[Cunninghamella bertholletiae-infective endocarditis complicated by tricuspid valve giant vegetation in a patient with aplastic anemia].

A 62-year-old female was presented to the hospital of the current study for pancytopenia and was diagnosed with severe aplastic anemia. She was treated with a combination therapy of antithymocyte globulin, cyclosporine A, and eltrombopag. The patient also presented with febrile neutropenia after commencement of the treatment and did not respond to the various antibiotics and antifungal agents. Echocardiography showed a giant vegetation attached to the tricuspid valve on Day 78 of the immunosuppressive therapy, and the tricuspid valve replacement was performed. The vegetation was formed by Cunninghamella bertholletiae, a mucor type, and was treated with high-dose liposomal amphotericin B (L-AMB), which was terminated after six weeks due to decreased renal function. In addition, mucormycosis was controlled by posttreatment with posaconazole (PSCZ). This is a rare case of mucormycosis that developed into a giant vegetation during the immunosuppressive therapy for aplastic anemia. It was believed to be a valuable case to consider in future mucormycosis treatment, including the success of the treatment by switching from L-AMB to PSCZ.

[Ochronosis of the Entire Aortic Root in Alkaptonuria;Report of a Case].

Alkaptonuria is a rare hereditary disorder of phenylalanine and tyrosine metabolism, which results in ochronosis of cardiovascular structures including valves, aortic intima, and coronary arteries. Aortic valve disease is the most frequently reported cardiac sequela of alkaptonuria. We report a case of 77-year-old woman with known alkaptonuria who underwent aortic valve replacement for severe aortic stenosis. Operative findings showed impressive ochronosis of the aortic valve and the aortic intima. The post-operative course was uneventful and she was discharged 25 days after the surgery.

Deep Hypothermic Circulatory Arrest Activates Neural Precursor Cells in the Neonatal Brain.

BACKGROUND: Use of antegrade cerebral perfusion (ACP) as an alternative neuroprotection strategy to deep hypothermic circulatory arrest (DHCA) in the setting of cardiopulmonary bypass in neonates has become a common approach, although the value of ACP over DHCA remains highly debated. This study investigated the disruption to neonatal brain homeostasis by DHCA and ACP. METHODS: Neonatal pigs (7 days old) undergoing bypass were assigned to 4 groups: DHCA at 18°C and ACP at 18°, 25°, and 32° for 45 minutes (n = 6 per group). ACP was initiated through the innominate artery and maintained at 40 mL/kg/min. After bypass, all animals were maintained sedated and intubated for 24 hours before being euthanized. Brain subventricular zone tissues were analyzed for histologic injury by assessing apoptosis and neural homeostasis (Nestin). RESULTS: Histologic examination showed no significant ischemic/hypoxic neuronal death at any cooling temperature among the 4 treatment groups. However, we detected a significantly higher apoptotic rate in DHCA compared with ACP at 18°C (P = .003-.017) or 25°C (P = .012-.043), whereas apoptosis at 32°C was not different from DHCA. Of note, we identified increased Nestin expression in the DHCA group compared with all ACP groups (P range = .011-.041). CONCLUSIONS: Neonatal piglet ACP at 18° or 25°C provides adequate protection from increased brain cellular apoptosis. In contrast to ACP, however, DHCA induces brain Nestin expression, indicating activation of neural progenitor cells and the potential of altering neonatal neurodevelopmental progression. DHCA has potential to more profoundly disrupt neural homeostasis than does ACP.

Effect of Inhaled Nitric Oxide on Hemodynamics in Lambs with 1½ Ventricle Circulation.

Inhaled nitric oxide (NO) is widely used to treat postoperative pulmonary hypertension in congenital heart disease. It is believed that NO increases cardiac output (CO) by decreasing pulmonary vascular resistance (PVR), leading to increased left ventricular preload. However, the effect of NO on CO in patients with 1½ ventricle circulation remains unclear. To evaluate this, a superior cavopulmonary (SCP) shunt was constructed in 10 juvenile sheep. A PTFE graft was inserted between the superior vena cava (SVC) and the main pulmonary artery (PA). The SVC was clamped at the right atrial junction to establish a 1½ ventricle circulation. Flows, pressures, and arterial blood gases were recorded before and during inhalation of NO. Mean arterial pressure (46.6 ± 5.4 to 44.6 ± 5.9 mm Hg; p = 0.06) and left atrial pressure (4.0 ± 2.5 to 4.0 ± 2.3 mm Hg; p = 1.0) did not change. Mean PA pressure (13.6 ± 2.4 to 11.7 ± 2.9 mm Hg; p = 0.006) and PVR (5.47 ± 2.99 to 4.54 ± 2.61 Wood Units; p = 0.037) decreased significantly. SVC flow (24.8 ± 11.3 to 22.0 ± 9.7 ml/min/kg; p = 0.09) did not change, and CO decreased (140.2 ± 37.2 to 132.1 ± 39.2 ml/min/kg; p = 0.033). Arterial PO2 improved (103.72 ± 29.30 to 132.43 ± 47.02 mm Hg; p = 0.007). In this 1½ ventricle model, NO surprisingly decreased cardiac output (CO) and did not increase left ventricular preload.

Surgical repair of axillary graft stump syndrome: report of two cases.

Late upper extremity embolic complications of occluded axillofemoral bypass graft (AxFG) or occluded axillo- axillary bypass graft (AxAG) are not frequently noted. A patient presented with acute right upper extremity thromboembolism 2 years after an AxFG occlusion. Computed tomography (CT) findings revealed kinking and occlusion of the axillary artery at the anastomosis. Another patient presented with acute left upper extremity thromboembolism 2 years and 6 years after an AxAG occlusion. CT indicated a thrombus progressing from the occluded graft to the axillary artery. Surgical repair of the axillary artery was performed in both patients without any complications.

Effects of atrial natriuretic peptide after prolonged hypothermic storage of the isolated rat heart.

Primary graft failure (PGF) caused by ischemia-reperfusion injury (IRI) is the strongest determinant of perioperative mortality after heart transplantation. Atrial natriuretic peptide (ANP) has been found to reduce the IRI of cardiomyocytes and may be beneficial in alleviating PGF after heart transplantation, although there is a lack of evidence to support this issue. The purpose of this study was to investigate the cardioprotective effects of ANP after prolonged hypothermic storage. For this purpose, an isolated working-heart rat model was used. After the preparation, the hearts were arrested with and stored in an extracellular-based cardioplegic solution at 3-4°C for 6 h and followed by 25 min of reperfusion. The hearts were divided into four groups (n = 7 in each group) according to the timing of ANP administration: Group 1 (in perfusate before storage), Group 2 (in cardioplegia), Group 3 (in reperfusate), and control (no administration of ANP). Left ventricular functional recovery and the incidence of ventricular fibrillation (VF) were compared. ANP administration at the time of reperfusion improved the percent recovery of left ventricular developed pressure (control, 45.5 ± 10.2; Group 1, 47.4 ± 8.8; Group 2, 45.3 ± 12 vs. Group 3, 76.3 ± 7; P < 0.05) and maximum first derivative of the left ventricular pressure (control, 47.9 ± 8.7; Group 1, 46.7 ± 8.8; Group 2, 49.6 ± 10.8 vs. Group 3, 76.6 ± 7.5; P < 0.05). The incidence of VF after reperfusion did not differ significantly among these four groups (71.4, 85.7, 57.1, and 85.7% in Groups 1, 2, 3, and control, respectively). This result suggests that the administration of ANP at the time of reperfusion may have the potential to decrease the incidence of PGF after heart transplantation.

Atrionatriuretic peptide improves left ventricular function after myocardial global ischemia-reperfusion in hypoxic hearts.

Atrionatriuretic peptide (ANP) is reported to be useful for attenuating myocardial ischemia-reperfusion injury and improving left ventricular function after reperfusion. However, ANP may be either ineffectual or harmful in cases where the myocardium has been chronically hypoxic since birth. This can be a result of the concomitant high levels of cyclic guanosine monophosphate (cGMP) produced within the myocardium. This study aimed to verify the validity of using ANP to improve left ventricular function after myocardial ischemia-reperfusion injury. For this purpose, a cyanotic congenital disease model that was developed using isolated rat hearts was used. Hearts were obtained from Sprague-Dawley rats that were housed from birth until 6 weeks of age either in a hypoxic environment with 13-14% FiO(2) (hypoxic group) or in ambient air (normoxic group). These hearts were subjected to 30min of normothermic global ischemia followed by 30min of reperfusion using the Langendorff technique. Left ventricular functional recovery in hearts administered ANP (0.1µM) into the reperfusion solution was compared with those hearts that were not administered ANP in both hypoxic (without ANP: n=6, with ANP: n=6, with ANP and HS-142-1[an antagonist of ANP]: n=6) and normoxic hearts (without ANP: n =6, with ANP: n=6). In the hypoxic hearts, ANP administration improved the percent recovery of the left ventricular developed pressure (76.3±9.2% without ANP vs. 86.9±6.7% with ANP), maximum first derivative of the left ventricular pressure (82.4±1.1% without ANP vs. 95.8±6.5% with ANP), and heart rate (85.6±4.7% without ANP vs. 96.1±5.2% with ANP) after reperfusion. The improvement and recovery of these cardiac functions were closely related to significantly increased levels of postischemic cGMP release after ANP administration. The effect of ANP was blocked by HS-142-1. The improvements observed in the hypoxic group were similar to those found in the normoxic group. ANP administration during reperfusion improved left ventricular function after myocardial acute global ischemia-reperfusion equally in both the chronically hypoxic and age-matched normoxic groups.

Patient with a massive idiopathic thrombosis in the inferior vena cava.

A 50 year-old man with no significant medical history was admitted for dyspnea and left femoral swelling. Contrast-enhanced computed tomography revealed pulmonary thromboembolism (PTE) and a thrombus in the inferior vena cava (IVC). The thrombus extended from the proximal IVC to the left popliteal vein. Therefore, we decided that an IVC filter insertion was difficult to indicate. Urgent IVC and peripheral vein thrombectomy was performed under cardiopulmonary bypass. On postoperative day 1, venous ultrasonography showed residual deep vein thrombosis in the left external iliac-femoral vein and the popliteal vein. The IVC filter insertion was performed to prevent the recurrence of PTE.

[Combined double valve replacement and abdominal aortic aneurysm repair in a patient with infective endocarditis; report of a case].

The choice of simultaneous or staged surgery in patients with valvular diseases and abdominal aortic aneurysms (AAA) remains controversial. We present a case of simultaneous surgery of double valve replacement and abdominal aorta replacement in a patient with infective endocarditis. A 74-year-old woman was admitted to our hospital because of general fatigue and appetite loss. Computed tomography (CT) scan showed a infrarenal AAA measuring 99 x 67 mm. Echocardiography showed severe regurgitation of mitral valve and aortic valve with vegetations. Electrocardiogram showed atrial fibrillation. She was diagnosed as heart failure due to infective endocarditis and treated with antibiotics, diuretics and catecholamine. However, heart failure did not improve; the patient underwent double valve replacement, pulmonary vein isolation and abdominal aorta replacement simultaneously. Postoperative course was uneventful.

Tolerance of the developing cyanotic heart to ischemia-reperfusion injury in the rat.

OBJECTIVE: Whether chronic hypoxia attenuates myocardial ischemia-reperfusion injury remains controversial because conflicting data have been reported probably due to the existence of many factors influencing the functional recovery of hearts. These factors include the differences of species, the time at which hypoxia begins, the degree of hypoxia, and so on. Regarding chronic hypoxia from birth, so far the only available data are based on findings in rabbit hearts. The purpose of this study was to describe the effect of chronic hypoxia from birth on myocardial reperfusion injury in the rat heart. METHODS: Normoxic hearts were obtained from rats housed in ambient air for 6 weeks (normoxic group); hypoxic hearts were obtained from rats housed in a hypoxic chamber (13%-14% oxygen) from birth for 6 weeks (hypoxic group). Isolated, crystalloid perfused working hearts were subjected to 30 min of global normothermic ischemia followed by 15 min of reperfusion; functional recovery was then measured in the two groups. The excretion of cyclic guanosine monophosphate (cGMP) in the coronary drainage was measured at the end of the preischemia and reperfusion periods. RESULTS: The percent recovery of the left ventricular developed pressure and the first derivative of left ventricular pressure were significantly better in the hypoxic group than in the normoxic group. cGMP excretion in the coronary drainage was significantly increased during both the preischemia and reperfusion periods. CONCLUSION: Chronic hypoxia from birth increased myocardial tolerance to ischemia-reperfusion injury with increased cGMP synthesis in the isolated heart model in rats.

Giant right coronary artery aneurysm complicated by acute myocardial infarction.

A coronary artery aneurysm is uncommon and frequently asymptomatic. This report presents a surgical case of a giant coronary artery aneurysm complicated by acute myocardial infarction. A 26-year-old man with sudden chest pain was referred to our hospital. Myocardial infarction was suspected, and emergency coronary angiography was performed. A giant coronary aneurysm was found in the mid-portion of the right coronary artery. The aneurysm, which was thrombosis-occluded, was successfully resected, and the right coronary artery was anastomosed in an end-to-end fashion. Although the strategy for treating a coronary artery aneurysm without myocardial ischemia remains controversial, surgical intervention should be considered in cases with a giant coronary artery aneurysm, even if asymptomatic, provided the surgical risk is low.

A case of double inflammatory aneurysms in the thoracic and abdominal aorta repaired simultaneously.

A 54-year-old male who had been experiencing a high fever for a month was admitted to a local hospital for examination. Computed tomography revealed saccular aneurysms in the descending thoracic aorta and infrarenal abdominal aorta. The walls of the aneurysms were thickened and enhanced by intravenous contrast which suggested the inflammatory change. He was transferred to this hospital and underwent graft replacement of both the descending thoracic aorta and the abdominal aorta simultaneously. Simultaneous surgery should be considered in patients presenting with multiple inflammatory aneurysms, since inflammatory aneurysms have a risk of demonstrating rapid enlargement.