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.

Pathological vascular remodeling is a hallmark of various vascular diseases. Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction, which leads to pathological vascular remodeling. Potassium dehydroandrographolide succinate (PDA), a derivative of andrographolide, has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections. This study investigates the potential of PDA in regulating pathological vascular remodeling. The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice. Experimental approaches, including rat aortic primary smooth muscle cell culture, flow cytometry, bromodeoxyuridine (BrdU) incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay, and Matrigel-based tube formation assay, were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells (SMCs). Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions. The results revealed that PDA exacerbates vascular injury-induced pathological remodeling, as evidenced by enhanced neointima formation. PDA treatment significantly increased the proliferation and migration of SMCs. Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88 (MyD88) expression in SMCs and interacted with T-cadherin (CDH13). This interaction augmented proliferation, migration, and extracellular matrix deposition, culminating in pathological vascular remodeling. Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling, mediated through the MyD88/CDH13 signaling pathway.
Mice ; Rats ; Animals ; Myeloid Differentiation Factor 88/metabolism* ; Vascular Remodeling ; Cell Proliferation ; Vascular System Injuries/pathology* ; Carotid Artery Injuries/pathology* ; Molecular Docking Simulation ; Muscle, Smooth, Vascular ; Cell Movement ; Mice, Inbred C57BL ; Signal Transduction ; Succinates/pharmacology* ; Potassium/pharmacology* ; Cells, Cultured ; Diterpenes ; Cadherins

Protein S deficiency causing arterial ischemic stroke during pregnancy is uncommon. Delay or omission of treatment with perfusion therapies may worsen outcomes for both the mother and the fetus. In this paper, we report a case of an early pregnant woman with protein S deficiency and multiple history of chronic cerebrovascular disease who underwent successful thrombolysis and mechanical thrombectomy. The patient is a 35-year-old woman, eight weeks pregnant, with a history of protein S deficiency and chronic cerebrovascular disease, presenting with rightsided weakness and aphasia. Initial National Institutes of Health Stroke Scale was 10 with cranial magnetic resonance imaging findings of acute infarcts on the left caudate, lentiform nucleus, insula, and frontal lobe with a large vessel occlusion on the proximal M1 segment of the left middle cerebral artery. Intravenous thrombolysis and mechanical thrombectomy were performed with complete recanalization. The patient improved and delivered without any complications after 8 months. Protein S deficiency can contribute to arterial thrombosis including ischemic stroke. Arterial ischemic stroke and large vessel occlusion can cause significant disability if not treated appropriately. Reperfusion therapies in pregnant women show favorable outcomes and should be performed if the benefits outweigh the risks.

Ruptured Sinus of Valsalva (RSOV) is a rarely encountered cardiac anomaly that can potentially lead to adverse clinical outcomes. RSOV increases the risk of morbidity during pregnancy due to the physiological changes associated with gestation, that can exacerbate the underlying cardiac pathology. We present the case of a 29-year-old female with an uncorrected RSOV who required an emergency cesarean section for abruptio placenta. The patient underwent the procedure under spinal anesthesia, with careful titration of norepinephrine infusion and close monitoring of hemodynamic parameters using an invasive intra-arterial line. Given the absence of established anesthetic protocols for parturients with RSOV undergoing cesarean delivery, a comprehensive understanding of the complex interaction between the hemodynamic effects of RSOV, pregnancy, and anesthesia is essential. This understanding enables the safe use of spinal anesthesia in urgent situations, leading to favorable patient outcomes.
Sinus of Valsalva ; Aortic Rupture ; Cesarean Section ; Anesthesia, Spinal

Objective: The varicocoele exist in approximately 35-40% of primary male factor infertility while two to 10 percent of cases presents with pain.1 Most surgeons favor subinguinal microscopic varicocoelectomy because it offers superior improvement in semen parameters and reproductive outcome with the least complication rate. This study aimed to show an innovative surgical technique in the management of men with varicoceles. Methods: Subinguinal varicocelectomies were performed by a single surgeon on all patients starting with a standard cystoscope stabilized by a customized mechanical holding system attached to the operating bed. All the presumed vascular channels, vas deferens and lymphatics were isolated and marked with vascular loops and surgical ties. After all the presumed vessels were tagged, the standard operating microscope was brought to the operative field and full microsurgical dissection was carried out. Results: Ten varicocelectomies were performed on six men with a mean age of 30.5 years. 13 arteries, 84 veins, and 20 lymphatics were identified by the cystoscope while 18 arteries, 93 veins, and 29 lymphatics were identified by the standard operating microscope. Comparing the two modalities, 72%, 90%, and 69% of the arteries, veins, and lymphatics, respectively, were correctly identified by the cystoscope when compared to the latter. Conclusion Subinguinal varicocelectomy using a standard cystoscope could be offered as an alternative surgical approach in men with varicoceles as it can identify veins comparable with that of the standard operating microscope. In addition, a standard cystoscope can also identify, to some degree, lymphatics and arteries during surgical dissection. This innovative surgical technique can serve as a valuable option in the treatment of men with varicoceles.
Cystoscopes ; Veins ; Arteries

Heart failure (HF) is a major cause of significant morbidity, mortality, and hospitalization worldwide including the Philippines. Congenitally corrected transposition of the great arteries (C-TGA) occurs when the right atrium enters the morphological left ventricle which gives rise to the pulmonary artery and the left atrium communicates with the right ventricle which gives rise to the aorta. Heart failure can occur in C-TGA especially if associated with other heart defects. Ideal management is anatomic correction via surgery to prevent or address heart failure. Peritoneal dialysis has been used as a therapeutic intervention for patients with refractory heart failure and kidney injury with or without kidney failure due to its gentler fluid removal compared to conventional ultrafiltration resulting in less myocardial stunning and neurohormonal activation. We present the case of a patient with heart failure who started on peritoneal dialysis (PD) as an adjunct therapy for fluid management after failing to satisfactorily achieve volume control with diuretics. The patient is a 56-year-old man with C-TGA admitted for decompensated heart failure. He was initially treated with intravenous diuretics on the first admission but was readmitted after 3 months for decompensation this time with borderline low blood pressure making diuresis difficult. The patient was given loop diuretics, tolvaptan, and angiotensin receptor neprilysin inhibitor (ARNI) but still with decreasing trends in urine output and inadequate symptom control. PD was initiated before discharge with subsequent improvement in heart failure symptoms. The patient was on regular follow-up for PD maintenance and titration of heart failure medication. In this case report, we have shown how PD can be an effective adjunct to guideline-directed medical therapy in patients with severely symptomatic heart failure who have an unstable hemodynamic status and for which volume management cannot be satisfactorily achieved with diuretics.
peritoneal dialysis ; heart failure ; congenital heart disease ; congenitally corrected transposition of the great arteries ; diuresis ; ultrafiltration

BACKGROUND: After major liver resection, the volume status of patients is still undetermined. However, few concerns have been raised about postoperative fluid management. We aimed to compare gut function recovery and short-term prognosis of the patients after laparoscopic liver resection (LLR) with or without inferior vena cava (IVC) respiratory variability-directed fluid therapy in the anesthesia intensive care unit (AICU). METHODS: This randomized controlled clinical trial enrolled 70 patients undergoing LLR. The IVC respiratory variability was used to optimize fluid management of the intervention group in AICU, while the standard practice of fluid management was used for the control group. The primary outcome was the time to flatus after surgery. The secondary outcomes included other indicators of gut function recovery after surgery, postoperative length of hospital stay (LOS), liver and kidney function, the severity of oxidative stress, and the incidence of severe complications associated with hepatectomy. RESULTS: Compared with patients receiving standard fluid management, patients in the intervention group had a shorter time to anal exhaust after surgery (1.5 ± 0.6 days vs. 2.0 ± 0.8 days) and lower C-reactive protein activity (21.4 [95% confidence interval (CI): 11.9-36.7] mg/L vs. 44.8 [95%CI: 26.9-63.1] mg/L) 24 h after surgery. There were no significant differences in the time to defecation, serum concentrations of D -lactic acid, malondialdehyde, renal function, and frequency of severe postoperative complications as well as the LOS between the groups. CONCLUSION: Postoperative IVC respiratory variability-directed fluid therapy in AICU was facilitated in bowel movement but elicited a negligible beneficial effect on the short-term prognosis of patients undergoing LLR. TRIAL REGISTRATION ChiCTR-INR-17013093.
Humans ; Hepatectomy ; Vena Cava, Inferior/surgery* ; Liver ; Laparoscopy ; Fluid Therapy

BACKGROUND: Right ventricular (RV)-arterial uncoupling is a powerful independent predictor of prognosis in heart failure with preserved ejection fraction (HFpEF). Coronary artery disease (CAD) can contribute to the pathophysiological characteristics of HFpEF. This study aimed to evaluate the prognostic value of RV-arterial uncoupling in acute HFpEF patients with CAD. METHODS: This prospective study included 250 consecutive acute HFpEF patients with CAD. Patients were divided into RV-arterial uncoupling and coupling groups by the optimal cutoff value, based on a receiver operating characteristic curve of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP). The primary endpoint was a composite of all-cause death, recurrent ischemic events, and HF hospitalizations. RESULTS: TAPSE/PASP ≤0.43 provided good accuracy in identifying patients with RV-arterial uncoupling (area under the curve, 0.731; sensitivity, 61.4%; and specificity, 76.6%). Of the 250 patients, 150 and 100 patients could be grouped into the RV-arterial coupling (TAPSE/PASP >0.43) and uncoupling (TAPSE/PASP ≤0.43) groups, respectively. Revascularization strategies were slightly different between groups; the RV-arterial uncoupling group had a lower rate of complete revascularization (37.0% [37/100] vs . 52.7% [79/150], P <0.001) and a higher rate of no revascularization (18.0% [18/100] vs . 4.7% [7/150], P <0.001) compared to the RV-arterial coupling group. The cohort with TAPSE/PASP ≤0.43 had a significantly worse prognosis than the cohort with TAPSE/PASP >0.43. Multivariate Cox analysis showed TAPSE/PASP ≤0.43 as an independent associated factor for the primary endpoint, all-cause death, and recurrent HF hospitalization (hazard ratios [HR]: 2.21, 95% confidence interval [CI]: 1.44-3.39, P <0.001; HR: 3.32, 95% CI: 1.30-8.47, P = 0.012; and HR: 1.93, 95% CI: 1.10-3.37, P = 0.021, respectively), but not for recurrent ischemic events (HR: 1.48, 95% CI: 0.75-2.90, P = 0.257). CONCLUSION RV-arterial uncoupling, based on TAPSE/PASP, is independently associated with adverse outcomes in acute HFpEF patients with CAD.
Humans ; Prognosis ; Prospective Studies ; Stroke Volume/physiology* ; Echocardiography, Doppler/adverse effects* ; Coronary Artery Disease/complications* ; Heart Failure ; Pulmonary Artery/diagnostic imaging* ; Ventricular Function, Right/physiology* ; Ventricular Dysfunction, Right

This study aimed to observe the effect of terpinen-4-ol(T4O) on the proliferation of vascular smooth muscle cells(VSMCs) exposed to high glucose(HG) and reveal the mechanism via the Krüppel-like factor 4(KLF4)/nuclear factor kappaB(NF-κB) signaling pathway. The VSMCs were first incubated with T4O for 2 h and then cultured with HG for 48 h to establish the model of inflammatory injury. The proliferation, cell cycle, and migration rate of VSMCs were examined by MTT method, flow cytometry, and wound healing assay, respectively. The content of inflammatory cytokines including interleukin(IL)-6 and tumor necrosis factor-alpha(TNF-α) in the supernatant of VSMCs was measured by enzyme-linked immunosorbent assay(ELISA). Western blot was employed to determine the protein levels of proliferating cell nuclear antigen(PCNA), Cyclin D1, KLF4, NF-κB p-p65/NF-κB p65, IL-1β, and IL-18. The KLF4 expression in VSMCs was silenced by the siRNA technology, and then the effects of T4O on the cell cycle and protein expression of the HG-induced VSMCs were observed. The results showed that different doses of T4O inhibited the HG-induced proliferation and migration of VSMCs, increased the percentage of cells in G_1 phase, and decreased the percentage of cells in S phase, and down-regulated the protein levels of PCNA and Cyclin D1. In addition, T4O reduced the HG-induced secretion and release of the inflammatory cytokines IL-6 and TNF-α and down-regulated the expression of KLF4, NF-κB p-p65/NF-κB p65, IL-1β, and IL-18. Compared with si-NC+HG, siKLF4+HG increased the percentage of cells in G_1 phase, decreased the percentage of cells in S phase, down-regulated the expression of PCNA, Cyclin D1, and KLF4, and inhibited the activation of NF-κB signaling pathway. Notably, the combination of silencing KLF4 with T4O treatment further promoted the changes in the above indicators. The results indicate that T4O may inhibit the HG-induced proliferation and migration of VSMCs by down-regulating the level of KLF4 and inhibiting the activation of NF-κB signaling pathway.
NF-kappa B/metabolism* ; Interleukin-18/metabolism* ; Proliferating Cell Nuclear Antigen/genetics* ; Cyclin D1/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Muscle, Smooth, Vascular ; Cell Proliferation ; Signal Transduction ; Cytokines/metabolism* ; Glucose/metabolism*

This study aims to explore the effect of Xiaoxuming Decoction on synaptic plasticity in rats with acute cerebral ischemia-reperfusion. A rat model of cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion(MCAO). Rats were randomly assigned into a sham group, a MCAO group, and a Xiaoxuming Decoction(60 g·kg~(-1)·d~(-1)) group. The Longa score was rated to assess the neurological function of rats with cerebral ischemia for 1.5 h and reperfusion for 24 h. The 2,3,5-triphenyltetrazolium chloride(TTC) staining and hematoxylin-eosin(HE) staining were employed to observe the cerebral infarction and the pathological changes of brain tissue after cerebral ischemia, respectively. Transmission electron microscopy was employed to detect the structural changes of neurons and synapses in the ischemic penumbra, and immunofluorescence, Western blot to determine the expression of synaptophysin(SYN), neuronal nuclei(NEUN), and postsynaptic density 95(PSD95) in the ischemic penumbra. The experimental results showed that the modeling increased the Longa score and led to cerebral infarction after 24 h of ischemia-reperfusion. Compared with the model group, Xiaoxuming Decoction intervention significantly decreased the Longa score and reduced the formation of cerebral infarction area. The modeling led to the shrinking and vacuolar changes of nuclei in the brain tissue, disordered cell arrangement, and severe cortical ischemia-reperfusion injury, while the pathological damage in the Xiaoxuming Decoction group was mild. The modeling blurred the synaptic boundaries and broadened the synaptic gap, while such changes were recovered in the Xiaoxuming Decoction group. The modeling decreased the fluorescence intensity of NEUN and SYN, while the intensity in Xiaoxuming Decoction group was significantly higher than that in the model group. The expression of SYN and PSD95 in the ischemic penumbra was down-regulated in the model group, while such down-regulation can be alleviated by Xiaoxuming Decoction. In summary, Xiaoxuming Decoction may improve the synaptic plasticity of ischemic penumbra during acute cerebral ischemia-reperfusion by up-regulating the expression of SYN and PSD95.
Rats ; Animals ; Rats, Sprague-Dawley ; Brain Ischemia/drug therapy* ; Reperfusion Injury/metabolism* ; Infarction, Middle Cerebral Artery ; Neuronal Plasticity ; Reperfusion