BACKGROUND

This case report describes a rare presentation of double-vessel Spontaneous Coronary Artery Dissection (SCAD) in a 54-year-old male. One dissection occurred in a coronary artery with atherosclerotic plaque deposition, while the second vessel exhibited dissection without evidence of plaque deposition, trauma or iatrogenic manipulation such as percutaneous coronary intervention. The patient, a known hypertensive and dyslipidemic, had a prior diagnosis of heart failure with reduced ejection fraction (HFrEF). He presented with progressively worsening shortness of breath and orthopnea (two-pillow orthopnea for three years. An initial coronary angiogram was recommended due to a high suspicion of underlying coronary artery disease (CAD).Subsequent diagnostic workup revealed multisegmental wall motion abnormalities on 2D echocardiography with Doppler imaging. Laboratory tests, including electrolytes, were unremarkable. A follow-up coronary angiogram revealed mild to moderate CAD in the left anterior descending (LAD) artery and spontaneous coronary artery dissection involving both the LAD and the right coronary artery (RCA). The patient was managed conservatively with aspirin and discharged on a regimen of sacubitril/valsartan, ivabradine, trimetazidine, and rosuvastatin. As typically seen in SCAD cases, conservative medical management was preferred over invasive procedures such as PCI or coronary artery bypass grafting (CABG), which are reserved for select clinical situations.

Human ; Male ; Middle Aged: 45-64 Yrs Old ; Arteries ; Dissection ; Hospitals ; Male ; Patients ; Research Report ; Tertiary Care Centers

Intraoperative hemorrhage is a life-threatening complication during neurosurgery, especially in posterior fossa surgery, where critical vasculature and brain structures are present. Adenosine has been used in neurovascular surgery, particularly in the management of intraoperative aneurysm rupture and hemorrhage for its ability to produce transient flow arrest. This case report describes a novel application for adenosine, in which adenosine-induced flow arrest was used to facilitate control of a vascular injury sustained during meningioma surgery.

A 46-year-old female diagnosed with a petroclival meningioma after presenting with a several-month history of headache, dizziness, and loss of balance underwent craniotomy and excision of the meningioma. The patient received general endotracheal anesthesia, and was maintained on remifentanil, propofol, and low-dose sevoflurane. During posterior excision of the meningioma, the basilar artery was inadvertently lacerated, resulting in significant blood loss. Adenosine was given through a subclavian catheter, and produced severe bradycardia, hypotension, then asystole for approximately 50 seconds. Adenosine-induced flow arrest allowed for initial control of the vascular injury through coagulation, while further hemostasis was achieved through hemostatic agents and muscle tamponade.

This case report demonstrates the usefulness of adenosine-induced flow arrest in the management of intraoperative hemorrhage from an intracranial vascular injury. Adenosine-induced flow arrest has documented safety and efficacy in other neurosurgical applications. As the management of intraoperative hemorrhage is an essential component of neuroanesthesia, this technique may be considered in similar circumstances of major vascular injury to facilitate hemostasis.

Human ; Female ; Middle Aged: 45-64 Yrs Old ; Adenosine ; Basilar Artery ; Meningioma

BACKGROUND

This case report describes a rare presentation of double-vessel Spontaneous Coronary Artery Dissection (SCAD) in a 54-year-old male. One dissection occurred in a coronary artery with atherosclerotic plaque deposition, while the second vessel exhibited dissection without evidence of plaque deposition, trauma or iatrogenic manipulation such as percutaneous coronary intervention. The patient, a known hypertensive and dyslipidemic, had a prior diagnosis of heart failure with reduced ejection fraction (HFrEF). He presented with progressively worsening shortness of breath and orthopnea (two-pillow orthopnea for three years. An initial coronary angiogram was recommended due to a high suspicion of underlying coronary artery disease (CAD).Subsequent diagnostic workup revealed multisegmental wall motion abnormalities on 2D echocardiography with Doppler imaging. Laboratory tests, including electrolytes, were unremarkable. A follow-up coronary angiogram revealed mild to moderate CAD in the left anterior descending (LAD) artery and spontaneous coronary artery dissection involving both the LAD and the right coronary artery (RCA). The patient was managed conservatively with aspirin and discharged on a regimen of sacubitril/valsartan, ivabradine, trimetazidine, and rosuvastatin. As typically seen in SCAD cases, conservative medical management was preferred over invasive procedures such as PCI or coronary artery bypass grafting (CABG), which are reserved for select clinical situations.

Human ; Male ; Middle Aged: 45-64 Yrs Old ; Arteries ; Dissection ; Hospitals ; Male ; Patients ; Research Report ; Tertiary Care Centers

INTRODUCTION

Secondary hypertension should be suspected among young individuals and patients with recent onset of hypertension or drug-resistant hypertension. Among the causes of secondary hypertension, renovascular hypertension is well-established and correctible if diagnosed appropriately. We report the case of a young female with an unusual cause of renovascular hypertension.

CLINICAL PRESENTATION:

A 29-year-old female was admitted for elevated blood pressure and headache, unresponsive to multiple antihypertensives. The workup for secondary hypertension was mostly unremarkable. However, renal Doppler ultrasound showed elevated peak systolic velocity in the left renal artery. CT angiogram revealed an outpouching between the left gonadal and renal veins. No renal artery stenosis was found on renal angiography, but venography revealed an aneurysm between the left gonadal and renal veins. An aberrant vein draining into the inferior vena cava (IVC) and severe reflux into a dilated left gonadal vein were also noted.

MANAGEMENTCONCLUSION

This case highlights a rare cause of renovascular hypertension due to renal vein congestion from severe left gonadal vein reflux and a renal/gonadal vein aneurysm. Additional mechanisms may include external compression of the renal artery or a suction effect caused by multiple venous outflows. Regardless of the exact pathophysiology, coiling of the aneurysm and gonadal vein successfully restored normal venous return and resolved hypertension.

Human ; Female ; Adult: 25-44 Yrs Old ; Veins ; Research Report ; Renal Veins ; Pharmaceutical Preparations ; Patients ; Hypertension, Renovascular ; Hypertension ; Female ; Aneurysm

Introduction: Pituitary apoplexy is a rare, life-threatening condition resulting from hemorrhage or infarction of the pituitary gland, most commonly in patients with pre-existing pituitary tumors. It typically presents with a sudden headache, visual disturbance, ophthalmoplegia, and altered mental status. An uncommon but serious complication is ischemic stroke in the middle cerebral artery (MCA) territory, particularly in the absence of direct internal carotid artery (ICA) compression. Case: We report a case of a 36-year-old male who presented with headache, visual impairment, and fever. Initial computed tomography (CT) brain imaging demonstrated a heterogeneous sellar lesion with peripheral calcification measuring 2.4 × 3.2 × 2.7 cm, suggestive of a pituitary mass with possible apoplexy, without evidence of acute cerebral infarction. The patient subsequently developed dysarthria, hemianopia, and reduced consciousness, prompting repeat neuroimaging. Follow-up CT revealed a large hypodense area in the right fronto-parieto-temporal region consistent with ischemic infarction. Magnetic resonance imaging confirmed an acute infarct in the right MCA territory without hemorrhagic transformation. A sellar-suprasellar mass measuring 2.3 × 2.8 × 3.8 cm was identified, consistent with a pituitary macroadenoma with intratumoral hemorrhage compressing the optic chiasm, but without direct right ICA compression. Time-of-flight mineralocorticoid receptor antagonists demonstrated attenuated flow in the right ICA (C2–C7), suggesting intracranial ICA thrombosis and reduced perfusion in the right MCA and its branches. Laboratory evaluation revealed hyperthyroidism and hypocortisolism, with no evidence of coagulopathy. The patient was treated with corticosteroid replacement and carbimazole and referred for neurosurgical management. Conclusion This case highlights a rare association between pituitary apoplexy and MCA stroke, possibly mediated by vasospasm, inflammation, or hypercoagulability. More research is needed to understand this connection and improve treatment strategies.
Middle Cerebral Artery ; Pituitary Apoplexy ; Infarction

The surgical treatment of the rare extracranial carotid artery aneurysm can lead to significant thromboembolic events in 4.4% of cases. Intraoperative monitoring has helped detect hypoperfusion and probable ischemic events, but this is not widely available in resource-limited hospitals in the Philippines. This case highlights the use of a portable standard 21-channel EEG machine for intraoperative monitoring in a tertiary government hospital. In addition, it highlights a conception of a protocol for the intraoperative electroencephalogram monitoring of carotid endoaneurysmorrhaphy procedures in a resource-limited setting. During the aneurysmorrhaphy procedure, the authors collaborated with the surgeons and the anesthesiologists to provide feedback about EEG changes during the operation. After a pre-induction baseline was recorded, continuous EEG monitoring was performed until the patient emerged from anesthesia. Mild EEG changes, attributed to relative hypotension, were observed during the procedure. These episodes were responsive to BP augmentation. There were no EEG changes observed during carotid cross-clamping. Shunting was not recommended to the surgical team. No new neurologic deficits were documented postoperatively and on follow-up after six months. This paper illustrates how an intraoperative team was formed, and intraoperative EEG was utilized for a complex carotid endoaneurysmorrhaphy for a patient with ECAA in a tertiary government hospital in the Philippines.

Human ; Resource-limited Settings ; Carotid Arteries ; Philippines

This paper explores the research progress of acupuncture for the prevention and treatment of Alzheimer's disease (AD) based on the "kidney-governor vessel-brain" axis. According to the fundamental pathogenesis of AD in traditional Chinese medicine (TCM), which attributes to kidney deficiency, marrow depletion, and impaired mental faculties, as well as the governor vessel's connection between the kidney and brain, the concept of the "kidney-governor vessel-brain" axis is proposed. The theoretical basis of the "kidney-governor vessel-brain" axis is analyzed based on the meridian pathway and physiological functions of the governor vessel, as well as the interdependent and mutually reinforcing relationships among the kidney, governor vessel, and brain. The relationship between AD and the "kidney-governor vessel-brain" axis is elucidated from both traditional medical theories and modern biological perspectives. Integrating clinical and mechanistic research on AD prevention and treatment based on this axis, it is suggested that the "kidney-governor vessel-brain" axis provides valuable insights and references for future research on AD prevention and treatment.
Humans ; Alzheimer Disease/physiopathology* ; Acupuncture Therapy ; Kidney/blood supply* ; Brain/blood supply* ; Meridians ; Blood Vessels/physiopathology*

BACKGROUND: The main cause of restenosis after percutaneous transluminal angioplasty (PTA) is the excessive proliferation and migration of vascular smooth muscle cells (VSMCs). Lin28a has been reported to play critical regulatory roles in this process. However, whether CCAAT/enhancer-binding proteins β (C/EBPβ) binds to the Lin28a promoter and drives the progression of restenosis has not been clarified. Therefore, in the present study, we aim to clarify the role of C/EBPβ-Lin28a axis in restenosis. METHODS: Restenosis and atherosclerosis rat models of type 2 diabetes ( n   =  20, for each group) were established by subjecting to PTA. Subsequently, the difference in DNA methylation status and expression of C/EBPβ between the two groups were assessed. EdU, Transwell, and rescue assays were performed to assess the effect of C/EBPβ on the proliferation and migration of VSMCs. DNA methylation status was further assessed using Methyltarget sequencing. The interaction between Lin28a and ten-eleven translocation 1 (TET1) was analysed using co-immunoprecipitation (Co-IP) assay. Student's t -test and one-way analysis of variance were used for statistical analysis. RESULTS: C/EBPβ expression was upregulated and accompanied by hypomethylation of its promoter in restenosis when compared with atherosclerosis. In vitroC/EBPβ overexpression facilitated the proliferation and migration of VSMCs and was associated with increased Lin28a expression. Conversely, C/EBPβ knockdown resulted in the opposite effects. Chromatin immunoprecipitation assays further demonstrated that C/EBPβ could directly bind to Lin28a promoter. Increased C/EBPβ expression and enhanced proliferation and migration of VSMCs were observed after decitabine treatment. Further, mechanical stretch promoted C/EBPβ and Lin28a expression accompanied by C/EBPβ hypomethylation. Additionally, Lin28a overexpression reduced C/EBPβ methylation via recruiting TET1 and enhanced C/EBPβ-mediated proliferation and migration of VSMCs. The opposite was noted in Lin28a knockdown cells. CONCLUSION Our findings suggest that the C/EBPβ-Lin28a axis is a driver of restenosis progression, and presents a promising therapeutic target for restenosis.
Animals ; Cell Proliferation/genetics* ; Cell Movement/genetics* ; Muscle, Smooth, Vascular/metabolism* ; Rats ; DNA Methylation/physiology* ; CCAAT-Enhancer-Binding Protein-beta/genetics* ; Male ; Myocytes, Smooth Muscle/cytology* ; Rats, Sprague-Dawley ; RNA-Binding Proteins/genetics* ; Cells, Cultured ; Coronary Restenosis/metabolism*

BACKGROUND: Epoxyeicosatrienoic acids (EETs), which are metabolites of arachidonic acid catalyzed by cytochrome P450 epoxygenase, are degraded into inactive dihydroxyeicosatrienoic acids by soluble epoxide hydrolase (sEH). Many studies have revealed that sEH gene deletion exerts protective effects against diabetes. Vascular calcification is a common complication of diabetes, but the potential effects of sEH on diabetic vascular calcification are still unknown. METHODS: The level of aortic calcification in wild-type and Ephx2-/- C57BL/6 diabetic mice induced with streptozotocin was evaluated by measuring the aortic calcium content through alizarin red staining, immunohistochemistry staining, and immunofluorescence staining. Mouse vascular smooth muscle cell lines (MOVAS cells) treated with β-glycerol phosphate (0.01 mol/L) plus advanced glycation end products (50 mg/L) were used to investigate the effects of sEH inhibitors or sEH knockdown and EETs on the calcification of vascular smooth muscle cells, which was detected by Western blotting, alizarin red staining, and Von Kossa staining. RESULTS: sEH gene deletion significantly inhibited diabetic vascular calcification by increasing levels of EETs in the aortas of mice. EETs (especially 11,12-EET and 14,15-EET) efficiently prevented the osteogenic transdifferentiation of MOVAS cells by decreasing nidogen-2 (NID2) expression. Interestingly, suppressing sEH activity by small interfering ribonucleic acid or specific inhibitors did not block osteogenic transdifferentiation of MOVAS cells induced by β-glycerol phosphate and advanced glycation end products. NID2 overexpression significantly abolished the inhibitory effect of sEH gene deletion on diabetic vascular calcification. Moreover, NID2 overexpression mediated by adeno-associated virus 9 vectors markedly increased insulin-like growth factor 2 (IGF2) and phospho-ERK1/2 expression in MOVAS cells. Overall, sEH gene knockout inhibited diabetic vascular calcification by decreasing aortic NID2 expression and, then, inactivating the downstream IGF2-ERK1/2 signaling pathway. CONCLUSIONS sEH gene deletion markedly inhibited diabetic vascular calcification through repressed osteogenic transdifferentiation of vascular smooth muscle cells mediated by increased aortic EET levels, which was associated with decreased NID2 expression and inactivation of the downstream IGF2-ERK1/2 signaling pathway.
Animals ; Mice ; Vascular Calcification/metabolism* ; Mice, Inbred C57BL ; Epoxide Hydrolases/metabolism* ; Diabetes Mellitus, Experimental/genetics* ; Male ; Gene Deletion ; MAP Kinase Signaling System/genetics* ; Cell Line ; Immunohistochemistry ; Muscle, Smooth, Vascular/metabolism* ; Signal Transduction/genetics* ; Mice, Knockout

Pancreatoduodenectomy with portal-superior mesenteric vein resection and reconstruction can provide radical surgical opportunities for patients with venous invasion and enable them to benefit from the surgery. With the development of minimally invasive concepts and surgical techniques, laparoscopic and robot-assisted pancreatoduodenectomy with portal-superior mesenteric vein resection and reconstruction is being increasingly widely carried out. This surgical procedure is highly technically demanding, and the perioperative management of patients is complex. However, there is a lack of high-quality and high-level evidence-based clinical studies in this regard. In order to better standardize the clinical application of laparoscopic or robot-assisted pancreatoduodenectomy with portal-superior mesenteric vein resection and reconstruction in China, the Study Group of Minimally Invasive Treatment for Pancreatic Cancer in China Anti-Cancer Association, guided by problems and based on evidence, formed 17 recommendations through full discussions among experts. The recommendations involve the safety, oncological benefits, and perioperative patient management of the minimally invasive approach to pancreatoduodenectomy with portal-superior mesenteric vein resection and reconstruction.
Humans ; Pancreaticoduodenectomy/methods* ; Mesenteric Veins/surgery* ; Laparoscopy ; Portal Vein/surgery* ; Robotic Surgical Procedures ; Pancreatic Neoplasms/surgery* ; Consensus