Masahide Chikada

Autoantigenicity of carbonic anhydrase 1 in patients with abdominal aortic aneurysm, revealed by proteomic surveillance

Abdominal aortic aneurysm (AAA) is sometimes detected in patients with atherosclerosis. One of the histological characteristics of AAA walls is infiltration of inflammatory cells, in which autoimmunity may be involved. Thereby, we here surveyed autoantigens in AAA walls by proteomics. Specifically, we separated proteins extracted from AAA wall samples by 2-dimensional electrophoresis and detected candidate autoantigens by western blotting. One of the detected candidates was carbonic anhydrase 1 (CA1). ELISA confirmed that the autoantibodies to CA1 were detected more frequently in AAA patients (n=13) than in healthy donors (n=25) (p=0.03). Interestingly, some serum samples from the AAA patients reacted to CA1 of the AAA walls stronger than to CA1 of peripheral blood mononuclear cells from healthy donors. Our data indicate that CA1 in the AAA walls would be modified to express neo-epitope(s) and that the autoimmunity to CA1 may be involved in the pathogenesis of AAA.

Communication between the right pulmonary artery and left atrium with aneurysm formation

Communication between the pulmonary artery and the left atrium is a rare congenital anomaly. A 7-year-old boy was referred to our hospital with a diagnosis of pulmonary arteriovenous fistula. Referral to a pediatric cardiologist had been delayed because he had only slight cyanosis and no heart murmur. Catheterization and computed tomography scans confirmed that the right pulmonary branches and pulmonary venous returns were normal and that an additional aneurysmal communication was located between the right pulmonary artery and the left atrium. Surgery proceeded uneventfully together with a cardiopulmonary bypass. The connection from the right pulmonary artery to the aneurysm was ligated, and the connection from the left atrium to the aneurysm was closed with a polytetrafluoroethylene patch. We describe this rare anomaly with cyanosis and no heart murmur.

Aberrant Glycosylation of Lumican in Aortic Valve Stenosis Revealed by Proteomic Analysis

To identify proteins related to the pathophysiology of aortic valve stenosis (AS), we investigated the protein profiles of AS aortic valves. Specifically, proteins were extracted from a thickened and calcified area (AS-C) and an apparently non-thickened and non-calcified area (AS-N) in an identical aortic valve leaflet in each of 6 AS patients. The proteins were then separated by 2-dimensional gel electrophoresis (2DE). Protein spots detected by 2DE were compared between the AS-C and AS-N samples. Protein spots of interest were subjected to protein identification by mass spectrometry.In total, 670 protein spots were detected by 2DE, 28 of which showed more than 1.5-fold different intensity (P < 0.05) between the AS-C and AS-N samples. Proteins were identified in 17 out of the 28 spots. Fibrinogen and lumican were identified in 9 and 3 spots, respectively. Intensity of these 12 spots was lower in the AS-C samples than in the AS-N samples. In the 1D-Western blot analysis, 4 lumican bands (80 kDa, 75 kDa, 65 kDa, and 53 kDa) were detected, of which 2 bands with 80 kDa and 75 kDa showed lower intensity in the AS-C samples than in the AS-N samples. When de-glycosylated protein samples were used in the 1D-Western blot, only a single lumican band with ~40 kDa was detected, indicating that lumican was variously glycosylated and that highly glycosylated lumican molecules were decreased in AS-C.Collectively, insufficient glycosylation of lumican in the thickened and calcified areas of AS aortic valves may be involved in the pathophysiology of AS.

Surgical Treatment or Conservative Therapy for Stanford Type A Acute Aortic Dissection with a Thrombosed False Lumen

OBJECTIVES Optimum treatment for acute aortic dissection (AAD) with a thrombosed false lumen (thrombosed AAD) remains controversial. We evaluated the outcome of thrombosed AAD according to treatment strategy. MATERIALS AND METHODS We examined 280 patients with AAD, of which 30 had thrombosed AAD. We compared computed tomography findings, cardiac performance, and clinical course in 28 of these patients. Patients were divided into three groups for the comparison: Group E (emergency surgery), Group C (conservative therapy), and Group S (conservative therapy switched to emergency surgery). RESULTS In Group E (n = 13), one patient died and 12 survived. In Group C (n = 10), all patients were discharged, of which two died of cancer and two of the remaining eight survivors underwent subsequent elective surgery. In Group S (n = 5), one patient died and four survived following surgery. CONCLUSIONS It was hard to predict re-dissection or rupture following conservative treatment for thrombosed AAD. Basically, we should perform emergency surgery following the diagnosis of thrombosed AAD, particularly in complicated cases such as those with pericardial effusion, tamponade, and large aorta. Conservative therapy has a very limited application in patients with the initial stages of thrombosed AAD.

Reports of four surgical treatments of acute pulmonary embolism with a floating thrombus in the right atrium.

Acute pulmonary embolism (APE) is a serious disease. Recently, multidetector-row computed tomography (MDCT) has proven to be valuable in detecting APE and deep vein thrombosis. APE is classified as massive, submassive, and nonmassive. The incidence of submassive APE and the number of therapeutic approaches for clinically diagnosed critical submassive APE have both increased. However, most strategies for submassive APE have been conservative, e.g., transvenous catheter pulmonary embolectomy, and there are few reports on surgical pulmonary embolectomy. We examined the surgical outcomes in four cases of submassive APE with a floating thrombus in the right atrium (RA) from August 2003 to July 2008. All patients appeared to have no neurological complications and showed an event-free survival of up to 65 months (37 ± 25 months). Surgical pulmonary embolectomy was effective for submassive APE with a floating thrombus in the RA.

Surgical Treatment for Angiosarcoma Occupying the Bilateral Atrial Cavities and the Atrial Septum

症例は喀血で発症した48歳の男性.胸部CT検査で,両側心房および心房中隔に発生した心臓悪性腫瘍とその肺転移と診断した.左房内腫瘍がきわめて大きく,心腔内閉塞による突然死の予防と病理診断を目的に手術を行った.腫瘍は右房から心房中隔を経て左房内を占有していた.肺静脈を含めた左房の一部を残し,残りの左房壁とほぼすべての心房中隔,右房壁を切除後,ウマ心膜で両側心房と心房中隔,上下大静脈を再建した.病理検査の結果は血管肉腫であった.術後第22病日に軽快退院し,その後,血液腫瘍内科に入院しInterleukin-2(IL-2)投与を行ったが,術後第107病日に死亡した.近年,血管肉腫に対する放射線療法やIL-2による治療の有用性が報告されている.自験例のように原発巣の完全切除が可能な症例は,可及的早期に原発巣を切除して病理診断を行い,術後に放射線療法やIL-2投与などを行うことで,治療の可能性が広がる.