Norikazu Nomura

Atrial natriuretic peptide reduces ischemia/reperfusion-induced spinal cord injury in rats by enhancing sensory neuron activation

We recently demonstrated that calcitonin gene-related peptide (CGRP) released from sensory neurons reduces spinal cord injury (SCI) by inhibiting neutrophil activation through an increase in the endothelial production of prostacyclin (PGI2). Carperitide, a synthetic α-human atrial natriuretic peptide (ANP), reduces ischemia/reperfusion (I/R)-induced tissue injury. However, its precise therapeutic mechanism(s) remains to be elucidated. In the present study, we examined whether ANP reduces I/R-induced spinal cord injury by enhancing sensory neuron activation using rats. ANP increased CGRP release and cellular cAMP levels in dorsal root ganglion neurons isolated from rats in vitro. The increase in CGRP release induced by ANP was reversed by pretreatment with capsazepine, an inhibitor of vanilloid receptor-1 activation, or with (9S, 10S, 12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3′,2′,1′-kl]pyrrolo[3,4-i][1,6]-benzodiazocine-10-carboxylic acid hexyl ester (KT5720), an inhibitor of protein kinase A (PKA), suggesting that ANP might increase CGRP release from sensory neurons by activating PKA through an increase in the cellular cAMP level. Spinal cord ischemia was induced in rats using a balloon catheter placed in the aorta. ANP reduced mortality and motor disturbances by inhibiting reduction of the number of motor neurons in animals subjected to SCI. ANP significantly enhanced I/R-induced increases in spinal cord tissue levels of CGRP and 6-keto-prostaglandin F1α. a stable metabolite of PGI2. ANP inhibited I/R-induced increases in spinal cord tissue levels of tumor necrosis factor and myeloperoxidase. Pretreatment with 4′-chloro-3-methoxycinnamanilide (SB366791), a specific vanilloid receptor-1 antagonist, and indomethacin reversed the effects of ANP. These results strongly suggest that ANP might reduce I/R-induced SCI in rats by inhibiting neutrophil activation through enhancement of sensory neuron activation.

Cardiotrophin-1 is a prophylactic against the development of chronic hypoxic pulmonary hypertension in rats.

BACKGROUND Cardiotrophin-1 (CT-1) reduces arterial blood pressure by activating nitric oxide synthesis. This study attempted to elucidate the effect of CT-1 on pulmonary arteries of pulmonary hypertensive rats. METHODS Pulmonary hypertension was induced in rats in a hypoxic chamber containing 10% to 11% oxygen. Rats kept in the hypoxic environment received either recombinant mouse CT-1 at a concentration of 50 micro g/kg (CT-1+hypoxia group, n = 21) or phosphate-buffered saline (hypoxia group, n = 30) once per day. Control rats housed in room air also received either the equivalent concentration of CT-1 (CT-1+normoxia group, n = 18) or phosphate-buffered saline (normoxia group, n = 39). Pulmonary arterial pressure, pulmonary vasorelaxation, and ventricular hypertrophy were measured. RESULTS The mean pulmonary arterial pressures were as follows (from lowest to highest; p values are relative to the hypoxia group): normoxia group (20.3 +/- 4.0 mm Hg, p < 0.0001), CT-1+normoxia group (21.1 +/- 2.4 mm Hg, p < 0.0001), CT-1+hypoxia group (27.9 +/- 4.1 mm Hg, p = 0.0019), and hypoxia group (33.9 +/- 6.6 mm Hg). The endothelium-dependent vasorelaxation value was largest in the normoxia group (59.5% +/- 17.4%, p < 0.0001), with it decreasing in the other groups in the following order (p values are relative to the hypoxia group): CT-1+normoxia group (52.8% +/- 15.5%, p = 0.0005), CT-1+hypoxia group (42.3% +/- 14.8%, p = 0.0061), and hypoxia group (17.4% +/- 4.8%). Right ventricular hypertrophy was significant only in the hypoxia group. CONCLUSIONS Our results demonstrate that treatment with CT-1 in a chronic hypoxic pulmonary hypertension model protects the endothelial function of the pulmonary artery; decreases pulmonary arterial pressure; and attenuates right ventricular hypertrophy.

Surgical management of an aneurysm of the left atrial appendage to prevent potential sequelae

An aneurysm of the left atrial appendage is an extremely rare anomaly that is commonly associated with supraventricular arrhythmia, compression of the coronary arteries, intracardiac thrombus and pulmonary venous stenosis. This condition may be caused by congenital dysplasia of the musculi pectinati and is usually diagnosed in the second to fourth decades of life. We report the surgical management of an asymptomatic 9-year old girl with this anomaly. She was referred to us because of abnormal chest X-ray findings, and investigation revealed an aneurysm of the left atrial appendage. As this condition may have potentially fatal complications, the aneurysm was completely resected under cardiac arrest with cardiopulmonary bypass to prevent recurrence and thrombus formation. We suggest that resection of an aneurysm of the left atrial appendage under cardiac arrest with cardiopulmonary bypass is a reasonable treatment option to prevent potential complications, particularly in children.

Ruptured Left Coronary Sinus of Valsalva Aneurysm Into the Left Ventricle

Ruptured aneurysm originating from the left coronary sinus toward the left ventricle (LV) is an extremely rare problem and the incidence was reported as 1.8% of all ruptured sinus Valsalva aneurysms [1]. This can cause severe aortic regurgitation, coronary insufficiency, and paroxysmal ventricular fibrillation [2]. A 59-year-old Japanese male presented with exertional dyspnea. Chest roentogenogram revealed bilateral pleural effusion and cardiomegaly. Two hours after his admission he required resuscitation because of sudden cardiopulmonary arrest. A two-dimensional echocardiogram demonstrated severe aortic regurgitation with compensated LV contractility. Initially he was treated with intensive medical care for congestive heart failure. Definitive diagnosis was confirmed on left-sided catheterization. The aortogram showed the “wind-sock” appearance of the aneurismal sac arising from the left coronary sinus extruding into the LV (arrow in Fig 1). The left coronary artery was intact (arrowhead in Fig 1) and no associated lesion, such as ventricular septal defect, was identified. Standard cardiopulmonary bypass was used during repair. The aneurysm was exposed through an oblique aortotomy. The aortic valvular ring at the left coronary sinus had detached completely from the aortic wall. The sac tightly adhered to the free wall of the LV and the bottom of the sac had perforated (asterisk in Fig 2). The left coronary cusp, valvular ring (arrowheads in Fig 2), and free wall of the aneurysmal sac were removed together. In order to obtain firm anchorage of a mechanical valve, mattress sutures with Teflon pledgets at the defect of valvular ring were directly placed on the aortoventricular junction where aneurismal wall adhering to the endocardium had turned into scar tissue. Histologic examination showed an accumulation of inflammatory cells (not only mononuclear cells but also neutrophiles) implying that a possible cause of aneurysmal formation was an infective endocarditis although any organisms could be identified from these specimens.

Surgical repair of tetralogy of Fallot with large conus artery.

The large conus artery transversing the right ventricular outflow tract may cause more confusion and concern in the surgery of tetralogy of Fallot with a small pulmonary annulus than other well-known coronary anomalies. We experienced an infantile case that precipitated into a critical left ventricular failure caused by transection of a large conus artery for the transannular right ventricular outflow tract reconstruction and rescued the patient with an extracorporeal lung–heart-assist system. Preoperative precise diagnosis of coronary anatomy should serve to protect against fatal mistakes, and various techniques for repair must be chosen individually for this subset of anomalies.

Surgical Treatment for Infected Thrombus in the Superior Vena Cava Using an Off-Pump Venoatrial Shunt

We report a septic patient who had an infected thrombus that extended from the right internal jugular vein to the right atrium 1 cm below the superior venocaval junction. The thrombus was successfully removed using an off-pump shunt placed between the innominate vein and the right atrium.

Infected pseudoaneurysm following a modified Blalock-Taussig shunt procedure

A 3-year-old boy with pulmonary atresia with ventricular septal defect, who had undergone placement of a modified Blalock-Taussig shunt, presented with a 1-week history of high fever. Computed tomography showed a pseudoaneurysm at the anastomosis between the right brachiocephalic artery and the graft. After intravenous antibiotic therapy, the pseudoaneurysm and infected graft were resected through a median sternotomy. This report describes successful management of a potentially fatal complication following placement of a modified Blalock-Taussig shunt.

Anatomical repair of aortopulmonary window with anomalous origin of the right coronary artery from the pulmonary artery.

Aortopulmonary window (APW) with an anomalous origin of a coronary artery is extremely rare. We report surgical management of a four‐week‐old infant with the association of a distal type of APW and an anomalous origin of the right coronary artery (RCA) from the pulmonary artery. Complete anatomical correction comprising division of the great arteries and transferring the RCA as an autologous flap to the aortic defect was successfully performed. doi: 10.1111/jocs.12205 (J Card Surg 2013;28:767–769)

Unruptured Sinus of Valsalva Aneurysm Suspected to Be a Cardiac Tumor

56-year-old man was referred to our hospital due to multiple paroxysmal ventricular contractions. During linical examination an intracardiac mass in the right atrium ttached to the interatrial septum was demonstrated by an nhanced computed tomographic scan (Fig 1, arrow) and agnetic resonance imaging (Fig 2, arrow) in which no pulsaile flow was observed. No other systemic inflammation or alvular lesions were observed. An intracardiac tumor, which as possibly a malignancy, was initially suspected. The operative findings revealed that the solid mass (30 2 36 mm) was attached to the right atrial wall adjacent to he commissure of the anterior and septal leaflet of the ricuspid valve. However, the mass was easily detached from he right atrial wall, and a defect hole appeared. The dimenions of the hole were 10 6 mm, which communicated with he noncoronary sinus, slightly toward the right of the center f the sinus of Valsalva. The aortic valve and annulus were ntact, and no ventricular septal defect was present. The urface of the mass was severely calcified and thickened, and huge solid thrombus, which appeared to be a tumor, occuied the interior. It was finally confirmed that the protrusion as not a tumor but a nonruptured aneurysm originating

Double-Outlet Technique for Tetralogy of Fallot-Type Disease with an Anomalous Coronary Artery

To reduce the right ventricular (RV) pressure and the pressure gradient between the RV and the pulmonary artery (PA) in Tetralogy of Fallot (TOF) with small pulmonary annulus, it is inevitable to enlarge the small annulus by incising and patching from RV to PA via PA annulus. If the anomalous coronary artery exists in the RV outflow tract, the procedure can not be done.