Myonephropathic Metabolic Syndrome Research Articles

Early surgical outcomes in the composite-valve root replacement with bioprosthesis after surgery for acute type A aortic dissection.

This study aimed to evaluate the surgical outcomes of composite-valve root replacement with bioprosthesis (b-CVRR) after acute type A aortic dissection (AAAD) repair. We included 41 patients who underwent b-CVRR after surgery for AAAD from 2007 to 2022. We excluded seven patients with VSRR, three with mechanical valve use, one with mycotic aneurysm, and one with cardiopulmonary resuscitation. The overlapping surgical indications for b-CVRR were pseudoaneurysm in 21 patients (51.2%), severe AI in 19 (46.3%), re-dissection in 15 (36.6%), root dilatation (> 50mm) in 12 (41.5%), and rupture in 3 (7.3%). The coronary artery reconstruction methods were bilateral Carrel patch in 13 patients (32%), Carrel patch with Piehler in 16 patients (38%), bilateral Piehler in six patients (15%), and Piehler with coronary artery bypass (CABG) in six patients (15%). Four patients who underwent the Carrel patch technique required additional intraoperative CABG. Three hospital mortality occurred (7.3%; myonephropathic metabolic syndrome, heart failure, bleeding from the thyroid carotid artery without injury). No thrombosis of the reconstructed site was observed with the Piehler procedure. Surgical outcomes for patients treated with b-CVRR after AAAD repair were acceptable. Intraoperative coronary artery events occurred due to stenosis caused by traction on the reconstructed coronary artery due to adhesions.

Three Cases of Compartment Syndrome Following Stanford Type-A Acute Aortic Dissection Surgery

Stanford type-A acute aortic dissection can cause lower limb ischaemia with malperfusion syndrome or femoral artery cannulation. Some reports suggest that muscular men aged <60 years may have risk factors for compartment syndrome and myonephropathic metabolic syndrome. This paper describes three cases of compartment syndrome after aortic dissection surgery.

Fatal myonephropathic metabolic syndrome after surgical repair of popliteal aneurysm rupture with distal occlusion

Fatal myonephropathic metabolic syndrome after surgical repair of popliteal aneurysm rupture with distal occlusion

A Case of Collapsed Stent Graft, Severe Lower Limb Ischemia, and Ruptured Abdominal Aortic Aneurysm Due to Type B Acute Aortic Dissection 3 Years after Endovascular Aneurysm Repair.

We report a case of stent graft occlusion, severe lower extremity ischemia, and ruptured abdominal aortic aneurysm due to type B acute aortic dissection 3 years after endovascular aneurysm repair. He admitted our hospital because of abrupt back pain and dysesthesia of bilateral lower limb. Contrast-enhanced computed tomography (CT) scan showed type B acute aortic dissection and occlusion of the stent graft due to dynamic compression by the false lumen. Emergent right axillo-bifemoral bypass operation was done for his critical limb ischemia. Immediately after the successful operation, he fell into shock vital and dissecting abdominal aortic aneurysm rupture was revealed by CT scan. We performed the stump occlusion of the infrarenal abdominal aorta and the bilateral common iliac arteries by abdominal midline incision. Postoperative myonephropathicmetabolic syndrome due to the left ischemia resulted in amputation of his left lower leg for lifesaving. While EVAR cases are increasing, various its complications come to be reported. We consider that this case report might be cautious about the indication of EVAR for the younger generation. (This is a translation of Jpn J Vasc Surg 2019; 28: 367–371.)

One-year limb outcome and mortality in patients undergoing revascularization therapy for acute limb ischemia: short-term results of the Edo registry.

The present study aimed to clarify the current status, therapeutic strategy, and 1-year outcome in acute limb ischemia (ALI) patients in Japan. The EnDOvascular treatment (Edo) registry database includes 324 patients from 10 institutes who were registered between November 2011 and October 2013. A total of 70 ALI patients (mean age 74.0years) from the Edo registry database were enrolled in this study. Of the 70 included patients, 72.9% were male and 35.7% had embolism. Of patients, 38.6%, 42.9%, and 18.6% underwent EVT, surgery, and hybrid thrombectomy, respectively, in primary revascularization strategy. Limb ischemia was categorized into four classes at initial evaluation: SVS/ISCVS class I (n = 13, 18.6%), SVS/ISCVS class IIa (n = 36, 51.4%), SVS/ISCVS class IIb (n = 21, 30%), and SVS/ISCVS class III (n = 0, 0%). Three patients with SVS/ISCVS class IIb limb ischemia developed myonephropathic metabolic syndrome. No catheter-directed thrombolysis was employed as a primary revascularization strategy. The 1-year rates of all-cause death, major amputation, and a composite of perioperative death or major adverse limb event were 28.6%, 5.7%, and 40.0%, respectively. Lower age, male sex, dyslipidemia, high estimated glomerular filtration rate, high albumin level, and low C-reactive protein level were independent positive predictors of all-cause death. In this registry, SVS/ISCVS class IIa ALI was predominant. Approximately 40% of primary revascularization strategy was surgery and EVT, followed by hybrid therapy. All-cause death and major amputation rates at 1 year were less than 30% and 6%, respectively.

A case of urgent blood purification therapies for myonephropathic metabolic syndrome caused by ischemia-reperfusion injury following abdominal aortic compression due to gastric volvulus

A case of urgent blood purification therapies for myonephropathic metabolic syndrome caused by ischemia-reperfusion injury following abdominal aortic compression due to gastric volvulus

A Case of Myonephropathic Metabolic Syndrome from Ischemia in the Right Upper Limb Caused by Right Axillary Artery Perfusion after Total Arch Replacement for Stanford Type A Aortic Dissection

A Case of Myonephropathic Metabolic Syndrome from Ischemia in the Right Upper Limb Caused by Right Axillary Artery Perfusion after Total Arch Replacement for Stanford Type A Aortic Dissection

Clinical application of ultrasound guided Fogarty balloon catheter in arterial crisis

To explore the effectiveness of arterial crisis after replantation of limb treated by ultrasound guided Fogarty balloon catheter. Between January 2012 and July 2016, 27 patients suffered from arterial crisis after replantation of limb were treated with ultrasound guided Fogarty balloon catheter combined with thrombolytic anticoagulant. There were 18 males and 9 females with the age of 19-51 years (mean, 32 years). The limb mutilation position was at knee joint in 3 cases, lower limb in 9 cases, ankle joint in 6 cases, elbow joint in 2 cases, forearm in 4 cases, and wrist joint in 3 cases. The arterial crisis happened at 2.5-18 hours (mean, 7.5 hours) after limb replantation surgery. Color doppler ultrasonography was used to diagnose the arterial thrombosis, finally the anastomotic thrombosis were found in 16 cases, non-anastomotic thrombosis in 7 cases, and combined thrombosis in 4 cases. All the thrombosis were deteced in the arteries with the length of 0.8-3.9 cm. No complication such as vascular perforation, rupture, air embolism, thromboembolism, wound infection, or sepsis happened after operation. Arterial crisis occurred again in 3 cases at 1.5-13.5 hours after limb replantation and treated by arterial exploration, 1 case was treated successfully; 2 cases had arterial occlusion and partial necrosis of limb, and got amputation treatment at last. The rest 24 cases survived with the incision healing by first stage. In the 24 cases, 1 case suffered from acute myonephropathic metabolic syndrome and corrected after hemodialysis; 1 case suffered from acute liver functional damage and corrected by comprehensive treatment of internal medicine. The 24 patients were followed up 7-38 months (mean, 11 months). At last follow-up, blood supply of the limb was good with normal skin temperature and improved sense of feeling, activity, and swelling. According to Chinese Medical Association of hand surgery to the upper extremity function assessment standard, the results were excellent in 12 cases, good in 8 cases, and fair in 4 cases with an excellent and good rate of 83.3%. Ultrasound guided Fogarty balloon catheter treatment of posterior replantation of arterial crisis can accurately locate the thrombosis, get the thrombus fast and invasive minimally to avoid the blind and repeated thrombectomy, and obtain certain effectiveness.

Pretreatment with the Free Radical Scavenger Edaravone Mitigates Kidney Glycogen Depletion and Neutrophil Infiltration after Leg Ischemia in a Rat Model: A Pilot Study.

Objective: We have previously shown that pretreatment with the free radical scavenger edaravone (Radicut®, Mitsubishi Tanabe Pharma Co., Japan) mitigated skeletal muscle damage due to ischemia reperfusion. In this study, we sought to validate its use in an experimental model of myonephropathic-metabolic syndrome (MNMS).Methods: Either edaravone (3.0 mg/kg; edaravone group; n=4) or saline (saline group; n=6) was intraperitoneally injected into male Lewis rats (508±31 g). Normal kidneys were harvested as control (n=3). MNMS was induced by bilaterally clamping the common femoral arteries for 5 h and declamping 5 h later. Kidney damage was evaluated by quantifying Periodic Acid Schiff (PAS)-positive area (glycogen storage) and esterase-positive cells (neutrophil infiltration).Results: The PAS-positive area in the saline group was significantly lower than that in the normal group (36.9±2.6 vs. 66.9±1.2%, P<0.01); the PAS-positive area in the edaravone group remained comparable to that in the normal group (52.9±0.9%, P<0.01). Esterase-positive cells in the saline group were significantly higher than in normal kidneys (62.4±5.6 vs. 17.5±2.4 cells/mm2, P<0.01), while they were significantly reduced in the edaravone group (32.8±5.7 cells/mm2, P<0.01).Conclusion: Edaravone pretreatment mitigates MNMS-induced kidney damage by reducing both glycogen depletion and neutrophil infiltration.

PC194. Edaravone Reduces Kidney Damage Induced by Myonephropathic Metabolic Syndrome in Rat

PC194. Edaravone Reduces Kidney Damage Induced by Myonephropathic Metabolic Syndrome in Rat

Abstract 720: Edaravone Reduces Kidney Damage Induced by Myonephropathic Metabolic Syndrome in Rats

Background: Free radicals cause myonephropathic metabolic syndrome (MNMS), which damages not only muscles but also kidneys. At ATVB 2014, we previously reported edaravone (Radicut®, Mitsubishi Tanabe Pharma Co., Japan), the free radical scavenger may suppress kidney damage induced by MNMS. Objective: In this study, we evaluated whether edaravone suppresses MNMS-induced kidney damage, focusing on active neutrophils and tubular function. Methods: Either 3.0 mg/kg of edaravone (edaravone group; n = 4), or saline (MNMS group; n = 6) was intraperitoneally injected into male Lewis male rats (508 ± 31 g). MNMS models were induced, by clamping the bilateral common femoral arteries for 5 hours, followed by de-clamping after more 5 hours. The both kidneys were stained with naphthol AS-D chloroacetate esterase to detect active neutrophils and with Periodic Acid Schiff (PAS) to assess glycogen storage. Normal kidneys were also stained as control (n = 3). Kidney damage was evaluated by counting the number of chloroacetate esterase-positive cells (neutrophil infiltration) and the percentage of PAS-positive area (tubular function). Results: The number of chloroacetate esterase-positive cells was significantly increased in the MNMS group than that in normal kidneys (62.4 ± 5.6 vs. 17.5 ± 2.4 cells/mm2, p&lt;0.01). However, the number of chloroacetate esterase-positive cells was significantly reduced in the edaravone group (32.8 ± 5.7 cells/mm2, p&lt;0.01, Figure attached). The percentage of PAS-positive area in the MNMS group was significantly decreased than that in normal kidneys (36.9 ± 2.6 vs. 66.9 ± 1.2%, p&lt;0.01). The percentage of PAS-positive area was maintained in the edaravone group (52.9 ± 0.9 %, p&lt;0.01, Figure attached). Conclusions: Edaravone may reduce neutrophil infiltration around the glomerulus and tubular dysfunction induced by MNMS.

Edaravone injected at the start of reperfusion suppresses myonephropathic metabolic syndrome in rats.

The purpose of this study was to evaluate whether edaravone (Radicut(®), Mitsubishi Tanabe Pharma Co., Osaka, Japan) injected at the start of reperfusion can suppress myonephropathic-metabolic syndrome (MNMS). MNMS models were made by clamping the bilateral common femoral arteries for 5 hours. At de-clamping (at the start of reperfusion), they were intra-peritoneal injected with 9.0 mg/kg of edaravone (the edaravone group, n = 5) or an equal volume of saline (the control group, n = 5). At five hours after de-clamping, the lower extremity muscles were stained with hematoxylin & eosin (H&E) to count the viable cells, and periodic acid- Schiff (PAS) to assess the glycogen storage. The lungs were also stained with H&E to expresse the alveolar wall thickness, and naphthol AS-D chloroacetate esterase to label infiltrating active neutrophils. The viable muscle cells in the edaravone group was significantly greater than that of the control group (593 ± 60 vs. 258 ± 31 cells/mm(2), p < 0.01). The PAS-positive area in the edaravone group was also significantly higher than that in the control group (30.1 ± 6.9 vs. 7.3 ± 2.1%, p < 0.001). The alveolar wall thickness in the edaravone group was significantly lower than that in the control group (63.6 ± 5.6 vs. 17.2 ± 5.2%, p < 0.001). The active neutrophil infiltration in the edaravone group was also significantly lower than that in the control group (249 ± 59 vs. 68 ± 8 cells/mm(2), p < 0.001). We conclude that edaravone injected at the start of reperfusion can suppress not only muscle reperfusion injury but also lung damage.

PS228. Can Edaravone Protect Kidney Damage Caused by Myonephropathic Metabolic Syndrome in Rats?

PS228. Can Edaravone Protect Kidney Damage Caused by Myonephropathic Metabolic Syndrome in Rats?

Abstract 323: Can Edaravone Protect From Kidney Damage Caused by Myonephropathic Metabolic Syndrome in Rats?

Introduction &amp; Hypothesis: Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which damages not only muscles but also kidneys. At ATVB 2012 &amp; 2013, we reported the free radical scavenger, edaravone (Radicut®, Mitsubishi Tanabe Pharma Co., Japan) suppresses muscle injury by MNMS. In this study, we evaluated whether edaravone can suppress kidney damage caused by MNMS. Methods: Lewis male rats (508 ±31 g, n = 10) were intraperitoneally injected with either 3.0 mg/kg of edaravone (edaravone group; n =4), or saline (MNMS group; n = 6). The MNMS models were induced, by clamping the bilateral common femoral arteries for 5 hours and then de-clamping. Five hours after de-clamping, the both kidneys were harvested and stained with hematoxylin &amp; eosin. Normal kidneys were also harvested as control (n = 3). Kidney damage was evaluated by counting the number of cells in glomerulus (glomerular infiltration) and the density of residual tubular cells (enlargement of tubular cells). Results: The number of cells in glomerulus was significantly increased in MNMS group than that in the control (77.2 ±3.7 vs. 49.6 ±2.8 cells/glomerulus, p &lt;0.01). However, the number of cells in glomerulus was alleviated in edaravone group (62.2 ±2.4 cells/glomerulus, p &lt;0.01). The density of residual tubular cells was significantly decreased in MNMS group than that in the control (555 ±24 vs. 957 ±44 cells/mm2, p &lt;0.001). The density of residual tubular cells was maintained in edaravone group (654 ±38 cells/mm2, p =0.06). Conclusions: MNMS was associated with significant glomerular infiltration and the enlargement of tubular cells. Edaravone may alleviate these kidney damages caused by MNMS.

Abstract 264: Edaravone Injected at the Start of Reperfusion Suppresses Lung Damage Caused by Myonephropathic Metabolic Syndrome in Rats

Introduction &amp; Hypothesis Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which damages not only muscles but also lungs. At ATVB 2012, we previously reported that radical scavenger, edaravone (Radicut®, Mitsubishi Tanabe Pharma Co., Japan) injected at the start of reperfusion suppresses muscle injury following leg ischemia in rats. In this study, we evaluated whether edaravone can suppress MNMS-induced lung damage following leg ischemia, if injected at the start of reperfusion. Methods The MNMS models (Male Lewis rats, 525 ± 78 g, n = 10) were induced, by clamping the bilateral common femoral arteries for 5 hours and then de-clamping. The rats were intraperitoneally injected with either 9.0 mg / kg of edaravone (edaravone group; n = 5), or saline (MNMS group; n = 5) at the same time as de-clamping, corresponding to the start of reperfusion. Five hours after de-clamping, the both lungs were harvested and stained with hematoxylin &amp; eosin (HE). Normal lungs without reperfusion were also harvested as control (n = 3). Lung damage was expressed as the percentage area of the alveolar wall thickness, determined by computerized densitometry (NIH Image Program J, Ver. 1.37). Results The lungs of MNMS group had extensive swelling. But the lungs of the edaravone group were filled with air, similar to that of normal lungs (Figure attached, original 200x). The mean percentage area in the edaravone group was significantly lower than that in MNMS group (17.2 ± 5.2 vs. 63.6 ± 5.6%, p &lt; 0.001). Conclusions Our results suggest that edaravone injected at the start of reperfusion can suppress MNMS-induced lung damage following leg ischemia in rats.

下肢虚血を合併した Stanford B 型急性大動脈解離に対する人工血管置換術後 MNMS の救命例

症例は52歳，男性．2011年9月，突然の胸背部痛と下肢の痺れを訴え当院に救急搬送された．CT検査でStanford B型急性大動脈解離と診断した．腎動脈以下の血栓化偽腔の圧排によって左総腸骨動脈の高度の狭小化を認めた．下肢の虚血解除を目的に緊急大腿動脈交叉（F-F）バイパス術を施行し左下肢の症状は消失した．しかし入院4日目に突然，両下肢の安静時痛およびチアノーゼが出現した．CT検査で血栓化偽腔の増大のために腎動脈下大動脈真腔が高度に狭小化していた．緊急開腹人工血管置換術を施行し，下肢血流の再還流をえた．術後血行再建後症候群（myonephropathic metabolic syndrome : MNMS）を併発し，急性腎不全に対して持続的血液濾過透析（CHDF）を行った．経過中に心室細動も発症し，術後管理に難渋したがその後，自尿を認め透析から離脱した．Ankle brachial pressure index（ABI）も改善し，入院34日目に麻痺なく独歩で退院した．

Intraoperative continuous hemodiafiltration with selective venous drainage of ischemic limbs

We report two cases of acute limb ischemia with threatened myonephropathic metabolic syndrome (MNMS) in which continuous hemodiafiltration (CHDF) was started before revascularization with selective drainage from the clamped femoral vein of ischemic limb and return of processed blood into the contralateral femoral vein. It was aimed to optimise the removal of metabolites which were produced by myolysis following reperfusion as well as to minimize the deviation of metabolites into the systemic circulation. Both cases had uneventful postoperative course without MNMS and the limbs were salvaged.

Acute Aortic Occlusion Due to False-Lumen Expansion After Repair of Abdominal Aortic Rupture in Type B Acute Aortic Dissection

We describe a patient with aortic occlusion due to false-lumen expansion after repair of abdominal aortic rupture in acute type B aortic dissection. A 70-year-old man presented to a nearby hospital with severe lower back pain, and was subsequently referred to our hospital with a diagnosis of abdominal aortic rupture. Computed tomography scanning on admission revealed type B aortic dissection with concomitant false-lumen rupture at the level of pre-existing infrarenal abdominal aortic aneurysm. The patient underwent abdominal aortic replacement with the true lumen reconstructed using a bifurcated knitted Dacron graft. On postoperative day 2, the patient developed severe lower body ischemia. Computed tomography scanning revealed complete true-lumen occlusion at the renal artery level because of false-lumen expansion. The patient underwent open fenestration by opening the bulging flap with a transverse graftotomy distal to the proximal graft anastomosis. After fenestration, the patient developed severe metabolic complications (i.e., myonephropathic-metabolic syndrome) and died a day later of cardiac arrest resulting from hyperkalemia. Abdominal aortic replacement with true-lumen reconstruction in patients with abdominal aortic rupture in type B acute aortic dissection could also lead to acute aortic occlusion due to re-dissection or true-lumen compromise accompanying retrograde propagation of false-lumen thrombosis. This lethal sequela after true-lumen reconstruction might be prevented by an adjuvant procedure such as concomitant fenestration.

Edaravone protects against tissue damage in the lung and kidney induced by myonephropathic metabolic syndrome

Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which not only damages muscles but also the kidneys and lungs. It was recently shown that the free radical scavenger edaravone suppressed reperfusion injury in rat extremities. The present study evaluated whether edaravone also protects against MNMS-induced tissue damage in the lungs and kidneys after reperfusion injury of rat extremities. Ten male Lewis rats (mean [± SD] weight 508±33 g) were divided into two groups. The MNMS models were created by clamping the bilateral common femoral arteries for 5 h, followed by declamping. In another group, 3.0 mg/kg of edaravone was injected into the peritoneal cavity before clamping the bilateral common femoral arteries. Five hours after starting reperfusion, the kidneys and lungs were harvested from each rat for histological study (n=10). Kidney damage was expressed as the number of infiltrating cells in the glomeruli. Lung damage was expressed as the percentage area of the alveolar wall thickness with cellular infiltration, using computerized densitometry. Kidneys in the edaravone group showed less cellular infiltration than in the control group (62.2±2.4 cells versus 75.8±3.6 cells per glomerulus, respectively; P=0.002). Lungs in the edaravone group also showed a significantly lower percentage of damaged lung tissue area than in the control group (20.5±1.5% versus 63.6±2.8%, respectively; P<0.001). The results suggest that the free radical scavenger edaravone might protect against kidney and lung damage induced by MNMS after reperfusion injury of rat extremities.

New Treatment With Human Atrial Natriuretic Peptide for Postoperative Myonephropathic Metabolic Syndrome

A 49-year-old man had sudden chest pain and paralysis of the lower right limb. An acute aortic dissection was diagnosed in a computed tomography scan and the patient underwent an emergency operation. After the operation, myonephropathic metabolic syndrome developed, and human atrial natriuretic peptide was administered for 11 days until the volume of daily urine output reached at least 10,000 mL, which would facilitate limb salvage and the preservation of life without hemodialysis. This report documents that postoperative myonephropathic metabolic syndrome improved due to the strong diuretic action of human atrial natriuretic peptide without hemodialysis.