Akira Mishima

Surgical treatment for right ventricular perforation caused by transvenous pacing electrodes: a report of three cases.

We experienced three cases of right ventricular perforation that were induced by transvenous pacing electrodes. The patients were a 72-year-old man who underwent percutaneous transluminal coronary recanalization and angioplasty, an 80-year-old woman who had temporary transvenous pacing for a complete atrioventricular block induced by acute valvular heart failure, and a 44-year-old man who had received a permanent pacemaker. All three patients were treated surgically. The first and second patients demonstrated either cardiac tamponade or hemopericardium necessitating pericardial drainage. Spontaneous hemostasis did not occur in cases 1 and 2, due to either anticoagulant therapy or myocardial degeneration. Such patients require surgical closure of the perforation and pericardial drainage as soon as pericardial effusion is confirmed. In contrast, middle-aged individuals without myocardial damage, such as patient 3, need only a simple removal and repositioning of the electrode followed by serial echocardiography.

Long-Term Outcome for Right Heart Function After Biventricular Repair of Pulmonary Atresia and Intact Ventricular Septum

OBJECTIVES The right heart function of the patients with pulmonary atresia and intact ventricular septum was assessed periodically during the process of staged biventricular repair, and the implications for its long-term outcome were analyzed. SUBJECTS AND METHODS During the period from 1971 to 1990, 21 neonates or infants with pulmonary atresia and intact ventricular septum had undergone initial palliative surgery. There were seven early postoperative deaths and one late death. Of the 13 survivors, 10 patients underwent subsequent biventricular repair and form the basis of this study. Their clinical records of roentgenography, electrocardiography, and catheterization studies at each staged period were reviewed retrospectively. RESULTS Arrhythmia occurred late in 2 patients, one of whom died by arrhythmia at 11 years after definitive surgical repair. Therefore the actuarial survival rate was 85.7% at 14 years. The catheterization study after the definitive biventricular repair revealed a significant fall in the right heart pressure (p = 0.0005) and significant improvement in the right ventricular ejection fraction (p = 0.0004). In angiocardiography, dilatation of the right atrium was noted in all patients and was more marked in those who developed arrhythmia in conjunction with rapid growth of the right ventricle. Moreover, the serial repeated electrocardiography disclosed progressive and significant prolongation of both PQ interval (p = 0.003) and QRS duration (p = 0.021). CONCLUSIONS Although biventricular repair for pulmonary atresia and intact ventricular septum proved to attain a satisfactory long-term result, it failed to resolve right heart dysfunction. Postoperative arrhythmia was prone to precipitate progressive dilatation of the right atrium.

Mitral regurgitation caused by ruptured chordae tendineae in Kawasaki disease

Kawasaki disease, a generalized vasculitis of unknown etiology, is becoming one of the leading causes of acquired heart disease in children. In the acute phase of illness, cardiac findings may reveal the involvement of the pericardium, myocardium, endocardium, and coronary arteries. Complications involving the coronary arteries are the most common causes of both early and late morbidity and mortality. I Valvular heart disease, such as primary mitral regurgitation, rarely occurs as a complication and may result in severe congestive heart failure. We report a case of mitral regurgitation caused by ruptured chordae tendineae in a patient with Kawasaki disease who underwent successful valve repair. Rupture of the chordae tendineae has not been previously reported as a cause of mitral regurgitation in Kawasaki disease. The patients Kawasaki disease was diagnosed at 3 months of age, when he had 5 days of fever, truncal rash, erythema of the palms and lips, bilateral conjunctival injection, and cervical lymphadenopathy. His serum C-reactive protein concentration was 9.1 mg/dl. He was treated 6 days after the onset of illness with high-dose aspirin and intravenous gamma globulin at a dosage of 400 mg/kg per day for 3 days. The patients clinical features improved rapidly, and his serum C-reactive protein concentration decreased to 0.7 mg/dl. His condition remained stable until day 24 of his illness, when a II/VI apical systolic murmur suddenly developed and his serum C-reactive protein concentration increased to 6.8 mg/dl. The patient had no fever at that time. Two-dimensional echocardiography and Doppler examination demonstrated mild mitral regurgitation without appreciable abnormalities of the coronary arteries. During a 3-day period, the patient came to have congestive heart failure as a result of mitral regurgitation. Intravenous gamma globulin was again administered to treat a recurrence of acute Kawasaki disease. Evaluation indicated rapid resolution of systemic inflammation, but severe heart failure resulting from significant mitral regurgitation persisted. Three months after the onset of illness, the patient was referred to our hospital for further evaluation. Cardiac catheterization confirmed the presence of grade 4/4 mitral regurgitation with associated pulmonary hypertension and a markedly dilatated left ventricle without evidence of hypokinesia or akinesia. Coronary angiography revealed

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.

Protective effects of calpain inhibitor for prolonged hypothermic cardiac preservation

PURPOSE For successful organ transplantation, it is important to properly preserve the donor organ. This study was carried out to investigate tissue damage generated by the activation of calpain during prolonged hypothermic cardiac preservation using specific antibodies for mu- and m-calpain proenzymes, and to ensure the protective effect of calpain inhibitor 1 (N-acetyl-leucyl-leucyl-norleucinal). METHODS Excised rat hearts were divided into two groups: in Group I, the heart was arrested and immersed in University of Wisconsin solution with 20 microM of calpain inhibitor 1 (n = 28) and in Group N, the heart was arrested and immersed in University of Wisconsin solution without calpain inhibitor (n = 27). After a 12-hour preservation period at 4 degrees C, the hearts were reperfused on an isolated perfusion apparatus. Separation of the myocardial calpain isozymes was carried out by DEAE cellulose chromatography and both calpain proenzymes were detected by immunoblotting. RESULTS The cardiac function was more satisfactorily maintained in Group I in comparison with Group N. Remarkable leakage of creatine kinase, glutamic-oxaloacetic transaminase and lactate dehydrogenase was detected in Group N, while it was efficiently suppressed in Group I. During ischemia, mu-calpain proenzyme decreased in Group N (p < 0.01), but there was no significant change in m-calpain. However, during reperfusion, both mu- and m-calpains decreased more in Group N (p < 0.01). CONCLUSION Activation of calpain proenzymes and a decrease in cardiac function during preservation and reperfusion were demonstrated. The use of calpain inhibitor to protect against tissue damage was suggested as being useful for the prolonged preservation of the heart.

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.

Modified subclavian flap aortoplasty for coarctation repair in patients less than three months of age

Subclavian flap aortoplasty is one of the best procedures for coarctation repair, but recoarctation still remains a problem in neonates and infants. We employed subclavian flap aortoplasty with resection of the whole layer of aortic ductal tissue in 9 patients less than 3 months of age with coarctation of the aorta and obtained satisfactory results.

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.