Dynamic left ventricular outflow tract obstruction in living donor liver transplantation recipients -A report of two cases-

Abstract

We present two cases of dynamic left ventricular outflow tract obstruction in 2 patients who were undergoing living donor liver transplantation. On the preoperative transthoracic echocardiography, the first patient showed normal ventricular function and a normal wall thickness, but severe hemodynamic deterioration developed during the anhepatic period and this was further aggravated after reperfusion in spite of volume resuscitation and catecholamine therapy. Intraoperative transesophageal echocardiography revealed the systolic anterior motion of the mitral valve leaflet together with left ventricular outflow tract obstruction. The second patient showed left ventricular hypertrophy with left ventricular outflow tract obstruction on the preoperative echocardiography. Intraoperative transesophageal echocardiography was used to guide fluid administration and the hemodynamic management throughout the procedure and a temporary portocaval shunt was established to mitigate the venous pooling during the anhepatic period. The purpose of this report is to emphasize the clinical significance of dynamic left ventricular outflow tract obstruction in patients who are undergoing living donor liver transplantation and the role of intraoperative echocardiography to detect and manage it.

Refractory Hypotension after Liver Allograft Reperfusion: A Case of Dynamic Left Ventricular Outflow Tract Obstruction

“…Systolic anterior motion/DLVOTO is a common occurrence after MV repair with an incidence between 2 and 16% ( 17 , 18 ). However, during liver transplantation, SAM/DLVOTO has been reported as the cause of hemodynamic compromise in a few cases where TEE was utilized for hemodynamic monitoring ( 6 – 8 , 16 , 19 , 20 ). Maslow et al characterized several preoperative echocardiographic parameters that can lead to anterior displacement of the MV coaptation point and cause DLVOTO in systole after MV repair ( 17 ).…”

“…Liver allograft reperfusion can be associated with significant cardiovascular instability and may require the administration of inotropes, vasopressors, and intravenous fluids, in order to avert cardiovascular collapse ( 1 – 8 ). The etiology of this cardiovascular depression is multifactorial and can result from several factors after unclamping of the portal vein, including: systemic release of the allograft preservative solution (cold and hyperkalemic fluid), blood-volume uptake by the liver allograft, the release of vasoactive mediators (such as inflammatory cytokines and free radicals), and acidic blood return from the liver and mesentery ( 1 – 5 , 9 , 10 ).…”

“…The combination of these factors can result in the postreperfusion syndrome (PRS), a phenomenon initially described by Aggarwal et al in 1987 ( 1 – 4 ). Significant hypotension may also occur after portal vein unclamping due to several other factors, such as: acute pulmonary embolus (from an inferior vena cava or portal vein thrombus), venous air embolism, acute right ventricular failure, dynamic left ventricular outflow tract obstruction (DLVOTO), and preload limitations (from torsion or obstruction of the inferior vena cava and massive blood loss) ( 1 , 2 , 6 – 8 , 11 ). The etiology of the hypotension therefore has to be investigated in a timely fashion, to ensure rapid and appropriate pharmacological therapy, and optimal patient outcomes.…”

Left ventricular outflow tract obstruction with systolic anterior motion of the mitral valve in patient with pericardial effusion caused by ascending aortic dissection -A case report-

“…However, LVOT obstruction also occurs in other conditions without cardiac history, such as mitral valve repair [2], myocardial infarction [3], dobutamine stress test [4], liver transplantation [5,6] and catecholamine infusion [7]. LVOT obstruction with SAM is induced by structural abnormalities such as small hyperdynamic left ventricular cavity, narrow LVOT, sigmoid septum, and displaced mobile elongated mitral leaflets [8].…”

Cirrhotic Cardiomyopathy and Liver Transplantation

“…Обычно данное осложнение становится ре-зультатом исходной гипертрофии левого желу-дочка, но может возникать и без нее при резком снижении нагрузки на миокард после ортотопи-ческой трансплантации печени. Именно поэтому дооперационные тесты с нагрузкой здесь не при-емлемы [31,32]. Для предоперационной оценки состояния миокарда и диагностики обструкции выходного тракта левого желудочка используют чреспище-водную эхокардиографию.…”