Percutaneous Ventricular Assist Device To Rescue a Patient with Profound Shock From a Thrombosed Prosthetic Mitral Valve

ABSTRACT: The TandemHeart® is a percutaneous ventricular assist device that has been approved to provide hemodynamic support in high-risk patients undergoing cardiac procedures, including percutaneous coronary interventions and aortic balloon valvuloplasty. Limited data exists for its role in stabilizing cardiogenic shock secondary to prosthetic valve dysfunction. In conclusion, we report the first case, to our knowledge, of profound cardiogenic shock secondary to an acutely thrombosed mechanical mitral valve in which the use of the TandemHeart was instrumental in rescuing a critically ill young female who made a full recovery. J INVASIVE CARDIOL 2008;20:E320–E323 The recent development of percutaneous left ventricular assist devices allows rapid achievement of circulatory support. One such device, the TandemHeart® percutaneous ventricular assist device (pVAD) (Cardiac Assist, Inc., Pittsburgh, Pennsylvania) provides a cardiac output of up to 5 L/min and has been approved for short-term hemodynamic support for high-risk patients undergoing cardiac procedures. It can be placed percutaneously in the cardiac catheterization laboratory using fluoroscopic guidance and has been primarily used to support patients undergoing high-risk percutaneous coronary intervention (PCI)1 and more recently during percutaneous aortic valve procedures.2 However, its use in the management of multiorgan failure secondary to a thrombosed prosthetic mitral valve has not been reported. We present the role of the TandemHeart device as a temporizing hemodynamic support for a critically ill young female with multiorgan failure secondary to a thrombosed prosthetic mitral valve. Case Report. A 35-year-old female presented on transfer from an outside hospital for further management of cardiogenic shock. The patient had a complicated past medical history including thoracic radiation and splenectomy for Hodgkin’s lymphoma, and subsequent chemotherapy for a relapse. In 1999 she developed symptomatic severe mitral regurgitation of unclear etiology. At that time, her left ventricular ejection fraction (LVEF) was normal and she underwent surgical repair of the mitral valve with insertion of a 26 mm Cosgrove flexible annuloplasty ring. One year later, in 2000, she presented with heart failure and was found to have severe mitral valve stenosis with coexisting severe tricuspid regurgitation. The patient underwent re-operation consisting of a mechanical mitral valve replacement using a 25 mm Carbomedics mechanical valve and a tricuspid ring annuloplasty with a 29 mm Duran ring. She remained asymptomatic until September, 2006, when she developed bilateral pleural effusions requiring thoracentesis. A transthoracic echocardiogram (TTE) in December 2006 revealed normal left ventricular function and a metallic prosthesis in the mitral position noted to have heavy reverberations precluding any comment on valvular excursion or stenosis. Over the subsequent months, she required 6 additional thoracenteses for recurrent bilateral pleural effusions prior to her admission in September 2007. While she had consistently taken warfarin for anticoagulation since the insertion of her prosthetic valve, warfarin therapy was temporarily discontinued during the periprocedural periods of each thoracentesis. In addition, she underwent a partial vulvectomy for cervical cancer 4 months prior to her presentation during which time warfarin therapy was held. Of note, although she did receive bridging anticoagulation with heparin during her vulvectomy, she was not given bridging anticoagulation for any of her thoracenteses procedures. She presented again to an outside institution in September 2007 with recurrent dyspnea and a large pleural effusion. Repeat TTE at the referring institution confirmed normal left ventricular function, severe pulmonary hypertension and elevated “E”-wave velocities across the mitral prosthesis, which was concerning for acute dysfunction of her mitral valve. On arrival to our institution, she appeared extremely ill with severe dyspnea and profound hypotension. She was noted to be centrally cyanosed, with a respiratory rate of 40 breaths/minute and an O2 saturation of 53% using a 100% re-breathing oxygen mask. She was on an intravenous dopamine infusion at 15 µg/kg/min, but remained hemodynamically unstable, with a resting sinus tachycardia of 130 beats per minute and a systemic blood pressure of 57/36 mmHg. On physical examination, she was noted to have marked distention of her jugular veins to the angle of her mandible, 3+ pitting edema of her lower extremities and inaudible mechanical clicks from her mitral valve. She was immediately intubated and placed on mechanical ventilation. Arterial blood gases post intubation revealed a pH of 7.0, pCO2 of 29 mmHg, and pO2 of 481 mmHg with a bicarbonate level of 7.6 mmol/L. TTE performed at the bedside demonstrated normal LVEF, the appearance of a thrombosed mechanical mitral valve with a peak gradient of 28 mmHg, severely decreased right ventricular function with dilation, severe tricuspid regurgitation and an estimated pulmonary pressure of 60 mmHg. Her general condition was adversely affected by the development of acute renal failure and a metabolic acidosis; her creatinine had risen to 1.9 mmol/L from a baseline of 0.9 mmol/L within 6 hours and her lactate level was elevated at 4.6 mmol/L. Cardiac surgery was consulted for consideration of emergent mitral valve replacement. However, this operation would be her third sternotomy in the setting of prior sternal radiation and given the acute decline in her respiratory, renal and metabolic status, it was felt that her outcome would be improved if she could first be stabilized with a percutaneous left ventricular assist device. In the catheterization laboratory, transesophageal echocardiography (TEE) confirmed that the prosthetic mitral valve leaflets were fixed in the semi-open position, with significant mitral regurgitation (Figures 1 and 2). The right and left atrial pressures were markedly elevated, with the left atrial pressure approaching the aortic diastolic pressures (Figure 3); the pulmonary artery pressure was 57/39 mmHg, with a mean of 46 mmHg (Figure 4) and a pulmonary arterial saturation of 36%. The systemic arterial pressure remained extremely low (69/47 mmHg, with a mean of 53 mmHg), and a systemic arterial saturation of 99% (Figure 3). The patient’s cardiac index using the Fick method was 1.1 L/min/m2 (body surface area of 1.8 m2). Based on the profoundly abnormal hemodynamics, the TandemHeart pVAD was placed. The technique for insertion of the TandemHeart pVAD has been previously described.1,3 Briefly, a transseptal puncture was made via the right femoral vein using intracardiac echocardiography (ICE) guidance and a 21 Fr cannula was placed in the left atrium. Arterial access was obtained from the left femoral artery and the tip of a 15 Fr cannula was positioned in the left external iliac artery. Thus, oxygenated blood was withdrawn from the left atrium, circulated via a centrifugal pump and re-entered into the left external iliac artery. Flow rates of 3.6 L/min were achieved with an increase in her cardiac index to 3.03 L/min/m2. Her pulmonary capillary wedge pressure decreased to 26 mmHg. Of note, selective coronary angiography demonstrated normal coronary arteries. Following the procedure, she returned to the coronary care unit and was weaned to low-dose inotropic support. Her urine output rapidly improved and her creatinine level returned to baseline by the next morning. Her metabolic state improved remarkably, with arterial blood gases showing a pH of 7.38, pCO2 of 42.3 mmHg, pO2 of 113 mmHg and a bicarbonate level at 22.6 mmol/L. However, as a consequence of her sustained low blood pressure prior to TandemHeart insertion, she developed “shock liver”, with a peak AST of 3,406 U/L and a INR of 5.3. These values rapidly improved with circulatory support and she was taken to the operating room 48 hours after placement of the pVAD. In the operating room, her valve was found to be thrombosed with pannus formation around the annulus (Figure 5). It was replaced with a 25 mm Medtronic Mosaic bioprosthetic valve (Medtronic, Inc., Santa Rosa, California). The TandemHeart pVAD was removed at the completion of the surgery. Postoperatively, the patient had acute tubular necrosis (ATN) which resolved spontaneously and she was discharged home 2 weeks later without further complications. Discussion. To our knowledge, this is the first reported use of the TandemHeart pVAD in a patient with cardiogenic shock from a thrombosed mechanical mitral valve. Case reports have been published using the TandemHeart pVAD for hemodynamic support in patients with cardiogenic shock from native aortic valve stenosis4 as a bridge to surgery, and also for hemodynamic support during percutaneous aortic balloon valvuloplasty.2 The role of the TandemHeart pVAD in our patient was specifically to provide hemodynamic support allowing improvement of the multiorgan failure that developed as a consequence of her cardiogenic shock and to optimize her outcome with a third cardiac surgery. The device clearly fulfilled this goal. Acute obstruction of the mitral valve, although rare, is a very serious and potentially fatal complication of a mechanical prosthetic valve. The AHA/ACC guidelines recommend surgery for an obstructed mechanical valve in patients with NYHA Class III–IV symptoms.5 However, surgical mortality in this group can be as high as 35%.6 In our patient, who had multiorgan failure and a third cardiac surgery, the operative risk was estimated at greater than 55%.7 Fibrinolysis, the only alternative treatment strategy for a thrombosed mechanical mitral valve, is not an optimal therapy. The largest study to date consists of 127 episodes of obstructive valve thrombosis (almost all left-sided) in 110 patients with mechanical valves who were treated with various thrombolytic agents.8 This study showed that thrombolytic therapy was only 71% successful, with greatest benefit in the aortic position. Multiple doses of thrombolytics were required in 40% of patients, and another 23% of patients required surgery because of a poor response to lysis. Importantly, the complication rate from fibrinolysis was 25%, including a 12% death rate. In the case presented, the patient was in dire condition and would have likely died soon after presentation without either surgery or the placement of hemodynamic support. Given the severe metabolic disarray and profound hemodynamic instability, it is doubtful that she would have survived an emergency operation. The TandemHeart pVAD allowed these factors to resolve prior to proceeding with an operation, likely improving her outcome by reducing her perioperative mortality risk to 20%.7 Alternative forms of hemodynamic support were considered, but thought inappropriate. Left ventricular assist device placement can be associated with significant time delay due to the complexity of the procedure, and we felt that it was not a suitable alternative due to the immediate need for hemodynamic support for this patient. Intra-aortic balloon pump (IABP) placement was also considered, but it would not help alleviate the increased preload due to the fixed, thrombosed prosthetic mitral valve. In this case, the TandemHeart pVAD not only restored cardiac output, but also decreased left atrial, and hence, pulmonary artery pressures. The hemodynamic benefits can be immediate,4 as they were for our patient in whom the acute metabolic, renal and pulmonary insults were reversed within 12 hours, rendering her a much better surgical candidate. The TandemHeart pVAD has been of proven benefit in a variety of clinical scenarios, including high-risk percutaneous transluminal coronary angioplasty,1 cardiogenic shock9 and percutaneous aortic valve replacement.10 We now report the first experience using the TandemHeart device in a patient with cardiogenic shock from a thrombosed mechanical mitral valve that provided an excellent patient outcome.

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