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We performed the 1st catheterization of an AbioCor™ implantable replacement heart, in a patient who had developed high right-sided pump pressures, to determine whether the high pressures were caused by graft kinking or obstruction.
Use of the AbioCor™ implantable replacement heart (ABIOMED®, Inc.; Danvers, Mass) in patients with refractory heart failure introduces a new physiology that returns their hemodynamic status to normal. We describe the case of a patient who underwent AbioCor implantation and developed high right-sided pump pressures during the early postoperative period. To determine whether the high pressures were caused by graft kinking or obstruction, we performed the 1st catheterization of an AbioCor pump.
The AbioCor implantable replacement heart is a fully implantable, mechanical replacement device that provides complete left- and right-sided pulsatile circulatory support. The 2-pound titanium and polyurethane pump consists of 2 artificial ventricles, 4 trileaflet valves, and a motor-driven hydraulic pumping system. A controller monitors and controls the pump rate. The AbioCor responds to the body's physiological changes through compensatory changes in motor speed, pump rate, or both. The AbioCor system transmits energy across the patient's skin by means of a transcutaneous energy transfer system, thereby minimizing the risk of infection that is generally associated with percutaneous power lines.
A 68-year-old man who had acute cardiac decompensation underwent AbioCor implantation after analysis of his prognostic markers showed a high probability of death within a month. He had a history of coronary artery disease, pulmonary hypertension, and severe congestive heart failure, as well as mild renal and hepatic dysfunction. Preoperatively, the pulmonary artery pressure was 90/32 mmHg (mean, 62 mmHg), and the pulmonary vascular resistance (PVR) was 6 Wood units. He was not eligible for heart transplantation because of the fixed, elevated PVR.
The AbioCor was implanted in the orthotopic position after complete excision of the native ventricles. The device was anastomosed to the left and right atria with a Dacron cuff. Portions of the atria were left intact. The complete implantation procedure has been described in detail elsewhere.1
During the early postoperative period, telemetry revealed an elevated right ventricular chamber pressure (95 mmHg), as indicated by high hydraulic pressures in the right ventricular pumping mechanism. Our efforts to decrease these pressures were unsuccessful, which led to concerns about impairment or restriction of blood flow in the outflow graft that led to the pulmonary artery. The results of transthoracic and transesophageal echocardiography were inconclusive; therefore, 1 week postoperatively, we performed a catheterization procedure.
A Swan-Ganz® pulmonary artery catheter (Baxter International, Inc.; Deerfield, Ill) was passed through the right atrial anastomosis and the right ventricular inflow valve into the right ventricular chamber (Fig. 1). After pressures were measured, the catheter was passed into the main pulmonary artery. The right ventricular pressure was 94/–13 mmHg (mean, 28 mmHg), and the pulmonary artery pressure was 72/33 mmHg (mean, 51 mmHg) (Fig. 2). Across the outflow valve of the device, the gradient was normal (~20 mmHg), with no evidence of pathologic flow obstruction. The pulmonary artery pressures remained high, but the device functioned normally for more than 6 months.
By performing catheterization of the AbioCor pump, we found that the pump was able to compensate for the patient's abnormal physiologic state. During the early postoperative period, high right-sided pump pressures resulted from the patient's elevated PVR—the condition that had precluded conventional cardiac transplanta-tion. Vasodilation to lower both the PVR and the high pump pressures subsequently led to peripheral vasodilatation that required volume infusions to maintain systemic perfusion. Although the device protects against left-sided heart failure and high left atrial pressures by automatically balancing right and left pump output, the volume overload eventually resulted in an elevated central venous pressure and hepatic dysfunction (de facto right heart failure) in our patient. Temporary dialysis and cessation of vasodilators resolved these problems. Although there was some risk of passing the catheter through the prosthetic valves of the device, we felt that the procedure was necessary to rule out the possibility of an obstruction in the pulmonic outflow conduit. The pulmonary pressures remained high but had no further effect on pulmonary function. Later, the right pump was able to overcome the high resistance and thus maintained adequate systemic cardiac output. Others have subsequently done similar catheterizations.2
The results of the catheterization procedure indicated no device abnormality or conduit obstruction; the knowledge gained was valuable in managing this patient and increased our understanding of the unique physiology created by this device. The AbioCor proved capable of compensating for a high PVR while maintaining normal systemic perfusion and low left atrial pressures. Although a high PVR does not require treatment, proper intravascular volume should be maintained in order to avoid high central venous pressures and passive congestion of the liver.
By recognizing the capabilities of the AbioCor and understanding the unique physiology that it creates, we may learn more about the physiologic derangement that occurs in patients who have chronic heart failure.
Address for reprints: Reynolds M. Delgado III, MD, Department of Cardiopulmonary Transplantation and Assist Devices, Texas Heart Institute, 6770 Bertner Avenue, Suite C-355, Houston, TX 77030. E-mail: ten.lop@odagledr