenyltetrazolium chloride (TTC). Ca2+ and troponin T (TnT) concentrations in coronary perfusion fluid were evaluated using the chromatometry method. Ca2+ concentration in cardiomyocytes was determined with detecting Ca2+ fluorescence intensity. The ultrastructure of cardiomyocytes was observed using transmission electron microscopy (TEM). ß-nicotinamide adenine dinucleotide (NAD+) of cardiomyocytes was also determined. RESULTS: The EGCG (I/R+EGCG) significantly reduced myocardial infarction size of isolated rat heart compared to I/R rats (p < 0.05), remarkably increased Ca2+ and decreased TnT concentrations in coronary perfusion fluid of I/R rats compared to the I/R model (p < 0.05), as well as markedly decreased intracellular Ca2+ concentration and promoted NAD+ concentration in cardiomyocytes compared to I/R rats (p < 0.05). It also obviously maintained the mitochondrial structure in cardiomyocytes of I/R rats and improved the ultrastructure of cardiomyocytes of MIRI rats. Lonidamine (LND) treatment (I/R+EGCG+LND group) significantly blocked the effects of EGCG on I/R injury compared to the I/R+EGCG group (p < 0.05). The EGCG (MIRI+EGCG) significantly decreased myocardial infarction size compared to MIRI rats (p < 0.05) and remarkably enhanced Ca2+ and reduced TnT concentrations in the pulmonary artery compared to that of MIRI rats (p < 0.05). CONCLUSIONS: The EGCG decreased myocardial infarction size in both I/R models and MIRI models by reducing intracellular Ca2+ concentration, increasing TnT concentration, promoting NAD+ concentration, and improving the ultrastructure of cardiomyocytes.

SIRT1 gene polymorphisms are associated with nondiabetic type 1 cardiorenal syndrome.

Type 1 cardiorenal syndrome (CRS1) is characterized by acute cardiac disease (e.g., acute heart failure [AHF]), leading to acute kidney injury. Sirtuin 1 (SIRT1), an NAD+ -dependent deacylase, has been found to be associated with CRS1. To confirm whether a correlation exists between SIRT1 variants and the risk of CRS1, the association between the prevalence of CRS1 and single-nucleotide polymorphisms (SNPs) within the SIRT1 gene was investigated in AHF patients. A total of 316 Chinese AHF participants (158 patients with CRS1 and 158 age- and sex-matched controls) were recruited for the present observational study to investigate the association between nine common SIRT1 SNPs (i.e., rs7895833 G > A, rs10509291 T > A, rs3740051 A > G, rs932658 A > C, rs33957861 C > T, rs7069102 C > G, rs2273773 T > C, rs3818292 A > G, and rs1467568 A > G) and the susceptibility to CRS1. Significant differences in genotype distribution between the control and CRS1 groups were found for rs7895833 and rs1467568. After applying a Bonferroni adjustment, the A allele of rs7895833 was still found to be protective (p = 0.001; odds ratio [OR] = 0.77) against CRS1 in this study population. The AA genotype of rs7895833 and the GA genotype of rs1467568 were associated with a significantly reduced risk of CRS1 (OR = 0.23 and 0.49, respectively). rs7895833 and rs1467568 were further analyzed as a haplotype, and the GA haplotype (rs7895833-rs1467568) exhibited a significant association with CRS1 (p = 0.008), while the AA haplotype showed a significant protective effect (p = 0.022). Our study showed that SIRT1 rs7895833 and rs1467568 polymorphisms had a significant effect on the risk of developing CRS1 in a population in China.

A vessel segmentation method for serialized cerebralvascular DSA images based on spatial feature point set of rotating coordinate system.

Cerebrovascular pathology is one of the main fatal diseases which seriously affect the human's health. Extracting the accurate image of cerebral vascular tissue is the key of clinical diagnosis. However, the motion artifacts in DSA images seriously affected the quality of vascular subtraction image. In this paper, an automatic and accurate segmentation method is presented to extract the vascular region in the live image of brain. Firstly, a coarse registration for the live image and the mask image is implemented. And then, the SIFT algorithm is utilized to detect geometrical feature points in the serialized subtraction images. After that, a spatial model of rotating coordinate system and a calculative strategy of contextual information are designed to eliminate the error feature points. Finally, based on a dynamic threshold method, the blood vessel image can be obtained by region growing. The context information in the adjacent subtraction images is fully used. The experimental result shows that the segmented cerebral vascular image is satisfactory. This method can provide accurate vessel image data for the clinical operation based on DSA interventional therapy.

An automatic segmentation system of acetabulum in sequential CT images for the personalized artificial femoral head design.

This paper describes an automatic and accurate segmentation method to extract the acetabulum tissue from sequential CT images. The hip joint consists of acetabulum and femoral head. In the personalized femoral head prosthesis designing by reverse engineering technology, obtaining the accurate acetabulum shape is the most important task. However, due to the necrotic femoral head's complex shape and the extremely narrow inter-bone region, obtaining the accurate acetabulum shape remains a challenging work. In this paper, we overcame these difficulties and developed an automatic segmentation method. First, we obtain the rough contour of the femoral head by utilizing the constraints of the great trochanter and the shape of femoral head in the initial slice. Second, we refine the rough contour by an orthogonal line edge detection approach and obtain a refined contour which will be used as the initial contour of the snake algorithm. Then, the snake algorithm is performed slice by slice upwards and downwards to generate the adjacent contours. During this process, the contour of the femoral head in a segmented slice is used as the initial contour of the next unsegmented slice. Finally, we can obtain the accurate sequential contours of the acetabulum by removing the femoral head and the femoral regions. And the 3D models of the acetabulum can be obtained correspondingly. The experimental result shows that the 3D models obtained by the proposed method are accurate and satisfactory. On this condition, we can reconstruct the personalized femoral head 3D models and design the personalized femoral head prosthesis.

[Effects of ANP upon ion pump activity and gene expression in aortic smooth muscle cells from spontaneously hypertensive rats].

OBJECTIVE: To explore the effects of atrial natriuretic peptide (ANP) upon the activities of Na(+), K(+)-ATPase, Ca(2+)-ATPase and mRNA expression levels of Na(+), K(+)-ATPase alpha(1)-subunit and plasma membrane Ca(2+)-ATPase isoform 1 (PMCA1) in cultured thoracic aortic vascular smooth muscle cells (ASMCs) isolated from spontaneously hypertensive rats (SHR). METHODS: ASMCs isolated from 14-week-old male SHR and Wistar-Kyoto (WKY) rats were interference-cultured in different doses of ANP and Angiotensin II (AngII). The contents of ANP and AngII in supernatant from ASMCs were measured by radioimmunoassay. The activities of the above two ATPases were measured by biochemistry and enzymology. RT-PCR assay was employed to determine the relative levels of Na(+), K(+)-ATPase alpha(1)-subunit and PMCA1 mRNA in ASMCs. RESULTS: The ANP level of supernatant in SHR ASMCs was significantly lower than those from WKY control [(7.3 +/- 2.4) pg x 10(-6) cells vs (19.3 +/- 3.3) pg x 10(-6) cells, P < 0.01] while the content of AngII in SHR ASMCs was significantly higher than those from WKY control [(57 +/- 4) pg x 10(-6) cells vs (44 +/- 4) pg x 10(-6) cells, P < 0.01]. The activity of Na(+), K(+)-ATPase [(4.3 +/- 0.8) micromol x h(-1) x mg(-1) vs (5.3 +/- 1.0) micromol x h(-1) x mg(-1)], Ca(2+)-ATPase [(3.2 +/- 0.7) micromol x h(-1) x mg(-1) vs (4.5 +/- 0.7) micromol x h(-1) x mg(-1)] in ASMCs from SHR were significantly lower than those from WKY control (both P < 0.01). The mRNA expression of Na(+), K(+)-ATPase alpha(1)-subunit (0.524 +/- 0.025 vs 0.704 +/- 0.116), PMCA1 (0.193 +/- 0.030 vs 0.547 +/- 0.045) significantly decreased in ASMCs from SHR versus the WKY control (both P < 0.01). As compared with SHR control, exogenous ANP improved obviously the activities of Na(+), K(+)-ATPase, Ca(2+)-ATPase and expression of alpha(1)-subunit, PMCA1 mRNA in a does-dependent manner (P < 0.05-P < 0.01). Exogenous AngII (1 x 10(-9), 1 x 10(-8), 1 x 10(-7) mol/L) significantly repressed activities of Ca(2+)-ATPase and attenuated the expression of PMCA1 mRNA (P < 0.05-P < 0.01). Only AngII (1 x 10(-7) mol/L) significantly inhibited the activity of Na(+), K(+)-ATPase and attenuated the expression of Na(+), K(+)-ATPase alpha(1)-subunit mRNA (both P < 0.05). ANP antagonized the effects of AngII (1 x 10(-7) mol/L) upon the activities of two ATPases and the expression of Na(+), K(+)-ATPase alpha(1)-subunit PMCA1 mRNA (P < 0.05-P < 0.01). AngII (1 x 10(-7) mol/L) increased the Na(+), K(+)-ATPase activity and the expression of Na(+), K(+)-ATPase alpha(1)-subunit mRNA, repressed the Ca(2+)-ATPase activity and the expression of PMCA1 mRNA in ASMCs from WKY rat (P < 0.05-P < 0.01). ANP antagonized the effects of AngII (1 x 10(-7) mol/L) upon the activity of Ca(2+)-ATPase and the expression of PMCA1 mRNA (P < 0.05-P < 0.01), but did not antagonize the effects of AngII (1 x 10(-7) mol/L) upon the activity of Na(+), K(+)-ATPase and the expression of alpha(1)-subunit mRNA in ASMCs from WKY rats (P > 0.05). CONCLUSION: The decreased activities of Na(+), K(+)-ATPase and Ca(2+)-ATPase may be related to the abnormal autocrine of ANP and AngII in ASMC of SHR. ANP can antagonize the effects of AngII upon the activities of two ATPases and the expression of Na(+), K(+)-ATPase alpha(1)-subunit PMCA1 mRNA.