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Introduction: We sought to examine midterm results and remodeling effect of false-lumen occlusion treatment using AFX VELA in case of chronic dissection repair. Material and Methods: From June 2019 to May 2022, we performed false lumen occlusion treatment using a modified Candy-Plug technique with AFX VELA on 8 chronic aortic dissection patients with a patent false lumen. We collected operative data, short-term clinical outcomes, mid-term clinical outcomes and imaging test results. We conducted follow-up examinations at postoperative, 6-month and 1-, 2- and 3-year intervals, including contrast-enhanced computed tomography to evaluate the diameter, false lumen thrombosis and any events. Results: The average time from the symptom onset to the thoracic endovascular repair was 81.5 (35-155) months. The aorta showed aneurysmal dilation with an average maximum short-axis diameter of 58.9 (41-91) mm. Two cases needed emergency surgery due to rupture and impending rupture. There were no postoperative deaths. Complete thrombosis within the false lumen was achieved in 6 cases (75%), but 2 cases had incomplete thrombosis, requiring additional treatment. The mean maximum diameter showed a significant decrease at 6 months, 1 year and 2 years postoperatively compared to preoperative measurements (P <.05). Conclusion: We showed the results of false lumen occlusion treatment using the AFX VELA cuff. We observed favorable clinical outcomes and remodeling effects. While the long-term durability and efficacy of this technique in aortic remodeling will need to be monitored with further observation, the use of this cuff is considered a reliable approach to false lumen occlusion treatment. [ABSTRACT FROM AUTHOR]

Myxomas are the most common type of benign cardiac tumors, and the right atrium is the second most common location among them, with an incidence ranging from 8.6% to 20% of all cardiac myxomas. Herein, we described a rare case of right atrial myxoma originating from the inferior vena cava orifice. In this case, main pulmonary artery cannulation and moderate hypothermic circulatory arrest were helpful to obtain a clear and simple view of the operative field without blood, which led to complete resection of the tumor with safety and better outcomes with no future recurrence. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide OBJECTIVES Thoracic endovascular aortic repair (TEVAR) for aortic arch aneurysms is challenging because of anatomical restrictions and the presence of cervical branches. Revascularization of the cervical branch is required when conventional commercial stent grafts are used. TEVAR using fenestrated stent grafts (FSG) often does not require additional procedures to revascularize cervical branches. This study aimed to evaluate the features and initial and midterm outcomes of TEVAR using fenestrated stent grafts. METHODS From April 2007 to December 2016, 101 consecutive patients underwent TEVAR using fenestrated stent grafts for distal aortic arch aneurysms at a single centre. Technical success, complications, freedom from aneurysm-related death, secondary intervention and aneurysm progression were retrospectively investigated. RESULTS All the patients underwent TEVAR using fenestrated stent grafts. The 30-day mortality rate was zero. Cerebral infarction, access route problems and spinal cord injury occurred in 4, 3 and 2 patients, respectively. Each type of endoleak was observed in 38 of the 101 patients during the course of the study; 20/38 patients had minor type 1 endoleaks at the time of discharge. The endoleak disappeared in 2 patients and showed no significant change in 8 patients; however, the aneurysm expanded over time in 10 patients. Additional treatment was performed in 8 of the 10 patients with type 1 endoleaks and dilatation of the aneurysm. The rate of freedom from aneurysm-related death during the observation period was 98%. CONCLUSIONS TEVAR with FSG is a simple procedure, with few complications. Additional treatment has been observed to reduce aneurysm-related deaths, even in patients with endoleaks and enlarged aneurysms. Based on this study, the outcomes of endovascular repair of aortic arch aneurysms using a fenestrated stent graft seem acceptable. [ABSTRACT FROM AUTHOR]

Phosphoglycerides are the major lipid component of all cell membranes. Phosphoglyceride crystal deposition disease (PCDD) is defined as the deposition of phosphoglyceride crystals and is considered a lipid metabolic disorder. It predominantly involves injured soft tissues, ultimately forming foreign body granulomas. We present a case of complete resection of PCDD in a 48-year-old woman, in whom the PCDD originated from a myocardial wound created at the time of surgical repair of a ventricular septal defect 40 years ago. We underscore that familiarity with this disease entity will help to stimulate accurate diagnosis and timely treatment. [ABSTRACT FROM AUTHOR]

Abstract: Background: The precise pathologic mechanisms underlying human thoracic aortic aneurysms (TAAs) remain uncertain, except that matrix metalloproteinase-9 (MMP-9) is considered a key enzyme for the degradation of extracellular matrix in aneurysm walls. The aim of this study was to elucidate the significance of the angiotensin II (AngII) pathway to MMP-9 production in human TAA walls. Methods and results: We examined the activation of Smad2, a common downstream molecule of AngII and transforming growth factor β (TGF-β) pathways, and the expression of MMP-9 in human nonsyndromic TAA walls. We observed significant increases in Smad2 activation and MMP-9 expression, associated with disruption of elastic lamellae. Using human TAA walls in ex vivo culture, we investigated whether AngII and/or TGF-β pathways are essential for MMP-9 production. Unexpectedly, TGF-β receptor inhibitor had no effect on MMP-9 production. We used PD98059, an inhibitor of extracellular signal–regulated kinase (ERK) activation, and demonstrated that PD98059 dramatically reduced MMP-9 production with attenuation of Smad2 activation. Moreover, exogenous AngII resulted in increases in Smad2 activation and MMP-9 production, in an ERK-dependent manner. Conclusion: Our findings indicate that the AngII/ERK pathway has an important role in the production of MMP-9 in human nonsyndromic TAA walls. [Copyright &y& Elsevier]

Six years after primary surgical treatment for gastric cancer, fluoro-deoxy-glucose positron emission tomography/computed tomography was performed in a 72-year-old man, and demonstrated an increased fluoro-deoxy-glucose uptake in the apex of the left ventricle. Magnetic resonance imaging also revealed a solitary small myocardial tumor. Under cardiopulmonary bypass, tumorectomy was performed with a macroscopically sufficient margin. Histopathologic examination showed adenocarcinoma with poor differentiation developed in the myocardium and pericardial fat; these findings were compatible with the previously resected gastric cancer. The postoperative course was uneventful; the patient has been alive for 29 months without any evidence of local recurrence or cardiac events. [ABSTRACT FROM AUTHOR]

p53 is a tumor suppressor gene contributing for genomic stability. p53 is involved in a broad range of cellular responses including cellular senescence, thereby mediates undesirable responses in some settings in age-related disorders. Recently it was shown that p53 promotes pathologies in age-related diseases including diabetes and heart failure. Here we show that endothelial p53 induces vascular dysfunction in hyperglycemia and ischemic conditions. First, we generated streptozotocin (STZ) -induced murine type I diabetic model. In these mice, endothelial p53 expression was increased and acetylcholine-induced vasodilatation was significantly impaired. Endothelial cell specific p53 depletion significantly improved endothelial dysfunction in hyperglycemic condition. Furthermore, p53 negatively regulated the phosphorylation of eNOS (p-eNOS) by up-regulating PTEN expression. We also found that p53 expression was increased in ischemic arteries. Endothelial cell specific p53 knockdown significantly augmented ischemia-induced angiogenesis. Next, we generated endothelial cell specific MDM4 knockout (EC-MDM4 KO) mice. EC-MDM4 KO mice increased p53 expression and decreased phospho-eNOS level in endothelial cells. Up-regulating endothelial p53 resulted in endothelial dysfunction together with reduced angiogenesis in ischemic arteries. These results suggest that endothelial p53 is critically involved in regulating vascular function under hyperglycemic and hypoxic conditions. Suppression of endothelial p53 would become a novel therapeutic target for metabolic diseases. [ABSTRACT FROM AUTHOR]

Mutations of the lamin A gene cause various premature aging syndromes, including Hutchinson-Gilford progeria syndrome (HGPS) and atypical Werner syndrome. In HGPS (but not atypical Werner syndrome), extensive loss of vascular smooth muscle cells leads to myocardial infarction with premature death. The underlying mechanisms how single gene mutations can cause various phenotypes are largely unknown. We performed an interactome analysis using mutant forms of lamin A involved in progeroid syndromes. We found that the mutant lamin A responsible for HGPS, known as progerin, could not bind to proteins related to the DNA damage response, including DNA-dependent protein kinase (DNA-PK). In contrast, wild-type lamin A and lamin A mutants causing atypical Werner syndrome were able to bind to these molecules. We also found that forced expression of progerin in vascular smooth muscle cells led to activation of DNA-PK and cellular growth arrest, while knockdown of DNA-PK attenuated this. Deletion of p53 also improved the inhibition of cell growth due to forced expression of progerin. These findings suggested that progerin activates the DNA damage response pathway and that dysregulation of this pathway may be responsible for the development of cardiovascular pathology in patients with HGPS.

HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors (statins) have been suggested to attenuate abdominal aortic aneurysm (AAA) growth. However, the effects of statins in human AAA tissues are not fully elucidated. The aim of this study was to investigate the direct effects of statins on proinflammatory molecules in human AAA walls in ex vivo culture. Simvastatin strongly inhibited the activation of nuclear factor (NF)-κB induced by tumor necrosis factor (TNF)-α in human AAA walls, but showed little effect on c-jun N-terminal kinase (JNK) activation. Simvastatin, as well as pitavastatin significantly reduced the secretion of matrix metalloproteinase (MMP)-9, monocyte chemoattractant protein (MCP)-2 and epithelial neutrophil-activating peptide (CXCL5) under both basal and TNF-α-stimulated conditions. Similar to statins, the Rac1 inhibitor NSC23766 significantly inhibited the activation of NF-κB, accompanied by a decreased secretion of MMP-9, MCP-2 and CXCL5. Moreover, the effect of simvastatin and the JNK inhibitor SP600125 was additive in inhibiting the secretion of MMP-9, MCP-2 and CXCL5. These findings indicate that statins preferentially inhibit the Rac1/NF-κB pathway to suppress MMP-9 and chemokine secretion in human AAA, suggesting a mechanism for the potential effect of statins in attenuating AAA progression.