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Cureus Dec 2023Even though cardiac computed tomography and magnetic resonance imaging are the gold standard for evaluating the aortic arch in the context of vascular rings in children,... (Review)
Review
Even though cardiac computed tomography and magnetic resonance imaging are the gold standard for evaluating the aortic arch in the context of vascular rings in children, echocardiography is usually the first-line modality. The echocardiographic evaluation of the aortic arch in the context of vascular rings in children has received little attention. This article details the step-by-step echocardiographic assessment of the aortic arch in vascular ring patients.
PubMed: 38249193
DOI: 10.7759/cureus.50899 -
Life (Basel, Switzerland) Jul 2023Mitral regurgitation (MR) is the most common form of valvular heart disease in the United States, and there are established guidelines for indications for requiring... (Review)
Review
Mitral regurgitation (MR) is the most common form of valvular heart disease in the United States, and there are established guidelines for indications for requiring mitral valve surgeries. However, there is an unmet clinical need for a subset of high-risk MR patients, especially those with advanced age, heart failure and/or secondary MR. Following the successes of transcatheter aortic valve replacements, significant advances have occurred over the last decade in transcatheter mitral valve interventions in order to manage these patients in both clinical practice and trials. The three main types of these interventions include a transcatheter edge-to-edge repair, percutaneous mitral annuloplasty (both direct and indirect) and transcatheter mitral valve replacement (including when applied to a prior prosthetic valve, annuloplasty ring and mitral annuloplasty ring). This review aims to discuss the contemporary techniques, evidence, indications, multimodality imaging evaluations and outcomes of the various transcatheter mitral valve interventions.
PubMed: 37511886
DOI: 10.3390/life13071511 -
Cardiovascular Diabetology Jul 2023Higher chemokine C-X-C motif ligand 5 (CXCL5) level was observed in type 2 diabetes mellitus (DM) patients; however, its role in diabetic vasculopathy was not clarified....
BACKGROUND
Higher chemokine C-X-C motif ligand 5 (CXCL5) level was observed in type 2 diabetes mellitus (DM) patients; however, its role in diabetic vasculopathy was not clarified. This study aimed to explore the impacts and mechanistic insights of CXCL5 in neovasculogenesis and wound healing in DM.
METHODS
Endothelial progenitor cells (EPCs) and human aortic endothelial cells (HAECs) were used in vitro. Streptozotocin-induced diabetic mice and Lepr/JNarl mice were used as type 1 and type 2 DM models. Moreover, CXCL5 knockout mice were used to generate diabetic mice. Hindlimb ischemia surgery, aortic ring assays, matrigel plug assay, and wound healing assay were conducted.
RESULTS
CXCL5 concentrations were increased in plasma and EPCs culture medium from type 2 DM patients. CXCL5 neutralizing antibody upregulated vascular endothelial growth factor (VEGF)/stromal cell-derived factor-1 (SDF-1) and promoted cell function in EPCs from type 2 DM patients and high glucose-treated EPCs from non-DM subjects as well as HAECs. CXCL5 directly up-regulated interleukin (IL)-1β/IL-6/tumor necrosis factor-α and down-regulated VEGF/SDF-1 via ERK/p65 activation through chemokine C-X-C motif receptor 2 (CXCR2). CXCL5 neutralizing antibody recovered the blood flow after hindlimb ischemia, increased circulating EPC number, and enhanced VEGF and SDF-1 expression in ischemic muscle. CXCL5 suppression promoted neovascularization and wound healing in different diabetic animal models. The above observation could also be seen in streptozotocin-induced CXCL5 knockout diabetic mice.
CONCLUSIONS
CXCL5 suppression could improve neovascularization and wound healing through CXCR2 in DM. CXCL5 may be regarded as a potential therapeutic target for vascular complications of DM.
Topics: Humans; Mice; Animals; Diabetes Mellitus, Type 2; Vascular Endothelial Growth Factor A; Diabetes Mellitus, Experimental; Streptozocin; Neovascularization, Pathologic; Endothelial Progenitor Cells; Chemokine CXCL12; Mice, Knockout; Wound Healing; Ischemia; Neovascularization, Physiologic; Chemokine CXCL5
PubMed: 37420254
DOI: 10.1186/s12933-023-01900-w -
Pharmaceutical Biology Dec 2023Gastrodin has been used as antihypertension therapy in China; however, the mechanisms underlying the effects of gastrodin have yet to be fully elucidated.
CONTEXT
Gastrodin has been used as antihypertension therapy in China; however, the mechanisms underlying the effects of gastrodin have yet to be fully elucidated.
OBJECTIVE
To explore the therapeutic efficiency of gastrodin as an antihypertensive and determine the mechanisms underlying this effect.
MATERIALS AND METHODS
C57BL/6 mice were continuously administered angiotensin II (Ang II) (500 ng/kg/min) to induce hypertension. Mice were randomly divided into control, Ang II and Ang II + gastrodin groups. Mice received intragastric administration of gastrodin (5 mg/kg) or double distilled water once a day for 4 weeks. Blood pressure, pulse wave velocity (PWV), thickness of the abdominal aorta, pathological morphology and differential expression transcripts (DETs) were assessed. Abdominal aorta rings and primary isolated vascular smooth muscle cells were subjected to Ang II stimulation to induce hypertension as and models, respectively. Vascular ring tension, release of Ca and levels of proteins involved in the myosin light chain kinase (MLCK)/phospho-myosin light chain 2 (p-MLC) pathway were determined.
RESULTS
Gastrodin treatment attenuated increases in blood pressure, PWV and thickness of the abdominal aorta. Treatment with gastrodin resulted in 2785 DETs and the enrichment of vascular contraction and calcium signalling pathways. Gastrodin treatment attenuated Ang II-induced vasoconstriction, produced a norepinephrine-precontracted vasodilation effect (attenuated by verapamil), and reduced intracellular Ca release. Furthermore, gastrodin suppressed activation of the MLCK/p-MLC pathway and .
CONCLUSIONS
Gastrodin treatment lowers blood pressure, suppresses Ang II-induced vascular contraction and MLCK/p-MLC pathway activation, thereby demonstrating the mechanisms underlying the therapeutic efficacy of gastrodin as an antihypertensive.
Topics: Animals; Mice; Angiotensin II; Antihypertensive Agents; Hypertension; Mice, Inbred C57BL; Muscle, Smooth, Vascular; Pulse Wave Analysis
PubMed: 37211627
DOI: 10.1080/13880209.2023.2207591 -
Seminars in Cardiothoracic and Vascular... Feb 2024Vascular rings represent an increasingly prevalent and diverse set of congenital malformations in which the aortic arch and its primary branches encircle and constrict... (Review)
Review
Vascular rings represent an increasingly prevalent and diverse set of congenital malformations in which the aortic arch and its primary branches encircle and constrict the esophagus and trachea. Perioperative management varies significantly based on the type of lesion, its associated comorbidities, and the compromise of adjacent structures. Multiple review articles have been published describing the scope of vascular rings and relevant concerns from a surgical perspective. This review seeks to discuss the perioperative implications and recommendations of such pathology from the perspective of an anesthesia provider.
PubMed: 38379198
DOI: 10.1177/10892532241234404 -
JACC. Cardiovascular Imaging Dec 2023The clinical value of high-risk coronary plaque characteristics (CPCs) to inform intensified medical therapy or revascularization of non-flow-limiting lesions remains... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The clinical value of high-risk coronary plaque characteristics (CPCs) to inform intensified medical therapy or revascularization of non-flow-limiting lesions remains uncertain.
OBJECTIVES
The authors performed a systematic review and meta-analysis to study the prognostic impact of CPCs on patient-level and lesion-level major cardiovascular adverse events (MACE).
METHODS
Thirty studies (21 retrospective, 9 prospective) with 30,369 patients evaluating the association of CPCs with MACE were included. CPCs included high plaque burden, low minimal lumen area, thin cap fibroatheroma, high lipid core burden index, low-attenuation plaque, spotty calcification, napkin ring sign, and positive remodeling.
RESULTS
CPCs were evaluated with the use of intracoronary modalities in 9 studies (optical coherence tomography in 4 studies, intravascular ultrasound imaging in 3 studies, and near-infrared spectroscopy intravascular ultrasound imaging in 2 studies) and by means of coronary computed tomographic angiography in 21 studies. CPCs significantly predicted patient-level and lesion-level MACE in both unadjusted and adjusted analyses. For most CPCs, accuracy for MACE was modest to good at the patient level and moderate to good at the lesion level. Plaques with more than 1 CPC had the highest accuracy for lesion-level MACE (AUC: 0.87). Because the prevalence of CPCs among plaques was low, estimated positive predictive values for lesion-level MACE were modest. Results were mostly consistent across imaging modalities and clinical presentations, and in studies with prevailing hard outcomes.
CONCLUSIONS
Characterization of CPCs identifies high-risk atherosclerotic plaques that place lesions and patients at risk for future MACE, albeit with modest sensitivity and positive predictive value (Coronary Plaque Characteristics Associated With Major Adverse Cardiovascular Events Among Atherosclerotic Patients and Lesions; CRD42021251810).
Topics: Humans; Plaque, Atherosclerotic; Coronary Artery Disease; Coronary Angiography; Retrospective Studies; Prospective Studies; Coronary Vessels; Predictive Value of Tests; Ultrasonography, Interventional
PubMed: 37804276
DOI: 10.1016/j.jcmg.2023.08.006 -
Acta Pharmacologica Sinica Aug 2023Vascular calcification is caused by the deposition of calcium salts in the intimal or tunica media layer of the aorta, which increases the risk of cardiovascular events...
Vascular calcification is caused by the deposition of calcium salts in the intimal or tunica media layer of the aorta, which increases the risk of cardiovascular events and all-cause mortality. However, the mechanisms underlying vascular calcification are not fully clarified. Recently it has been shown that transcription factor 21 (TCF21) is highly expressed in human and mouse atherosclerotic plaques. In this study we investigated the role of TCF21 in vascular calcification and the underlying mechanisms. In carotid artery atherosclerotic plaques collected from 6 patients, we found that TCF21 expression was upregulated in calcific areas. We further demonstrated TCF21 expression was increased in an in vitro vascular smooth muscle cell (VSMC) osteogenesis model. TCF21 overexpression promoted osteogenic differentiation of VSMC, whereas TCF21 knockdown in VSMC attenuated the calcification. Similar results were observed in ex vivo mouse thoracic aorta rings. Previous reports showed that TCF21 bound to myocardin (MYOCD) to inhibit the transcriptional activity of serum response factor (SRF)-MYOCD complex. We found that SRF overexpression significantly attenuated TCF21-induced VSMC and aortic ring calcification. Overexpression of SRF, but not MYOCD, reversed TCF21-inhibited expression of contractile genes SMA and SM22. More importantly, under high inorganic phosphate (3 mM) condition, SRF overexpression reduced TCF21-induced expression of calcification-related genes (BMP2 and RUNX2) as well as vascular calcification. Moreover, TCF21 overexpression enhanced IL-6 expression and downstream STAT3 activation to facilitate vascular calcification. Both LPS and STAT3 could induce TCF21 expression, suggesting that the inflammation and TCF21 might form a positive feedback loop to amplify the activation of IL-6/STAT3 signaling pathway. On the other hand, TCF21 induced production of inflammatory cytokines IL-1β and IL-6 in endothelial cells (ECs) to promote VSMC osteogenesis. In EC-specific TCF21 knockout (TCF21) mice, VD and nicotine-induced vascular calcification was significantly reduced. Our results suggest that TCF21 aggravates vascular calcification by activating IL-6/STAT3 signaling and interplay between VSMC and EC, which provides new insights into the pathogenesis of vascular calcification. TCF21 enhances vascular calcification by activating the IL-6-STAT3 signaling pathway. TCF21 inhibition may be a new potential therapeutic strategy for the prevention and treatment of vascular calcification.
Topics: Animals; Humans; Mice; Basic Helix-Loop-Helix Transcription Factors; Cells, Cultured; Endothelial Cells; Interleukin-6; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Osteogenesis; Plaque, Atherosclerotic; Signal Transduction; STAT3 Transcription Factor; Vascular Calcification
PubMed: 36997664
DOI: 10.1038/s41401-023-01077-8 -
Cardiovascular Diabetology Dec 2023Data are limited on the association of metabolic dysfunction-associated fatty liver disease (MAFLD) with systemic atherosclerosis. This study aimed to examine the...
BACKGROUND
Data are limited on the association of metabolic dysfunction-associated fatty liver disease (MAFLD) with systemic atherosclerosis. This study aimed to examine the relationship between MAFLD and the extent of atherosclerotic plaques and stenosis, and presence of polyvascular disease (PolyVD).
METHODS
In this cross-sectional study, MAFLD was diagnosed based on the presence of metabolic dysfunction (MD) and fatty liver disease (FLD). MAFLD was divided into three subtypes: MAFLD with diabetes mellitus (DM), MAFLD with overweight or obesity (OW), as well as MAFLD with lean/normal weight and at least two metabolic abnormalities. Atherosclerosis was evaluated, with vascular magnetic resonance imaging for intracranial and extracranial arteries, thoracoabdominal computed tomography angiography for coronary, subclavian, aorta, renal, iliofemoral arteries, and ankle-brachial index for peripheral arteries. The extent of plaques and stenosis was defined according to the number of these eight vascular sites affected. PolyVD was defined as the presence of stenosis in at least two vascular sites.
RESULTS
This study included 3047 participants, with the mean age of 61.2 ± 6.7 years and 46.6% of male (n = 1420). After adjusting for potential confounders, MAFLD was associated with higher extent of plaques (cOR, 2.14, 95% CI 1.85-2.48) and stenosis (cOR, 1.47, 95% CI 1.26-1.71), and higher odds of presence of PolyVD (OR, 1.55, 95% CI 1.24-1.94) as compared with Non-MAFLD. In addition, DM-MAFLD and OW-MAFLD were associated with the extent of atherosclerotic plaques and stenosis, and presence of PolyVD (All P < 0.05). However, lean-MAFLD was only associated with the extent of atherosclerotic plaques (cOR, 1.63, 95% CI 1.14-2.34). As one component of MAFLD, FLD per se was associated with the extent of plaques and stenosis in participants with MAFLD. Furthermore, FLD interacted with MD to increase the odds of presence of systemic atherosclerosis (P for interaction ≤ 0.055).
CONCLUSIONS
MAFLD and its subtypes of DM-MAFLD and OW-MAFLD were associated with the extent of atherosclerotic plaques and stenosis, and presence of PolyVD. This study implicated that FLD might be a potential target of intervention for reducing the deleterious effects of MAFLD on systemic atherosclerosis.
Topics: Male; Humans; Middle Aged; Aged; Plaque, Atherosclerotic; Cross-Sectional Studies; Constriction, Pathologic; Atherosclerosis; Non-alcoholic Fatty Liver Disease
PubMed: 38093371
DOI: 10.1186/s12933-023-02083-0