RESUMEN
BACKGROUND: The effect of a narrow chest on minimally invasive mitral valve surgery (MIMVS) is unclear.MethodsâandâResults: We enrolled 206 MIMVS patients and measured anteroposterior diameter (APD) between the sternum and vertebra, transverse thoracic diameter (TD), right and left APD of the hemithorax (RD and LD, respectively), and the Haller index (HI; TD/APD ratio) on computed tomography. Preoperative characteristics and operative outcomes were compared between patients with a narrow chest (Group N; HI >2.5; n=53) and those with a normal chest (control [C]; HI ≤2.5; n=153), and the correlations of these measurements with operation time were evaluated in 133 patients undergoing an isolated mitral procedure. Groups N and C differed significantly in APD (89.4 vs. 114.3 mm, respectively; P<0.001), TD (251.5 vs. 240.3 mm, respectively; P=0.002), RD (152.5 vs. 172.5 mm, respectively; P<0.001), LD (155.0 vs. 172.4 mm, respectively; P<0.001), and HI (2.84 vs. 2.12, respectively; P<0.001). Procedural characteristics were comparable, except for a longer aortic cross-clamp time (ACCT) in Group N (118.7 vs. 105.8 min; P=0.047). Rates of surgical death, re-exploration, cerebral infarction, and prolonged ventilation were comparable between the 2 groups. TD was significantly correlated with ACCT (R2=0.037, P=0.028) in patients undergoing an isolated mitral procedure. CONCLUSIONS: Early MIMVS outcomes in patients with narrow chests are satisfactory. TD prolongs ACCT during MIMVS.
RESUMEN
Distribution of phosphatidylserine (PS) in the erythrocyte membrane is essential for its activity. Flippase transports phospholipids from the outer to the inner leaflet of the lipid bilayer and maintains asymmetric distribution of phospholipids in the plasma membrane. ATP11C, a flippase, catalyzes PS flipping at the plasma membrane in association with cell cycle control protein 50A (CDC50A). ATP11C T418â¯N mutation causes 90% decrease in erythrocyte PS-flippase activity. However, the mechanism of the activity reduction remains unknown. To study the endogenous expression of ATP11C in erythrocytes, we produced a monoclonal antibody against human ATP11C. Immunoblotting analyses with this antibody revealed the absence of ATP11C in erythrocyte membranes derived from a patient with the T418â¯N mutation. Transiently expressed ATP11C wild-type in cultured cells localized in the cell membranes in the presence of CDC50A. Contrastingly, ATP11C T418â¯N mutants stacked at the endoplasmic reticulum (ER) even in the presence of CDC50A, suggesting improper intracellular trafficking. Expression of the T418â¯N mutant in cultured cells was lower than that in the wild-type. However, reduced expression of the T418â¯N mutant was partially restored by treatment with proteasome inhibitors, suggesting ER-associated degradation of the mutant protein. Cells expressing T418â¯N did not show flippase activity at the plasma membrane. These data show that the loss of PS-flippase activity in erythrocytes carrying ATP11C T418â¯N mutation is due to impaired enzymatic activity, improper membrane trafficking, and increased proteasome degradation.
Asunto(s)
Adenosina Trifosfatasas/genética , Anemia Hemolítica Congénita/genética , Predisposición Genética a la Enfermedad/genética , Proteínas de Transporte de Membrana/genética , Mutación Missense , Adenosina Trifosfatasas/metabolismo , Anemia Hemolítica Congénita/metabolismo , Animales , Transporte Biológico/genética , Células COS , Chlorocebus aethiops , Retículo Endoplásmico/metabolismo , Membrana Eritrocítica/química , Membrana Eritrocítica/metabolismo , Eritrocitos/metabolismo , Femenino , Células HeLa , Humanos , Immunoblotting , Masculino , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Proteínas de Transporte de Membrana/metabolismo , Fosfatidilserinas/química , Fosfatidilserinas/metabolismoRESUMEN
BACKGROUND: Thromboembolic occlusion of the superior mesenteric artery (SMA) is a grave complication in individuals diagnosed with atrial fibrillation (AF). This condition often necessitates extensive bowel resection, culminating in short bowel syndrome, which presents challenges for anticoagulant administration and/or antiarrhythmic therapy. CASE PRESENTATION: Presented here are findings of two patients, aged 78 and 72 years, respectively, who underwent comprehensive thoracoscopic AF surgery subsequent to extensive small bowel resection following SMA embolization. In each, onset of AF precipitated an embolic event, while the concurrent presence of short bowel syndrome complicated anticoagulation management. Total thoracoscopic AF surgery, comprised stapler-closure of the left atrial appendage (LAA) and bilateral epicardial clamp-isolation of the pulmonary veins, an operative modality aimed at addressing AF rhythm control and mitigating embolic events such as cerebral infarction, led to favorable outcomes in both cases. Additionally, computed tomography (CT) conducted one month post-surgery revealed the absence of residual tissue in the LAA, with the left atrium demonstrating a well-rounded, spherical shape. At the time of writing, the patients have remained asymptomatic following surgery regarding thromboembolic and arrhythmic manifestations for 29 and 10 months, respectively, notwithstanding the absence of anticoagulant or antiarrhythmic pharmacotherapy. Additionally, electrocardiographic surveillance has revealed persistent sinus rhythm. CONCLUSIONS: The present findings underscore the feasibility and efficacy of a total thoracoscopic AF surgery procedure for patients presented with short bowel syndrome complicating SMA embolization, thus warranting consideration for its broader clinical application.