Management of three cardiogenic pulmonary edemas occurring in a patient scheduled for left ventricular assist device implantation: indicators for determining left ventricular assist device pump speed.

A male patient with Marfan syndrome underwent aortic root replacement and developed left ventricular (LV) failure. Four years later, he underwent aortic arch and aortic valve replacement. Thereafter, his LV failure progressed, and cardiogenic pulmonary edema (CPE) appeared, which we treated with extracorporeal LV assist device (LVAD) placement. Three months later, the patient developed aspiration pneumonia, which caused hyperdynamic right ventricle (RV) and CPE. We treated by changing his pneumatic LVAD to a high-flow centrifugal pump. A month later, he underwent thoracoabdominal aortic replacement. After four weeks, he developed septic thrombosis and LVAD failure, which caused CPE. We treated with LVAD circuit replacement and an additional membrane oxygenator. Four months later, he underwent DuraHeart(®) implantation. During this course, pulmonary artery wedge pressure (PAWP) varied markedly. Additionally, systolic pulmonary artery pressure (sPAP), left atrial diameter (LAD), RV end-diastolic diameter (RVEDD) and estimated RV systolic pressure (esRVP) changed with PAWP changes. In this patient, LV failure and hyperdynamic RV caused the CPEs, which we treated by adjusting the LVAD output to the RV output. Determining LVAD output, RV function and LV end-diastolic diameter are typically referred, and PAWP, LAD, RVEDD, and sPAP could be also referred.

A case of a giant cell myocarditis that developed massive left ventricular thrombus during percutaneous cardiopulmonary support.

BACKGROUND: Giant cell myocarditis, characterized by infiltration of multinucleated giant cells in the myocardium, is a rare type of myocarditis. It often progresses rapidly into fulminant heart failure and indicates a poor prognosis. When a patient with giant cell myocarditis develops into severe myocarditis presenting with a cardiogenic shock, we should use a percutaneous cardiopulmonary support (PCPS), which could occur complications. We experienced a patient with giant cell myocarditis, who developed left ventricular thrombus formations during the circulation support therapy with PCPS for cardiogenic shock. CASE PRESENTATION: A 60-year-old man who developed a cardiogenic shock was transferred to our hospital. After the admission, inotropic agents were increased and an intra-aortic balloon pumping was started. But these therapies did not improve his hemodynamic status. He was placed PCPS. Then, he underwent endomyocardial biopsy and was diagnosed with giant cell myocarditis. On the next morning, he developed complete atrioventricular block, and subsequently, thrombus formations occurred in his left ventricular outlet tract and Valsalva sinus despite an anticoagulant therapy. Thereafter, we intensified the anticoagulant therapy to prevent further thrombus formation, but he developed an intracranial hemorrhage. He did not recover from heart failure and died 16 days after the admission. CONCLUSIONS: We present a patient with giant cell myocarditis who developed widespread thrombosis in the left ventricle during the circulatory support with PCPS, despite anticoagulant therapy. In this case, decreased left myocardial contractility caused by giant cell myocarditis and increased left ventricular afterload by the retrograde perfusion from the PCPS induced the thrombotic tendency and congestion in the left ventricle. In addition, he developed complete atrioventricular block, which reduced the left ventricular ejection and enhanced the thrombus formation. Because patients with giant cell myocarditis have a low probability of spontaneous recovery, heart transplantation or ventricular assist device implantation may be required for circulatory support. We should establish mechanical circulatory support rapidly to improve the prognosis of patients with giant cell myocarditis. Moreover, a ventricular assist device, which can prevent both ventricular congestion and retrograde blood flow, might be suitable to prevent complications as this case.

[Pulmonary Artery Catheter Injured by Ablation Device during Maze Procedure].

We report a case of pulmonary artery catheter (PAC) injury by radio frequency device for maze procedure. A 64-year-old female with severe mitral insufficiency, tricuspid insufficiency and paroxysmal atrial fibrillation was scheduled for mitral valve repair, tricuspid annulo- plasty and maze procedure including right-sided maze. Under general anesthesia, a PAC was inserted to pul- monary artery (PA) uneventfully. After radio frequency maze procedure and mitral valve repair, PAC was removed from right atrium by the surgeon for tricus- pid annuloplasty. Thereafter, the surgeon reinserted the PAC under transesophageal echocardiographic guidance since PAC balloon could not be inflated. PA pressure and cardiac output were not shown despite other parameters were correct We removed the PAC and reinserted a new one after the surgery. The PAC was compressed at about 25 cm from the tip and it appears to have been injured during right-sided maze procedure with radio frequency device. Complications of PAC are well known, including PA rupture and suture entrapment to the right atrium. To best of our knowledge, this is the first reported case of PAC injury by radio frequency device. Fortunately the PAC was not torn in our case ; however, there might have been a risk of infection through the thermodilu- tion cable.

Fabrication of tin-filled carbon nanofibres by microwave plasma vapour deposition and their in situ heating observation by environmental transmission electron microscopy.

Sn-filled carbon nanofibres (CNFs) are fabricated by microwave plasma chemical deposition. Scanning electron microscopy observations revealed the existence of a Sn island under the CNFs. The structure of the CNFs is investigated, and the behaviour of Sn in the internal space of CNFs is revealed by performing in situ heating observations by environmental transmission electron microscopy (ETEM). ETEM observations reveal that they have low-crystallized carbon wall and Sn occupies not only the CNF's internal space but also its carbon wall. The Sn inside the CNF is completely covered by the carbon wall. Further, the in situ heating observations reveal that Sn within the internal space and the carbon wall of the CNFs diffused to the outside during heating. Moreover, it is found that higher membered carbon rings and defects in the graphite layer act as diffusion routes between disordered carbon layers.