miR-144-3p Regulates Vascular Smooth Muscle Cell Phenotypic Switch via FBN1

Background: Carotid artery dissection (CAD) represents a commonly reported factor causing stroke in young and middle-aged adults. Vascular wall remodeling is one of its important pathogenetic mechanisms. FBN1 is a common pathogenic gene leading to Marfan syndrome, whose mutation can cause the formation of aneurysm and arterial dissection. It was recently demonstrated multiple miRNAs contribute to the development of arterial dissection, while miR-144-3p’s function is undefined.Methods: In the current study, vascular smooth muscle cells (VSMCs) were transfected with miR-144-3p mimic and inhibitor, as well as siFBN1 and miR-144-3p + siFBN1, to determine vascular smooth muscle’s contractile genes, extracellular matrix-associated proteins. In addition, miR-144-3p’s effects on cell proliferation, migration, adhesion, invasion and apoptosis were evaluated.Results: The results revealed miR-144-3p had elevated amounts, while the fibrillin-1 protein showed reduced expression in arterial dissection tissues. Meanwhile, FBN1 was shown to be a miR-144-3p target by dual-luciferase gene reporter assay. In response to miR-144-3p mimic transfection, decreased expression of VSMC contractile gene markers, increased apoptosis, and decreased proliferation, migration, and invasion were found.Conclusions: Overall, miR-144-3p affects the biological function of VSMCs by targeting and regulating FBN1, decreases the expression of contractile genes，transforms the phenotype and leads to vascular wall remodeling.

Unilateral Thalamic Infarction Associated with Rupture of Dissecting Posterior Cerebral Artery in Childhood-Onset Systemic Lupus Erythematosus: A Case Report

BackgroundCerebrovascular diseases are well-known complications of systemic lupus erythematosus (SLE). Among them, cerebral arterial dissection is a rare vascular complication, in which an intimal tear of the blood vessel leads to an intramural hematoma. Cerebral arterial dissection leads to arterial stenosis, thrombosis, and aneurysm, resulting in cerebral infarction or subarachnoid hemorrhage (SAH). Herein, we report a case of posterior cerebral artery (PCA) dissection in SLE that presented as unilateral thalamic infarction followed by SAH and intraventricular hemorrhage (IVH). Case PresentationA 16-year-old boy hospitalized with prolonged fever, hair loss, and skin eruption was newly diagnosed with SLE based on the 2019 EULAR/ACR SLE classification criteria. He suddenly complained of headache, diplopia, and impairment of lateral gaze during hospitalization. Brain magnetic resonance imaging revealed left thalamic infarction, although cerebral vessel inflammation or thrombosis was not observed. Antiphospholipid antibodies such as lupus anticoagulant, anti-cardiolipin antibody, and anti-β2-glycoprotein antibody were not detected. His symptoms improved with high-dose steroid, low-dose aspirin, and mannitol therapy. Five days later, he experienced severe headache and generalized tonic-clonic seizures. Brain computed tomography revealed SAH and IVH with hydrocephalus. Even though emergent external ventricular drainage was performed, the ventricle size did not decrease. Transfemoral cerebral angiography revealed a ruptured dissecting PCA pseudoaneurysm, and immediate coil embolization was successfully performed. The patient fully recovered without any neurologic sequelae, although he underwent ventriculoperitoneal shunting for hydrocephalus following SAH. ConclusionsTo the best of our knowledge, this is the first reported case of PCA dissection in a patient with childhood-onset SLE. Moreover, the subsequent progression from cerebral infarction to SAH caused by PCA dissection makes this case unique. In SLE patients presenting with cerebral infarction and hemorrhage, cerebral arterial dissection and pseudoaneurysm should be considered to achieve favorable outcomes.

Progress in Diagnosis and Endoscopic Treatment of Stanford B Penetrating Aortic Ulcers

Penetrating aortic ulcers is rare in clinical practice, and it is necessary to intervene in this type of aortic perforating ulcer because it can be accompanied by major arterial dissection and intermural hematoma. With the widespread application and technical advancement of follow-up thoracic aortic endovascular repair (TEVAR), endovascular treatment has become the first choice for symptomatic aortic perforating ulcers. In this review, we will review the diagnosis, diagnosis and endovascular treatment of aortic perforating ulcer.

A near-fatal consequence of chiropractor massage: massive stroke from carotid arterial dissection and bilateral vertebral arterial oedema

A 35-year-old Chinese man with no risk factors for stroke presented with a 2-day history of expressive dysphasia and a 1-day history of right-sided weakness. The presentation was preceded by multiple sessions of neck, shoulder girdle and upper back massage for pain relief in the prior 2 weeks. CT of the brain demonstrated an acute left middle cerebral artery infarct and left internal carotid artery dissection. MRI cerebral angiogram confirmed left carotid arterial dissection and intimal oedema of bilateral vertebral arteries. In the absence of other vascular comorbidities and risk factors, massage-induced internal carotid arterial dissection will most likely precipitate the near-fatal cerebrovascular event. The differential diagnosis of stroke in a younger population was consequently reviewed and discussed.